Fibrinogen Promotes Neutrophil Activation and Delays Apoptosis1 (original) (raw)

Journal Article

Carolina Rubel ,

División Inmunología, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina

,

Buenos Aires

,

Argentina

Address correspondence and reprint requests to Dr. Carolina Rubel, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina, Pacheco de elo 3081, 1425 Buenos Aires, Argentina. E-mail address: [email protected]

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Gabriela C Fernández ,

División Inmunología, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina

,

Buenos Aires

,

Argentina

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Graciela Dran ,

División Medicina Experimental, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina

,

Buenos Aires

,

Argentina

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Macarena Beigier Bompadre ,

Macarena Beigier Bompadre

División Inmunología, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina

,

Buenos Aires

,

Argentina

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Martín A Isturiz ,

División Inmunología, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina

,

Buenos Aires

,

Argentina

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Marina S Palermo

División Inmunología, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina

,

Buenos Aires

,

Argentina

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Accepted:

14 November 2000

Published:

01 February 2001

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Carolina Rubel, Gabriela C Fernández, Graciela Dran, Macarena Beigier Bompadre, Martín A Isturiz, Marina S Palermo, Fibrinogen Promotes Neutrophil Activation and Delays Apoptosis, The Journal of Immunology, Volume 166, Issue 3, February 2001, Pages 2002–2010, https://doi.org/10.4049/jimmunol.166.3.2002
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Abstract

The acute phase of the inflammatory response involves an increase in the concentrations of different plasma proteins that include fibrinogen (Fbg) and multiple proinflammatory mediators. In parallel, neutrophil activation is thought to play a crucial role in several inflammatory conditions, and it has been recently demonstrated that Fbg specifically binds to the α-subunit of CD11b/CD18 on neutrophil surface. Although several reports have shown that CD11b engagement modulates neutrophil responses, the effect of human Fbg (hFbg), one of CD11b physiologic ligands, has not been exhaustively investigated. We have now shown that incubation of purified neutrophils with hFbg induces a transient and rapid elevation of free intracellular Ca2+. This early intracellular signal is accompanied by changes in the expression of neutrophil activation markers, including enhancement of CD11b and CD66b, and down-regulation of FcγRIII. In addition, we have evaluated the effect of hFbg on two functional events related to expression and resolution of inflammation: cytotoxic capacity and rate of neutrophil apoptosis. We have found that activation of neutrophils by hFbg resulted in both enhancement of phagocytosis and Ab-dependent cellular cytotoxicity, and delay of apoptosis. We conclude that during inflammatory processes, soluble Fbg could influence neutrophil responses, increasing and prolonging their functional capacity.

Copyright © 2001 by The American Association of Immunologists

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