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Suppression of cytokine‐mediated β 2 ‐integrin activation on circulating neutrophils in critically ill patients
Author(s) -
Rosenbloom Alan J.,
Pinsky Michael R.,
Napolitano Christopher,
Nguyen ThuSong,
Levann Douglas,
Pencosky Nicole,
Dorrance Adrienne,
Ray Barry K.,
Whiteside Theresa
Publication year - 1999
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.66.1.83
Subject(s) - integrin alpha m , integrin , tumor necrosis factor alpha , receptor , immunology , inflammation , biology , alpha (finance) , cytokine , microbiology and biotechnology , medicine , endocrinology , immune system , biochemistry , construct validity , nursing , patient satisfaction
The β 2 integrin CD11b plays a central role in inflammation and the systemic inflammatory response syndrome (SIRS). The CD11b molecule activates in two ways: the density of membrane‐bound CD11b up‐regulates and the molecule undergoes a conformational change that confers adhesiveness to counter‐receptors. We studied the kinetics of CD11b activation in patients with SIRS. We found a significantly diminished CD11b activation in response to tumor necrosis factor α (TNF‐α). This affected all circulating polymorphonuclear neutrophils (PMN) and was an intrinsic property of the cells and not due to antagonism by soluble TNF‐α receptors or loss of cellular receptors for TNF‐α. Diminished responsiveness correlated with the severity of organ failure and lasted for months in some patients but had no impact on mortality. We speculate that reduced CD11b responsiveness in SIRS contributes to the high risk of recurrent infection, but that it may also be protective against excessive PMN activation within the vascular space. J. Leukoc. Biol. 65: 83–89; 1999.