Toll-like receptor (TLR) family is an important group of receptors through which the innate
immune systems recognizes invasive microbes, and is crucial for many aspects of microbial
elimination, including recruitment of phagocytes to infected tissue. However, when activated to
excess, TLRs can mediate pathology. Here, we comparatively assessed cytokines production,
TLR2 and TLR4 expressions, apoptotic rate and leucocytes recruitment in heart and liver of
C57BL/6 and BALB/c infected with Tulahuen strain. Plasma transaminases activity was also
investigated.
GOT and GPT activities were increased in infected BALB/c and C57BL/6 mice at all times
tested, although it was higher at 14 days post infection (dpi) in C57BL/6. Moreover, C57BL/6
liver showed a stronger pro-inflammatory cytokine profile (IL6, IL12 and TNF��) concomitantly
with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression.
Toll-like receptor (TLR) family is an important group of receptors through which the innate immune systems recognizes invasive microbes, and is crucial for many aspects of microbial elimination, including recruitment of phagocytes to infected tissue. However, when activated to excess, TLRs can mediate pathology. Here, we comparatively assessed cytokines production, TLR2 and TLR4 expressions, apoptotic rate and leucocytes recruitment in heart and liver of C57BL/6 and BALB/c infected with Tulahuen strain. Plasma transaminases activity was also investigated. GOT and GPT activities were increased in infected BALB/c and C57BL/6 mice at all times tested, although it was higher at 14 days post infection (dpi) in C57BL/6. Moreover, C57BL/6 liver showed a stronger pro-inflammatory cytokine profile (IL6, IL12 and TNF��) concomitantly
with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. Toll-like receptor (TLR) family is an important group of receptors through which the innate immune systems recognizes invasive microbes, and is crucial for many aspects of microbial elimination, including recruitment of phagocytes to infected tissue. However, when activated to excess, TLRs can mediate pathology. Here, we comparatively assessed cytokines production, TLR2 and TLR4 expressions, apoptotic rate and leucocytes recruitment in heart and liver of C57BL/6 and BALB/c infected with Tulahuen strain. Plasma transaminases activity was also investigated. GOT and GPT activities were increased in infected BALB/c and C57BL/6 mice at all times tested, although it was higher at 14 days post infection (dpi) in C57BL/6. Moreover, C57BL/6 liver showed a stronger pro-inflammatory cytokine profile (IL6, IL12 and TNF��) concomitantly
with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. Toll-like receptor (TLR) family is an important group of receptors through which the innate immune systems recognizes invasive microbes, and is crucial for many aspects of microbial elimination, including recruitment of phagocytes to infected tissue. However, when activated to excess, TLRs can mediate pathology. Here, we comparatively assessed cytokines production, TLR2 and TLR4 expressions, apoptotic rate and leucocytes recruitment in heart and liver of C57BL/6 and BALB/c infected with Tulahuen strain. Plasma transaminases activity was also investigated. GOT and GPT activities were increased in infected BALB/c and C57BL/6 mice at all times tested, although it was higher at 14 days post infection (dpi) in C57BL/6. Moreover, C57BL/6 liver showed a stronger pro-inflammatory cytokine profile (IL6, IL12 and TNF��) concomitantly
with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. Toll-like receptor (TLR) family is an important group of receptors through which the innate immune systems recognizes invasive microbes, and is crucial for many aspects of microbial elimination, including recruitment of phagocytes to infected tissue. However, when activated to excess, TLRs can mediate pathology. Here, we comparatively assessed cytokines production, TLR2 and TLR4 expressions, apoptotic rate and leucocytes recruitment in heart and liver of C57BL/6 and BALB/c infected with Tulahuen strain. Plasma transaminases activity was also investigated. GOT and GPT activities were increased in infected BALB/c and C57BL/6 mice at all times tested, although it was higher at 14 days post infection (dpi) in C57BL/6. Moreover, C57BL/6 liver showed a stronger pro-inflammatory cytokine profile (IL6, IL12 and TNF��) concomitantly
with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression.
Toll-like receptor (TLR) family is an important group of receptors through which the innate immune systems recognizes invasive microbes, and is crucial for many aspects of microbial elimination, including recruitment of phagocytes to infected tissue. However, when activated to excess, TLRs can mediate pathology. Here, we comparatively assessed cytokines production, TLR2 and TLR4 expressions, apoptotic rate and leucocytes recruitment in heart and liver of C57BL/6 and BALB/c infected with Tulahuen strain. Plasma transaminases activity was also investigated. GOT and GPT activities were increased in infected BALB/c and C57BL/6 mice at all times tested, although it was higher at 14 days post infection (dpi) in C57BL/6. Moreover, C57BL/6 liver showed a stronger pro-inflammatory cytokine profile (IL6, IL12 and TNF��) concomitantly
with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. Toll-like receptor (TLR) family is an important group of receptors through which the innate immune systems recognizes invasive microbes, and is crucial for many aspects of microbial elimination, including recruitment of phagocytes to infected tissue. However, when activated to excess, TLRs can mediate pathology. Here, we comparatively assessed cytokines production, TLR2 and TLR4 expressions, apoptotic rate and leucocytes recruitment in heart and liver of C57BL/6 and BALB/c infected with Tulahuen strain. Plasma transaminases activity was also investigated. GOT and GPT activities were increased in infected BALB/c and C57BL/6 mice at all times tested, although it was higher at 14 days post infection (dpi) in C57BL/6. Moreover, C57BL/6 liver showed a stronger pro-inflammatory cytokine profile (IL6, IL12 and TNF��) concomitantly
with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. with high levels of IL10 and TGF��. Hepatic leukocytes with CD3+, CD4+, CD11c+, and Gr1+
markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. markers were increased at 14 and 21dpi whereas F4/80+ only augmented at 14dpi in both mouse strains. NK+ cells from infected C57BL/6 were increased at 14 and 21dpi, and only at 14dpi in BALB/c.TLR2 and TLR4 mRNA were up-regulated in BALB/c at 14, 21 and 24dpi; however in C57BL/6 only was detected at 14dpi. Apoptotic nucleus from hepatic and cardiac tissue was observed in all infected mice, but the apoptotic rate was higher in liver of C57BL/6. Additionally, the caspase-3 cleavage was not detected in liver lysates. Altogether, our results suggest that the fatal hepatic injury found in infected C57BL/6 could be related to unbalance pro and anti-inflammatory cytokines production and differential TLR expression. Toll-like receptor (TLR) family is an important group of receptors through which the innate immune systems recognizes invasive microbes, and is crucial for many aspects of microbial elimination, including recruitment of phagocytes to infected tissue. However, when activated to excess, TLRs can mediate pathology. Here, we comparatively assessed cytokines production, TLR2 and TLR4 expressio
