“In a skin-infection model involving pathogenic bacteria and fungi, microbial adhesion to myeloid cells initiated an early innate-defense phase through Piezo1-dependent leukotriene B4, interleukin-1α, and CXCL1 signaling that recruited neutrophils before canonical pattern-recognition signaling; a later phase depended on Toll-like receptors and CXCL2.”

Checks out so far. 2 hold up so far.

0.8963 under ledger-default@0.3.0 at snapshot 27745 for all claims together. The number is the model's figure for every checkable claim holding at once, treating them as independent.

The statement as a whole, read from the 2 claims below. Each claim is scored on its own; this reading only counts them. Provisional until audited.

Review 75% done · 25% counted in review coverage · 50% by the claims' own author only (2 claims, 8 checks)

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Checked in Galedra: score 0.90, strongly supported · not yet reviewed by anyone else “In a skin-infection model involving pathogenic bacteria and fungi, microbial adhesion to myeloid cells initiated an early innate-defense phase through Piezo1-dependent leukotriene B4, interleukin-1α…” https://galedra.org/investigations/01a0ead7-10e9-720b-ab9a-9a4abc19760f

“In a skin-infection model with pathogenic bacteria and fungi, microbial adhesion initiated an early PRR-independent neutrophil-recruitment phase by engaging Piezo1 and promoting leukotriene B4, interleukin-1α, and CXCL1 signaling.”

Supported · 0.9601 under ledger-default@0.3.0 at snapshot 27745 · review checks 1 of 4 · provisional until audited.

3 of 4 review checks done · 1 counted · 2 by the author only

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“In the same skin-infection model, a later neutrophil-recruitment phase depended on Toll-like receptor and CXCL2 signaling, marking a transition to canonical pathogen-driven innate immunity.”

Supported · 0.9335 under ledger-default@0.3.0 at snapshot 27745 · review checks 1 of 4 · provisional until audited.

3 of 4 review checks done · 1 counted · 2 by the author only

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