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多种微生物败血症会破坏正常的中性粒细胞细胞外基质蛋白相互作用。

Polymicrobial sepsis disrupts normal neutrophil extracellular matrix protein interactions.

作者信息

Simms H H, D'Amico R

机构信息

Department of Surgery, Rhode Island Hospital/Brown University School of Medicine, Providence 02903.

出版信息

Circ Shock. 1992 Sep;38(1):1-8.

PMID:1327574
Abstract

The purpose of this study was to examine how intra-abdominal sepsis and extracellular matrix proteins (fibronectin, laminin) affect adherent polymorphonuclear leukocyte (PMN) function. Two groups of swine were studied: Group I (n = 5) underwent sham laparotomy; Group II (n = 8) underwent cecal ligation and incision. PMN adherent to either fibronectin (F) or laminin (L) had increased candicidal activity over buffer (B) by Group I but not by post-operative day 8 Group II PMN. (Percent specific release 51Cr-Group I--35.00, 68.25, 64.75% for B, F, and L; P less than 0.001 comparing B vs. F or L; Group II--14.25, 12.50, 12.75% for B, F, and L; P = NS comparing B vs. F or L.) To determine the mechanism for this finding, PMN priming was then assessed by evaluating both PMN adherence to extracellular matrix proteins and the cell surface expression of CR1/CR3 by using sheep RBC opsonized with C3b or C3bi. PMN activation was assayed by using MTT-Formazan, myeloperoxidase, and hypochlorous acid (HOCl) production. Fibronectin and laminin increased PMN adherence and CR1/CR3 expression over buffer by Group I and Group II animals. Fibronectin and laminin increased MTT-Formazan, myeloperoxidase, and HOCl production over buffer by Group I PMN but not POD 8 Group II PMN. These results suggest that untreated intra-abdominal sepsis partially abrogates the effect of extracellular matrix proteins on PMN function; in particular, the activation but not priming of adherent PMN by extracellular matrix proteins is reduced in this clinical situation.

摘要

本研究的目的是探讨腹腔内脓毒症和细胞外基质蛋白(纤连蛋白、层粘连蛋白)如何影响黏附的多形核白细胞(PMN)功能。研究了两组猪:第一组(n = 5)进行假剖腹手术;第二组(n = 8)进行盲肠结扎和切开。第一组PMN黏附于纤连蛋白(F)或层粘连蛋白(L)时,其杀菌活性相对于缓冲液(B)有所增加,但术后第8天的第二组PMN则没有。(51Cr特异性释放百分比——第一组——B、F和L分别为35.00%、68.25%和64.75%;B与F或L比较,P<0.001;第二组——B、F和L分别为14.25%、12.50%和12.75%;B与F或L比较,P =无显著性差异)。为了确定这一发现的机制,随后通过评估PMN对细胞外基质蛋白的黏附以及使用用C3b或C3bi调理的绵羊红细胞来评估CR1/CR3的细胞表面表达,来评估PMN的预激。通过使用MTT-甲臜、髓过氧化物酶和次氯酸(HOCl)生成来检测PMN的活化。第一组和第二组动物中,纤连蛋白和层粘连蛋白相对于缓冲液增加了PMN的黏附及CR1/CR3的表达。第一组PMN中,纤连蛋白和层粘连蛋白相对于缓冲液增加了MTT-甲臜、髓过氧化物酶和HOCl的生成,但术后第8天的第二组PMN则没有。这些结果表明,未经治疗的腹腔内脓毒症部分消除了细胞外基质蛋白对PMN功能的影响;特别是,在这种临床情况下,细胞外基质蛋白对黏附的PMN的活化作用降低,但预激作用未受影响。

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Polymicrobial sepsis disrupts normal neutrophil extracellular matrix protein interactions.多种微生物败血症会破坏正常的中性粒细胞细胞外基质蛋白相互作用。
Circ Shock. 1992 Sep;38(1):1-8.
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Granulocyte colony-stimulating factor reverses septic shock-induced polymorphonuclear leukocyte dysfunction.粒细胞集落刺激因子可逆转脓毒性休克诱导的多形核白细胞功能障碍。
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Interaction of human neutrophils and HL-60 cells with the extracellular matrix.人类中性粒细胞和HL-60细胞与细胞外基质的相互作用。
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Divalent cation substitution reveals CD18- and very late antigen-dependent pathways that mediate human neutrophil adherence to fibronectin.二价阳离子替代揭示了介导人类中性粒细胞黏附于纤连蛋白的CD18和极迟抗原依赖性途径。
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Untreated intra-abdominal sepsis: lack of synergism between polymorphonuclear leukocyte (PMN) complement receptors CR1/CR3 and IgG receptor FcRIII.未治疗的腹腔内脓毒症:多形核白细胞(PMN)补体受体CR1/CR3与IgG受体FcRIII之间缺乏协同作用。
J Trauma. 1990 Aug;30(8):1027-31. doi: 10.1097/00005373-199008000-00013.

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