title: Pathogenesis I: interactions of host cells and fungi.
abstract: The interactions of host cells and fungi during infection represent a complex interplay. Although T helper 1 (Th1)-mediated immunity is primarily responsible for acquired resistance to Paracoccidioides brasiliensis, studies have demonstrated that polymorphonuclear neutrophils play a critical role in providing an early resistance to this organism. One study has shown that the invasiveness of Candida albicans requires adherence, particularly to endothelial cells, which in turn are stimulated to express various cell-markers and pro-inflammatory cytokines as part of a proactive resistance to invasion. 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 migration of host-inflammatory cells to sites of infection and likely explains, in part, the reduced host inflammatory response to this organism. Resistance to aspergillosis is often associated with the immune status of the host. In one set of studies, it has been demonstrated that lymphocytes have little direct effect on the organism, but that antigen-presenting dendritic cells stimulate the production of Th1 cytokines, suggesting a positive role for 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 the host to Aspergillus fumigatus.
authors.affiliation: Division of Infectious Diseases, Santa Clara Valley Medical Center, and California Institute for Medical Research, San Jose 95128-2699, USA. Karl.Clemons@slip.net
authors.forename: K V
authors.initials: KV
authors.lastname: Clemons
authors.forename: V L
authors.initials: VL
authors.lastname: Calich
authors.forename: E
authors.initials: E
authors.lastname: Burger
authors.forename: S G
authors.initials: SG
authors.lastname: Filler
authors.forename: M
authors.initials: M
authors.lastname: Grazziutti
authors.forename: J
authors.initials: J
authors.lastname: Murphy
authors.forename: E
authors.initials: E
authors.lastname: Roilides
authors.forename: A
authors.initials: A
authors.lastname: Campa
authors.forename: M R
authors.initials: MR
authors.lastname: Dias
authors.forename: J E
authors.initials: JE
authors.lastname: Edwards
authors.forename: Y
authors.initials: Y
authors.lastname: Fu
authors.forename: G
authors.initials: G
authors.lastname: Fernandes-Bordignon
authors.forename: A
authors.initials: A
authors.lastname: Ibrahim
authors.forename: H
authors.initials: H
authors.lastname: Katsifa
authors.forename: C G
authors.initials: CG
authors.lastname: Lamaignere
authors.forename: L H
authors.initials: LH
authors.lastname: Meloni-Bruneri
authors.forename: J
authors.initials: J
authors.lastname: Rex
authors.forename: C A
authors.initials: CA
authors.lastname: Savary
authors.forename: C
authors.initials: C
authors.lastname: Xidieh
mesh_terms: D000818:Animals; D001232:Aspergillus fumigatus / Q000276:immunology / Q000472:pathogenicity*; D002176:Candida albicans / Q000276:immunology / Q000472:pathogenicity*; D003455:Cryptococcus neoformans / Q000276:immunology / Q000472:pathogenicity*; D006801:Humans; D007109:Immunity; D051379:Mice; D009181:Mycoses / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology; D010228:Paracoccidioides / Q000276:immunology / Q000472:pathogenicity*