Pathogenesis I: interactions of host cells and fungi

The interactions of host cells and fungi during infection represent a compl ex interplay. Although T helper 1 (Th1)-mediated immunity is primarily resp onsible for acquired resistance to Paracoccidioides brasiliensis, studies h ave demonstrated that polymorphonuclear neutrophils play a critical role in providing an early resistance to this organism. One study has shown that t he invasiveness of Candida albicans requires adherence, particularly to end othelial cells, which in turn are stimulated to express various cell-marker s and pro-inflammatory cytokines as part of a proactive resistance to invas ion. Somewhat in contrast to infection with C. albicans, it has been shown that the capsular glucuronoxylomannan of Cryptococcus neoformans causes the shedding of host-cell adherence molecules (L-selectins) needed for the mig ration of host-inflammatory cells to sites of infection and likely explains , in part, the reduced host inflammatory response to this organism. Resista nce to aspergillosis is often associated with the immune status of the host . In one set of studies, it has been demonstrated that lymphocytes have lit tle direct effect on the organism, but that antigen-presenting dendritic ce lls stimulate the production of Th1 cytokines, suggesting a positive role f or the dendritic cell in host-response. Similarly, another study has shown that among the regulatory cytokine networks that Th2-associated cytokines ( e.g., interleukin-10) likely play a detrimental role in the resistance of t he host to Aspergillus fumigatus.