Literature DB >> 16107231

Complement-induced Impairment of the Innate Immune System During Sepsis.

Eric A Albrecht1, Peter A Ward.   

Abstract

The complement system is an integral part of innate immunity and is chiefly responsible for controlling bacterial infections, especially those involving gram- negative organisms. To accomplish this task, serum proteins engage in a series of enzymatic cascades. The cleaved proteins assemble pores on membranous structures, which lead to cell lysis. During this process, powerful inflammatory mediators are produced, including the anaphylatoxins, C5a, C3a, and the membrane attack complex (MAC). Under systemic inflammatory conditions, an overactive complement system may compromise the effectiveness of innate immunity. We review the detrimental effects that are caused by uncontrolled complement activation during sepsis.

Entities:  

Year:  2005        PMID: 16107231     DOI: 10.1007/s11908-005-0008-y

Source DB:  PubMed          Journal:  Curr Infect Dis Rep        ISSN: 1523-3847            Impact factor:   3.725


  50 in total

Review 1.  Complement components of the innate immune system in health and disease in the CNS.

Authors:  P Gasque; Y D Dean; E P McGreal; J VanBeek; B P Morgan
Journal:  Immunopharmacology       Date:  2000-08

2.  The classical and alternative pathways of complement activation play distinct roles in spontaneous C3 fragment deposition and membrane attack complex (MAC) formation on human B lymphocytes.

Authors:  Robert Graham Quinton Leslie; Claus Henrik Nielsen
Journal:  Immunology       Date:  2004-01       Impact factor: 7.397

3.  Inhibition of C5a-induced inflammation with preserved C5b-9-mediated bactericidal activity in a human whole blood model of meningococcal sepsis.

Authors:  Tom Sprong; Petter Brandtzaeg; Michael Fung; Anne M Pharo; E Arne Høiby; Terje E Michaelsen; Audun Aase; Jos W M van der Meer; Marcel van Deuren; Tom E Mollnes
Journal:  Blood       Date:  2003-07-24       Impact factor: 22.113

Review 4.  Complement and autoimmunity.

Authors:  Susan A Boackle
Journal:  Biomed Pharmacother       Date:  2003-09       Impact factor: 6.529

5.  Mechanisms for the diminished neutrophil exudation to secondary inflammatory sites in infected patients with a systemic inflammatory response (sepsis).

Authors:  N A Ahmed; S McGill; J Yee; F Hu; R P Michel; N V Christou
Journal:  Crit Care Med       Date:  1999-11       Impact factor: 7.598

6.  Untreated intra-abdominal sepsis: lack of synergism between polymorphonuclear leukocyte (PMN) complement receptors CR1/CR3 and IgG receptor FcRIII.

Authors:  H H Simms; R D'Amico; K Burchard
Journal:  J Trauma       Date:  1990-08

7.  Trauma serum suppresses superoxide production by normal neutrophils.

Authors:  M E Lanser; G E Brown; R Mora; W Coleman; J H Siegel
Journal:  Arch Surg       Date:  1986-02

8.  Expression of the complement C3a and C5a receptors after permanent focal ischemia: An alternative interpretation.

Authors:  Scott R Barnum; Robert S Ames; Peter R Maycox; Sarah J Hadingham; Jackie Meakin; David Harrison; Andrew A Parsons
Journal:  Glia       Date:  2002-04-15       Impact factor: 7.452

9.  Septic plasma suppresses superoxide anion synthesis by normal homologous polymorphonuclear leukocytes.

Authors:  J J Zimmerman; J R Millard; C Farrin-Rusk
Journal:  Crit Care Med       Date:  1989-12       Impact factor: 7.598

10.  Complement C5a receptor antagonist attenuates multiple organ injury in a model of ruptured abdominal aortic aneurysm.

Authors:  Denis W Harkin; Alex Romaschin; Stephen M Taylor; Barry B Rubin; Thomas F Lindsay
Journal:  J Vasc Surg       Date:  2004-01       Impact factor: 4.268

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  1 in total

Review 1.  Bench-to-bedside review: the role of C1-esterase inhibitor in sepsis and other critical illnesses.

Authors:  Mervyn Singer; Annie M Jones
Journal:  Crit Care       Date:  2011-01-26       Impact factor: 9.097

  1 in total

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