Resumen:
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.