Host-fungal interface in the liver during C. albicans infection: steatosis, apoptosis hepathocellular and association with fungal infectivity

RENNA M.S; CORREA SG; PARAJE G; PORPORATTO C; CORREA S.G; SOTOMAYOR C.E

Montreal, Canada

Congreso; 12th International Congress of Immunology and 4th Annual Conference of FOCIS.; 2004

  Candida albicans is the major fungal pathogen in humans, particularly in immunocompromised patients. C.albicans grows as a member of the flora in normal hosts; however in immunocompromised hosts, the transition of C. albicans into an opportunistic pathogen is not uncommon and disseminated candidiasis of endogenous origin may occur. The gastrointestinal mucosa is probably the most common portal of entry of C.albicans for hematogenous dissemination. During the progression of disease transcriptional program linking morphogenesis with other virulence factor are activated. Little is know about lipases produced by the fungus and its role in the pathogenesis of infection.  At early stages of the infection, the liver constitutes the first barrier for the control of fungal spreading. The ability of this organ to limit the growth of the yeast and to mount an efficient inflammatory reaction may be crucial in determining the outcome of the fungal infection. Liver function depends on the integrated activity of different hepatic cells and the injury of the organ could result of disintegrated intracellular functions. Recently, we developed a model of C. albicans infection suitable to evaluate the contribution of innate immune mechanisms and the role of the liver in the control of this opportunistic fungal infection in normal and immunossuppresed hosts. In our approach, the exposure to stress modifies the immune status of the host increasing the susceptibility for this fungal infection.