Luissint, Anny-ClaudeWilliams, Holly C.Kim, WookiFlemming, SvenHilgarth, Roland S.O'Leary, Monique N.Denning, Tomothy L.Nusrat, AsmaParkos, Charles A.Azcutia Criado, Verónica2025-01-302025-01-302019Luissint, AC., Williams, H.C., Kim, W. et al. Macrophage-dependent neutrophil recruitment is impaired under conditions of increased intestinal permeability in JAM-A-deficient mice. Mucosal Immunol 12, 668–678 (2019). https://doi.org/10.1038/s41385-019-0143-710.1038/s41385-019-0143-7https://hdl.handle.net/20.500.14352/117343Junctional adhesion molecule-A (JAM-A) is a transmembrane glycoprotein expressed on leukocytes, endothelia, and epithelia that regulates biological processes including barrier function and immune responses. While JAM-A has been reported to facilitate tissue infiltration of leukocytes under inflammatory conditions, the contributions of leukocyte-expressed JAM-A in vivo remain unresolved. We investigated the role of leukocyte-expressed JAM-A in acute peritonitis induced by zymosan, lipopolysaccharide (LPS), or TNFα using mice with selective loss of JAM-A in myelomonocytic cells (LysM-Cre;Jam-afl/fl). Surprisingly, in LysM-Cre;Jam-afl/fl mice, loss of JAM-A did not affect neutrophil (PMN) recruitment into the peritoneum in response to zymosan, LPS, or TNFα although it was significantly reduced in Jam-aKO mice. In parallel, Jam-aKO peritoneal macrophages exhibited diminished CXCL1 chemokine production and decreased activation of NF-kB, whereas those from LysM-Cre;Jam-afl/fl mice were unaffected. Using Villin-Cre;engAttribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/journal articlehttps://doi.org/10.1038/s41385-019-0143-7https://www.sciencedirect.com/science/article/pii/S1933021922004135?via%3Dihubopen access612JAM-ANeutrophilsIntestinalPermeabilityFisiología animal (Farmacia)24 Ciencias de la Vida