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Neutrophil recruitment to inflamed joints can occur without cellular priming.

Journal article
Authors Lena Björkman
Karin Christenson
Lisa Davidsson
Jonas Mårtensson
Firoozeh Amirbeagi
Amanda Welin
Huamei Forsman
Anna Karlsson
Claes Dahlgren
Johan Bylund
Published in Journal of leukocyte biology
Volume 105
Issue 6
Pages 1123-1130
ISSN 1938-3673
Publication year 2019
Published at Institute of Odontology
Institute of Medicine, Department of Rheumatology and Inflammation Research
Pages 1123-1130
Language en
Subject categories Other Medical Sciences


Recruitment of neutrophils from blood to tissues is a cardinal event in inflammation during which neutrophils switch from a resting, naive state to a preactivated, primed phenotype; the priming process is characterized by alterations in the composition of cell surface adhesins, for example, shedding of l-selectin and mobilization of granule-stored integrins to the cell surface. Ligation of chemotactic receptors and interactions with the endothelial lining are established triggers of neutrophil priming and in line with this, in vivo transmigrated neutrophils obtained from tissues are typically highly primed. We here characterize the priming of neutrophils brought about by in vivo recruitment from blood to inflamed joints by the analyses of synovial fluid and blood from patients with inflammatory arthritis. For comparisons, we used controlled in vivo models of neutrophil transmigration to skin of healthy subjects. In contrast to the residing view and in vivo transmigrated neutrophils from skin models, neutrophils from synovial fluid were often surprisingly resting and phenotypically very similar to naive cells isolated from peripheral blood; synovial fluid cells often retained l-selectin and had undergone minimal up-regulation of integrin receptors. In complete agreement with our in vivo findings, cell-free synovial fluid was potently chemotactic without triggering alteration of surface receptors also in vitro. We conclude that tissue recruitment of neutrophils does not by default trigger l-selectin shedding and granule mobilization, and the chemoattractant(s) guiding neutrophils to synovial fluid apparently operate without inducing cellular priming.

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