PMID: 2490078Jan 1, 1989Paper

Pulmonary defense mechanisms against opportunistic fungal pathogens

Immunology Series
A R Waldorf

Abstract

Though of critical importance, nonimmune host defense mechanisms against aspergillosis and mucormycosis are not completely understood. Prevention of these infections presumably requires control of either spore germination and/or hyphal growth by the host. The data suggest that the host provides an important barrier to infection by control of spore or conidia germination, the critical step involving conversion of the fungus to its tissue-invasive form. The mechanisms of host defense against A. fumigatus are not strictly dependent on inhibition of conidia germination. Rather, pulmonary defense against Aspergillus appears to depend to a greater degree on early killing of fungal conidia by alveolar macrophages. In contrast, prevention of mucormycosis appears to require inhibition of fungal spore germination by the bronchoalveolar macrophage, thereby preventing conversion of the fungus to its hyphal form, although resident bronchoalveolar macrophages are unable to kill R. oryzae spores. Thus, host pulmonary defenses to Rhizopus and Aspergillus vary, even in normal animals. The tissue-invasive hyphal forms of the fungi which cause aspergillosis and mucormycosis are too large to be ingested by phagocytic cells. Although macrophages an...Continue Reading

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