Format

Send to:

Choose Destination
See comment in PubMed Commons below
PLoS One. 2011 Apr 11;6(4):e18404. doi: 10.1371/journal.pone.0018404.

Paracrine IL-33 stimulation enhances lipopolysaccharide-mediated macrophage activation.

Author information

  • 1Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan.

Abstract

BACKGROUND:

IL-33, a member of the IL-1 family of cytokines, provokes Th2-type inflammation accompanied by accumulation of eosinophils through IL-33R, which consists of ST2 and IL-1RAcP. We previously demonstrated that macrophages produce IL-33 in response to LPS. Some immune responses were shown to differ between ST2-deficient mice and soluble ST2-Fc fusion protein-treated mice. Even in anti-ST2 antibody (Ab)-treated mice, the phenotypes differed between distinct Ab clones, because the characterization of such Abs (i.e., depletion, agonistic or blocking Abs) was unclear in some cases.

METHODOLOGY/PRINCIPAL FINDINGS:

To elucidate the precise role of IL-33, we newly generated neutralizing monoclonal Abs for IL-33. Exogenous IL-33 potentiated LPS-mediated cytokine production by macrophages. That LPS-mediated cytokine production by macrophages was suppressed by inhibition of endogenous IL-33 by the anti-IL-33 neutralizing mAbs.

CONCLUSIONS/SIGNIFICANCE:

Our findings suggest that LPS-mediated macrophage activation is accelerated by macrophage-derived paracrine IL-33 stimulation.

PMID:
21494550
[PubMed - indexed for MEDLINE]
PMCID:
PMC3073971
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Public Library of Science Icon for PubMed Central
    Loading ...
    Write to the Help Desk