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革兰氏阴性菌血症患者血液吞噬细胞上Fcα受体I的表达增强与FcR-γ亚基的酪氨酸磷酸化有关。

Enhanced expression of Fc alpha receptor I on blood phagocytes of patients with gram-negative bacteremia is associated with tyrosine phosphorylation of the FcR-gamma subunit.

作者信息

Chiamolera M, Launay P, Montenegro V, Rivero M C, Velasco I T, Monteiro R C

机构信息

Divisions of Emergency Medicine, University of São Paulo, São Paulo, Brazil.

出版信息

Shock. 2001 Nov;16(5):344-8. doi: 10.1097/00024382-200116050-00004.

DOI:10.1097/00024382-200116050-00004
PMID:11699071
Abstract

Sepsis caused by gram-negative bacteria is a common finding having high incidence and mortality. Fc alpha RI (CD89), a receptor for immunoglobulin A (IgA), has been shown to mediate bacterial phagocytosis, which might play a role in the pathogenesis of sepsis. In this study the expression and function of Fc alpha RI were analyzed on blood monocytes and neutrophils of patients with bacteremia. We found a marked increased in expression of the alpha- and gamma-subunits of the Fc alpha RI on both types of cells in patients with gram-negative bacteremia, but not in patients with gram-positive bacteremia. This increase was independent of serum IgA levels. Fc alpha RI M(r) was lower on cells from gram-negative patients than on cells from controls (50-65 kDa versus 55-75 kDa), despite a similar 32-kDa backbone, indicating altered glycosylation. Increased levels of Fc alpha RI on blood phagocytes correlated with enhanced serum IL-6 levels, but not with IFN gamma or TNF-alpha. FcR-gamma chain associated with Fc alpha RI was phosphorylated in patients neutrophils, indicating functional engagement of this receptor during gram-negative sepsis. Increased expression and activation of Fc alpha RI-gamma 2 complexes following gram-negative infections suggests its involvement in host defense against bacteria.

摘要

革兰氏阴性菌引起的败血症很常见,发病率和死亡率都很高。免疫球蛋白A(IgA)的受体FcαRI(CD89)已被证明可介导细菌吞噬作用,这可能在败血症的发病机制中起作用。在本研究中,分析了菌血症患者血液单核细胞和中性粒细胞上FcαRI的表达和功能。我们发现革兰氏阴性菌血症患者的这两种细胞上FcαRI的α和γ亚基表达均显著增加,而革兰氏阳性菌血症患者则未出现这种情况。这种增加与血清IgA水平无关。尽管有相似的32 kDa主链,但革兰氏阴性菌血症患者细胞上的FcαRI M(r)低于对照组细胞(50 - 65 kDa对55 - 75 kDa),表明糖基化改变。血液吞噬细胞上FcαRI水平的升高与血清IL - 6水平升高相关,但与IFNγ或TNF - α无关。革兰氏阴性菌血症患者中性粒细胞中与FcαRI相关的FcR - γ链发生磷酸化,表明在革兰氏阴性菌败血症期间该受体发挥了功能作用。革兰氏阴性菌感染后FcαRI - γ2复合物表达和激活的增加表明其参与了宿主对细菌的防御。

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