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Mechanoregulation of Human Neutrophil Host Defense and Survival
Author(s) -
O'Brien Xian,
Elisseou Nicholas,
Flores Estefany,
Patel Dipan,
Morrissette Cole,
Loosley Alex,
Reichner Jonathan
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.505.1
Subject(s) - phagocytosis , chemotaxis , respiratory burst , microbiology and biotechnology , degranulation , immunology , biology , motility , innate immune system , mechanosensitive channels , inflammation , receptor , immune system , biochemistry , ion channel
Neutrophils are an essential component of the inflammatory response, acting as the first responders to injury and infection. Because they are able to migrate into any tissue in the body, they necessarily encounter different physical microenvironments. Neutrophils traveling through different tissues encounter distinctive mechanical cues that affect their morphology, motility, and function. To understand how mechanosensing affects the phagocytic and antimicrobial functions of primary human neutrophils, we examined dectin‐mediated, Fcγ‐mediated. and complement‐mediated phagocytosis, the phagocytosis of apoptotic bodies, markers of respiratory burst and degranulation, IL‐8 production, NETosis, and cell survival on fibronectin coated subtracted of differing compliance. While respiratory burst and IL‐8 production were independent of substrate stiffness, we found a mechanoregulatory component to neutrophil degranulation, NETosis, and cell survival. We additionally characterize mechanosensitive differences in phagocytic receptor function and identify an oppositional regulatory role for Rho Kinase. These data provide clear evidence that neutrophil host defense and survival are directly affected by mechanical cues in the tissue microenvironment.