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Am J Physiol Regul Integr Comp Physiol (December 4, 2003). doi:10.1152/ajpregu.00585.2003
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Submitted on October 7, 2003
Accepted on November 27, 2003

Interleukin-6 and Interleukin-15 are Selectively Regulated by Lipopolysaccharide and Interferon-{gamma} in Primary Pig Adipocytes

Kolapo M Ajuwon1, Sheila K Jacobi1, Joanne L Kuske1, and Michael E Spurlock1*

1 Department of Animal Sciences, Comparative Medicine Program, Purdue University, West Lafayette, IN, USA

* To whom correspondence should be addressed. E-mail: spurloc0{at}purdue.edu.

3T3-L1 adipocytes express the lipopolysaccharide (LPS) receptor, and respond to direct stimulation with the antigen by increasing the expression of inflammatory mediators. Activation of this receptor by its ligand in the macrophage causes the activation and translocation of nuclear factor kappa-B (NFkB) to the nucleus where it regulates the expression of proinflammatory cytokines and other target genes. We investigated whether LPS could stimulate NFkB translocation in primary pig adipocytes and regulate the expression and secretion of TNF-{alpha} and IL-6. LPS clearly induced the nuclear translocation of NFkB, and also up-regulated (P < 0.05) the mRNA expression and secretion of IL-6 into the culture medium. An induction of TNF-{alpha} expression by LPS was not detected, but with extended incubation (8 hours), there was a modest increase (P < 0.09) in the media concentration of this cytokine. Inhibition of either ERK1/2, PKC, or the inhibitory G protein (Gi) with U0126, Bisindolylmaleimide HCl, and pertussis toxin, respectively, blocked (P < 0.05) the increase in IL-6 expression caused by LPS. Because LPS administration in vivo increases circulating concentrations of IFN-{gamma}, and because this cytokine also regulates multiple immune modulators in the adipocyte, we also determined whether IFN-{gamma} regulates cytokine expression in primary adipocytes. Although the expression of IL-6 and TNF-{alpha} were unresponsive to IFN-{gamma}, the expression of IL-15 was markedly up-regulated (P < 0.01). Furthermore, the induction of IL-15 expression by IFN-{gamma} was blocked by inhibition of PKC. These data indicate that NFkB is responsive to LPS in the adipocyte, and also identify key mediators of LPS-induced IL-6 expression. In addition, we provide novel evidence that IFN-{gamma} targets the adipocyte to induce IL-15 expression, thus indicating a possible role for the adipocyte in the regulation of T-cell function and muscle metabolism during the innate immune response.




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