Candida albicans infection produces elongated hyphae resistant to phagocytic clearance compelling alternative neutrophil effector mechanisms to destroy these physically large microbial structures. Additionally, all tissue-based neutrophilic responses to fungal infections necessitate contact with the extracellular matrix (ECM). Neutrophils undergo a rapid, ECM-dependent mechanism of homotypic aggregation and NETosis in response to C.
View Article and Find Full Text PDFRelease of neutrophil extracellular traps (NETs) is a significant antimicrobial host defense mechanism in adults. In neonates, fungal sepsis is a frequent cause of morbidity and mortality and may be a consequence of inadequate neutrophil defense functions. Like neutrophils from adult donors, we found that neutrophils from neonates formed robust cellular aggregates and released NETs in response to fungal β-glucan and Candida albicans hyphae when presented with extracellular matrix.
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