Neutrophils are key for host protection from fungal infection due to their potent intra- and extracellular defense mechanisms against fungi. How neutrophils, which do not normally reside in the tissue, find their way to the site of infection is not fully understood. Although IL-17 was proposed to be involved in this process, we have recently shown that the neutrophil recruitment during oropharyngeal candidiasis is independent of the IL-17 pathway. This project addresses the role of keratinocyte-derived IL-1α for neutrophil recruitment in response to C. albicans infection and how IL-1 signaling coordinates a cellular crosstalk between keratinocytes and endothelial cells to promote an effective neutrophil response for optimal control of acute fungal infection in the oral mucosa.
Funding: Swiss National Science Foundation (Sinergia)
IL-1α expression in the C. albicans-infected oral epithelium