Interleukin 1α Is Critical for Resistance against Highly Virulent Aspergillus fumigatus Isolates.

摘要: ABSTRACT Heterogeneity among Aspergillus fumigatus isolates results in unique virulence potential and inflammatory responses. How these drive specific immune responses how this affects fungally induced lung damage disease outcome are unresolved. We demonstrate that the highly virulent CEA10 strain is able to rapidly germinate within immunocompetent environment, inducing greater damage, vascular leakage, interleukin 1α (IL-1α) release than low-virulence Af293 strain, which germinates with a lower frequency environment. Importantly, clearance of was consequently dependent on IL-1α, contrast Af293. The IL-1α occurred by caspase 1/11- P2XR7-independent mechanism but calpain activity. Our finding early fungal conidium germination drives IL-1α-dependent inflammation supported three independent experimental lines. First, pregermination prior vivo challenge an neutrophil response. Second, more EVOL20 derived from Af293, airways, leading enhanced clearance. Third, primary environmental A. under airway conditions follow same trend toward dependency. data support hypothesis phenotypic variation significantly contributes outcomes.