Chlamydophila pneumoniae Inhibits Differentiation of Progenitor Adipose Cells and Impairs Insulin Signaling.

Chlamydophila pneumoniae Inhibits Differentiation of Progenitor Adipose Cells and Impairs Insulin Signaling. Research Abstract Details 

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Chlamydophila pneumoniae Inhibits Differentiation of Progenitor Adipose Cells and Impairs Insulin Signaling. Abstract Text:

Yu Shi,Youan Liu,Andrew Murdin,Ausra Raudonikiene-Mancevski,Bilal B Ayach,Zhiwen Yu,I George Fantus,Peter P Liu,Yu Shi,Youan Liu,Andrew Murdin,Ausra Raudonikiene-Mancevski,Bilal B Ayach,Zhiwen Yu,I George Fantus,Peter P Liu,Yu Shi,Youan Liu,Andrew Murdin,Ausra Raudonikiene-Mancevski,Bilal B Ayach,Zhiwen Yu,I George Fantus,Peter P Liu,

Background. @nbsp; Recent clinical studies have shown Chlamydophila pneumoniae seropositivity to be related to overweight status and inversely related to insulin sensitivity. The present study was performed to investigate the potential effects of C. pneumoniae infection of adipocytes. Methods. @nbsp; 3T3-L1 cells and primary epididymal preadipocytes were infected with C. pneumoniae either before or after induction of differentiation, and the effects on adipogenesis and insulin signaling were determined. Tumor necrosis factor (TNF)-alpha signaling was examined by assessing the effects of C. pneumoniae infection in preadipocytes isolated from epididymal adipose tissue of both wild-type and TNF-alpha(-/-) mice. Results. @nbsp; C. pneumoniae successfully infected both undifferentiated and differentiated 3T3-L1 cells in vitro. The bacteria were also detected in adipose tissue of infected low-density lipoprotein receptor-deficient mice. TNF-alpha protein levels were significantly increased in cells infected with either live or heat-killed C. pneumoniae or treated with lipopolysaccharide or heat-shock protein 65; this increase was associated with inhibition of adipocyte differentiation and down-regulation of insulin-stimulated tyrosine-phosphorylated insulin receptor and its substrate. In contrast, C. pneumoniae infection in TNF-alpha(-/-) adipocytes produced no apparent changes, but addition of recombinant TNF-alpha reversed this effect. Conclusions. @nbsp; We demonstrate for the first time that C. pneumoniae can infect murine pre- and postdifferentiated adipocytes and, through a TNF-alpha-mediated inflammatory mechanism, can impair differentiation and insulin signaling.

Chlamydophila pneumoniae Inhibits Differentiation of Progenitor Adipose Cells and Impairs Insulin Signaling. Publishing Authors By Initials

Y Shi,Y Liu,A Murdin,A Raudonikiene-Mancevski,BB Ayach,Z Yu,IG Fantus,PP Liu,Y Shi,Y Liu,A Murdin,A Raudonikiene-Mancevski,BB Ayach,Z Yu,IG Fantus,PP Liu,Y Shi,Y Liu,A Murdin,A Raudonikiene-Mancevski,BB Ayach,Z Yu,IG Fantus,PP Liu,

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Chlamydophila pneumoniae Inhibits Differentiation of Progenitor Adipose Cells and Impairs Insulin Signaling. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: The Journal of infectious diseases

VOLUME: 197

Page Numbers: 439-48

Journal Abbreviation: J. Infect. Dis.

ISSN: 0022-1899

DAY: 1

MONTH: Feb

YEAR: 2008

Chlamydophila pneumoniae Inhibits Differentiation of Progenitor Adipose Cells and Impairs Insulin Signaling. Information

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LANGUAGE: eng

NlmUniqueID: 413675

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Grant and Affiliation Information for Chlamydophila pneumoniae Inhibits Differentiation of Progenitor Adipose Cells and Impairs Insulin Signaling.

AFFILIATION: 1Toronto General Hospital Research Institute, 2Sanofi Pasteur Canada, 3Banting and Best Diabetes Centre, and 4University of Toronto, Toronto, Ontario, Canada.

Country: United States

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MEDLINETA: J Infect Dis

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