Format

Send to

Choose Destination
See comment in PubMed Commons below
Ann N Y Acad Sci. 1996 Oct 31;796:104-12.

Role of complement, chemokines, and regulatory cytokines in acute lung injury.

Author information

  • 1Department of Pathology, University of Michigan Medical School, Ann Arbor 48109, USA.

Abstract

The roles of complement, proinflammatory cytokines and regulatory cytokines in lung inflammatory injury are becoming defined. Like the proinflammatory cytokines (TNF alpha and IL-1), complement activation products (C5a and/or the membrane attack complex, C5b-9) can directly activate endothelial cells to cause upregulation of adhesion molecules (P-selectin) or can function in a synergistic manner with TNF alpha to cause enhanced upregulation of ICAM-1 and E-selectin. The beta chemokine, MIP-1 alpha, appears to function in vivo as an autocrine activator, enhancing TNF alpha production by pulmonary macrophages, which, in turn, enhances the inflammatory response. Finally, IL-4 and IL-10 have strong regulatory effects by suppressing in vivo production of TNF alpha. There is now compelling evidence to suggest that, in IgG immune-complex-induced lung inflammation in rats, endogenous IL-10 is produced and regulates the intensity of the inflammatory response. Blocking of endogenous IL-10 substantially increases lung TNF alpha production, the recruitment of neutrophils, and the intensity of lung inflammatory injury. Accordingly, the network of cytokines carefully regulates lung inflammatory responses.

PMID:
8906217
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley
    Loading ...
    Write to the Help Desk