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The Journals of Gerontology Series A: Biological Sciences and Medical Sciences Advance Access published online on April 17, 2009
The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, doi:10.1093/gerona/glp046
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© The Author 2009. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

Age-Associated Increase in Cytokine Production During Systemic Inflammation: Adipose Tissue as a Major Source of IL-6

Marlene E. Starr1, B. Mark Evers1,2 and Hiroshi Saito1,2

1 Department of Biochemistry and Molecular Biology
2 Department of Surgery, University of Texas Medical Branch, Galveston

Address correspondence to Hiroshi Saito, PhD, Department of Surgery, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-0828. Email: hsaito{at}utmb.edu


  Abstract

Increased mortality and overexpression of interleukin-6 (IL-6) during inflammatory stress are well-documented age-associated phenomena; however, the site of IL-6 overexpression is not entirely known. Here, we report that white adipose tissue is a major source of IL-6 in aged animals during lipopolysaccharide (LPS)-induced systemic inflammation. Among the various tissues examined, white adipose tissue from the epididymal fat pad (located in the abdominal cavity) expressed the highest level of IL-6 messenger RNA in both young and aged mice with a 5.5-fold higher level in the aged. Immunohistochemistry revealed that, within the adipose tissue, LPS-induced IL-6 expression is localized to both the adipocytes and stromal cells. Compared with age-matched wild-type mice, aged IL-6(–/–) mice exhibited reduced mortality to LPS suggesting a deleterious effect of IL-6 overexpression in the aged. These results demonstrate that increased vulnerability to systemic inflammation with age is due in part, to augmented IL-6 production by the adipose tissue.

Keywords Aging; IL-6; Adipose tissue; Sepsis; Endotoxemia

Received: September 7, 2008; Accepted: February 24, 2009

Decision Editor: Huber R. Warner, PhD


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