INTRACELLULAR AND EXTRACELLULAR DEFENSES OF HUMAN PHAGOCYTES AGAINST BLASTOMYCES DERMATITIDIS CONIDIA AND YEASTS

  • 1 January 1985
    • journal article
    • research article
    • Vol. 105  (6) , 737-750
Abstract
The lesions of blastomycosis are characterized by both suppuration and granuloma formation, but the relative roles of human neutrophils, monocytes and macrophages against B. dermatitidis are poorly defined. B. dermatitidis yeasts are generally too large to be ingested by polymorphonuclear neutrophils (PMN), and are killed predominantly by external PMN attachment and degranulation, whereas conidia are first ingested, then killed. PMN function is maximal in the presence of serum, divalent cations and complement, and killing is more efficient for conidia (.apprx. 50%) than for yeasts (.apprx. 20%). PMN that have degranulated, but remain attached to yeasts, block access by contiguous PMN. When degranulated PMN are removed, allowing access by fresh PMN, there is a further increment in yeast killing. Both conidia and yeasts are killed by predominantly oxidative PMN mechanisms, with conidia being greater activators of the respiratory burst, and proportionately more influenced by oxidative inhibitors. Peripheral blood monocytes can kill conidia (.apprx. 35%), but are feebly active against yeasts (.apprx. 5%). Monocyte-derived macrophages kill .apprx. 90% of conidia and 40% of yeasts. The dramatic susceptibility of conidia, the infective particles of B. dermatitidis, to nonspecific phagocytic host defenses may help to explain the relative rarity of blastomycosis as a clinical problem. The presence of PMN in lesions of blastomycosis may indicate an active, although limited, role of these cells in host defense against B. dermatitidis yeasts.