ABSTRACT Batrachochytrium dendrobatidis continues to cause declines in amphibian populations worldwide, and it remains unclear why skin defenses often fail to control the infection. Although amphibians have a complex, multifunctional immune system, the chytridiomycosis agent seems to have evolved countermeasures that enable it to survive and eventually impair critical skin functions. Previous studies show that B. dendrobatidis cells or cell-free supernatants inhibit lymphocytes by inducing apoptosis, suggesting impaired local cell killing. However, there is little evidence of lymphocyte recruitment to chytrid-infected skin, implying the fungus may also inhibit the functions of antigen-presenting cells. Here, we demonstrate that phagocytosis by peritoneal macrophages is significantly reduced by co-culture with live or heat-killed B. dendrobatidis zoosporangia, freeze-thawed zoospores, fungal cell-free supernatants, or cell-wall fragments. The phagocytic capacity of frog bone marrow-derived macrophages, differentiated by colony-stimulating factor-1 (CSF-1) or interleukin-34 (IL-34) (key macrophage growth factors), as well as immortalized mammalian macrophages, is also impaired. Inhibition of mammalian macrophages suggests that these inhibitory factors are not restricted to amphibian cells. Overall, these studies indicate that B. dendrobatidis cells and their components can hinder the recognition and function of macrophages that reside in or enter the skin to clear infections. This disabling of host phagocytosis is undoubtedly central to how B. dendrobatidis prevents effective innate and adaptive immune responses in the skin.
Rollins-Smith et al. (Tue,) studied this question.