Batrachochytrium dendrobatidis, an emergent pathogen linked to amphibian declines, produces factors that inhibit adaptive immunity in amphibians and mammals


Meeting Abstract

126.2  Monday, Jan. 7  Batrachochytrium dendrobatidis, an emergent pathogen linked to amphibian declines, produces factors that inhibit adaptive immunity in amphibians and mammals. FITES , JS*; PARKER COLLIER, SM; OSWALD-RICHTER, KA; RAMSEY, JR; GAMMILL, WM; ROLLINS-SMITH, LA; Vanderbilt University; Vanderbilt University; Vanderbilt University; James Madison University; Vanderbilt University; Vanderbilt University jeffrey.s.fites@vanderbilt.edu

Batrachochytrium dendrobatidis (Bd) is a pathogenic chytrid fungus that infects the keratinized epithelium of amphibian skin to cause the lethal disease chytridiomycosis, which is linked to global amphibian declines. While adaptive immune defenses appear to be involved in resistance, a robust response is often lacking; and the mechanisms by which Bd avoids immune surveillance are not well understood. One hypothesis to explain the ineffective immune responses is that this fungus produces virulence factors that inhibit lymphocyte functions. To address this hypothesis, we studied the effects of Bd cells or supernatants on in vitro proliferation of Xenopus laevis splenic lymphocytes induced by PHA or other activators. Proliferation was inhibited by Bd cells or cell-free factors released by Bd. A closely related non-pathogenic chytrid, Homolaphlyctis polyrhiza, was poorly able to inhibit lymphocyte functions suggesting that Bd has unique virulence factors. These factors induced splenocyte apoptosis, activating both caspase 8 and caspase 9 pathways. Bd factors also inhibited activation and induced apoptosis in murine and human lymphocytes. Ongoing studies of the molecular nature of the fungal virulence factors suggest that they are soluble, non-protein components of the Bd cell wall. These results suggest that Bd has evolved a mechanism to impair adaptive immunity in host amphibians in order to colonize the skin. The inhibitory factors appear to target a pathway shared between amphibians and mammals. Research Support: NSF grants 0843207 and 1121758 to LR-S

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