Neurocandidiasis is a serious form of bloodstream infection with 50% of mortality, associated
with congenital or acquired immunodeficiencies. With the aim to explore the ethiopathogenic
mechanisms involved in this mycosis, we developed a murine in vivo model. C57Bl/6 mice were
injected iv with 5.105, 1.106 or 2,5.106 viable yeasts of C. albicans and the colonization
assessed 4, 12, 24, 48 and 72h post-infection. Candida was able to impinge, get through the BBB and settle down in the brain parenchyma as was confirmed by the recovery of the CFU 4h after the microorganism administration. The immunostaining with anti-GFAP and anti-CD11b (Astrocytes and Microglia marker respectively), revealed the presence of both reactive astroand microgliosis (IF). Interestingly, we detected neuronal degeneration associated to the infection (FJB/A-Cu-Ag stain) and a significant number of TUNEL+ cells. The local balance
between pro- (IL-1â and TNF-á) and anti-inflammatory (TGF-â and IL-10) cytokines indicated a
break-up of the niche homeostasis promoting a Th1 profile (ELISA). This model reproduces human pathology and provides evidence not reported yet in support of neuronal degeneration and apoptosis+ and/or pyroptosis+ cells after a systemic induced infection with C. albicans.
injected iv with 5.105, 1.106 or 2,5.106 viable yeasts of C. albicans and the colonization
assessed 4, 12, 24, 48 and 72h post-infection. Candida was able to impinge, get through the BBB and settle down in the brain parenchyma as was confirmed by the recovery of the CFU 4h after the microorganism administration. The immunostaining with anti-GFAP and anti-CD11b (Astrocytes and Microglia marker respectively), revealed the presence of both reactive astroand microgliosis (IF). Interestingly, we detected neuronal degeneration associated to the infection (FJB/A-Cu-Ag stain) and a significant number of TUNEL+ cells. The local balance
between pro- (IL-1â and TNF-á) and anti-inflammatory (TGF-â and IL-10) cytokines indicated a
break-up of the niche homeostasis promoting a Th1 profile (ELISA). This model reproduces human pathology and provides evidence not reported yet in support of neuronal degeneration and apoptosis+ and/or pyroptosis+ cells after a systemic induced infection with C. albicans.
assessed 4, 12, 24, 48 and 72h post-infection. Candida was able to impinge, get through the
BBB and settle down in the brain parenchyma as was confirmed by the recovery of the CFU 4h
after the microorganism administration. The immunostaining with anti-GFAP and anti-CD11b
(Astrocytes and Microglia marker respectively), revealed the presence of both reactive astroand
microgliosis (IF). Interestingly, we detected neuronal degeneration associated to the
infection (FJB/A-Cu-Ag stain) and a significant number of TUNEL+ cells. The local balance
between pro- (IL-1â and TNF-á) and anti-inflammatory (TGF-â and IL-10) cytokines indicated a
break-up of the niche homeostasis promoting a Th1 profile (ELISA). This model reproduces human pathology and provides evidence not reported yet in support of neuronal degeneration and apoptosis+ and/or pyroptosis+ cells after a systemic induced infection with C. albicans.
between pro- (IL-1â and TNF-á) and anti-inflammatory (TGF-â and IL-10) cytokines indicated a
break-up of the niche homeostasis promoting a Th1 profile (ELISA). This model reproduces human pathology and provides evidence not reported yet in support of neuronal degeneration and apoptosis+ and/or pyroptosis+ cells after a systemic induced infection with C. albicans.
break-up of the niche homeostasis promoting a Th1 profile (ELISA). This model reproduces
human pathology and provides evidence not reported yet in support of neuronal degeneration
and apoptosis+ and/or pyroptosis+ cells after a systemic induced infection with C. albicans.
+ and/or pyroptosis+ cells after a systemic induced infection with C. albicans.