Skip NavigationSkip to Content

Induction of human monocyte interleukin (IL)-8 by fibrinogen through the Toll-like receptor pathway

  1. Author:
    Kuhns, D. B.
    Priel, D. A. L.
    Gallin, J. I.
  2. Author Address

    NIAID, NIH, Host Def Lab, Bethesda, MD 20892 USA. NCI Frederick, SAIC Frederick, Clin Serv Program, Ft Detrick, MD 21702 USA.;Gallin, JI, NIAID, NIH, Host Def Lab, Bldg 10,Rm 6-2551, Bethesda, MD 20892 USA.;jgallin@cc.nih.gov
    1. Year: 2007
    2. Date: Oct
  1. Journal: Inflammation
    1. 30
    2. 5
    3. Pages: 178-188
  2. Type of Article: Article
  3. ISSN: 0360-3997
  1. Abstract:

    Fibrinogen, in addition to its role in coagulation, is also an acute phase protein of inflammation. Treatment of adherent human monocytes with fibrinogen increases IL-8, IL-6, and TNF-alpha, but has no effect on MCP-1, IFN-beta, or IP-10. Treatment of monocytes with fibrinogen and C5a doubles IL-8 and IL-6 production, compared to fibrinogen alone. The increase in cytokine production was accompanied by a transient increase in IL-8 mRNA and increased NF-kappa B activity. Monocytes from an IRAK-4- and two NEMO-deficient patients had 80% reduced IL-8 responses to fibrinogen. Moreover, responses to fibrinogen were blocked with anti-CD14 antibody (MY4), a subunit of the LPS receptor. The data indicate that fibrinogen alone and fibrinogen plus C5a are potent inducers of cytokine production in monocytes, and that signaling by fibrinogen is mediated through the TLR-4 pathway.

    See More

External Sources

  1. DOI: 10.1007/s10753-007-9035-1
  2. WOS: 000250118500007

Library Notes

  1. No notes added.
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel