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Evidence item

The excerpt directly reports the pathogenic bacteria/fungi skin-infection model and the early PRR-independent, adhesion-triggered Piezo1–LTB4–IL-1α–CXCL1 pathway that recruits neutrophils. DIRECT_TEXT

Authenticity UNVERIFIED · extraction UNVERIFIED · independence group none (unreviewed) · created seq 24025

Source: Microbial adhesion promotes Piezo1 activation to initiate innate immunity · locator {} · excerpt hash sha256:9b031e087bfafcad202526359a564e49d1cfacd714576f150ff1e3d71b7c06f6

Exact excerpt
Using a skin infection model with pathogenic bacteria and fungi, we demonstrate that neutrophil recruitment occurs in two sequential phases. The early phase is PRR-independent and instead driven by microbial adhesion, which engages the mechanosensitive ion channel Piezo1 to promote leukotriene (LT)B4 production. Together with interleukin-1α, LTB4 induces CXCL1 release, triggering neutrophil infiltration via the same circuit at play during sterile inflammation. By contrast, the late phase is toll-like receptor (TLR)- and CXCL2-dependent, marking a transition to the canonical, pathogen-driven response.

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