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    CD40L Deficiency Attenuates Diet-Induced Adipose Tissue Inflammation by Impairing Immune Cell Accumulation and Production of Pathogenic IgG- Antibodies

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    Author
    Wolf, D; Jehle, F; Rodriguez, AO; Dufner, B; Hoppe, N; Colberg, C; Lozhkin, A; Bassler, N; Rupprecht, B; Wiedemann, A; ...
    Date
    2012-03-08
    Source Title
    PLoS One
    Publisher
    PUBLIC LIBRARY SCIENCE
    University of Melbourne Author/s
    Peter, Karlheinz
    Affiliation
    Melbourne Medical School
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Wolf, D., Jehle, F., Rodriguez, A. O., Dufner, B., Hoppe, N., Colberg, C., Lozhkin, A., Bassler, N., Rupprecht, B., Wiedemann, A., Hilgendorf, I., Stachon, P., Willecke, F., Febbraio, M., Binder, C. J., Bode, C., Zirlik, A. & Peter, K. (2012). CD40L Deficiency Attenuates Diet-Induced Adipose Tissue Inflammation by Impairing Immune Cell Accumulation and Production of Pathogenic IgG- Antibodies. PLOS ONE, 7 (3), https://doi.org/10.1371/journal.pone.0033026.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/253133
    DOI
    10.1371/journal.pone.0033026
    Abstract
    BACKGROUND: Adipose tissue inflammation fuels the metabolic syndrome. We recently reported that CD40L--an established marker and mediator of cardiovascular disease--induces inflammatory cytokine production in adipose cells in vitro. Here, we tested the hypothesis that CD40L deficiency modulates adipose tissue inflammation in vivo. METHODOLOGY/PRINCIPAL FINDINGS: WT or CD40L(-/-) mice consumed a high fat diet (HFD) for 20 weeks. Inflammatory cell recruitment was impaired in mice lacking CD40L as shown by a decrease of adipose tissue macrophages, B-cells, and an increase in protective T-regulatory cells. Mechanistically, CD40L-deficient mice expressed significantly lower levels of the pro-inflammatory chemokine MCP-1 both, locally in adipose tissue and systemically in plasma. Moreover, levels of pro-inflammatory IgG-antibodies against oxidized lipids were reduced in CD40L(-/-) mice. Also, circulating low-density lipoproteins and insulin levels were lower in CD40L(-/-) mice. However, CD40L(-/-) mice consuming HFD were not protected from the onset of diet-induced obesity (DIO), insulin resistance, and hepatic steatosis, suggesting that CD40L selectively limits the inflammatory features of diet-induced obesity rather than its metabolic phenotype. Interestingly, CD40L(-/-) mice consuming a low fat diet (LFD) showed both, a favorable inflammatory and metabolic phenotype characterized by diminished weight gain, improved insulin tolerance, and attenuated plasma adipokine levels. CONCLUSION: We present the novel finding that CD40L deficiency limits adipose tissue inflammation in vivo. These findings identify CD40L as a potential mediator at the interface of cardiovascular and metabolic disease.

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