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Visfatin, an Adipocytokine with Proinflammatory and Immunomodulating Properties¹

Alexander R. Moschen^*, Arthur Kaser^*, Barbara Enrich^*, Birgit Mosheimer, Milan Theurl, Harald Niederegger and Herbert Tilg^2,*

^* Department of Medicine, Christian Doppler Research Laboratory for Gut Inflammation and Clinical Division of Gastroenterology and Hepatology, Department of Medicine, Clinical Division of General Internal Medicine, and Innsbruck Biocentre, Division of Experimental Pathophysiology and Immunology, Innsbruck Medical University, Innsbruck, Austria

Adipocytokines are mainly adipocyte-derived cytokines regulating metabolism and as such are key regulators of insulin resistance. Some adipocytokines such as adiponectin and leptin affect immune and inflammatory functions. Visfatin (pre-B cell colony-enhancing factor) has recently been identified as a new adipocytokine affecting insulin resistance by binding to the insulin receptor. In this study, we show that recombinant visfatin activates human leukocytes and induces cytokine production. In CD14⁺ monocytes, visfatin induces the production of IL-1, TNF-, and especially IL-6. Moreover, it increases the surface expression of costimulatory molecules CD54, CD40, and CD80. Visfatin-stimulated monocytes show augmented FITC-dextran uptake and an enhanced capacity to induce alloproliferative responses in human lymphocytes. Visfatin-induced effects involve p38 as well as MEK1 pathways as determined by inhibition with MAPK inhibitors and we observed activation of NF-B. In vivo, visfatin induces circulating IL-6 in BALB/c mice. In patients with inflammatory bowel disease, plasma levels of visfatin are elevated and its mRNA expression is significantly increased in colonic tissue of Crohn’s and ulcerative colitis patients compared with healthy controls. Macrophages, dendritic cells, and colonic epithelial cells might be additional sources of visfatin as determined by confocal microscopy. Visfatin can be considered a new proinflammatory adipocytokine.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by a grant from the Austrian Science Foundation (P17447).

² Address correspondence and reprint requests to Dr. Herbert Tilg, Department of Medicine, Clinical Division of Gastroenterology and Hepatology, Innsbruck Medical University and Christian Doppler Research Laboratory for Gut Inflammation, Anichstrasse 35, 6020 Innsbruck, Austria. E-mail address: Herbert.Tilg{at}uibk.ac.at

³ Abbreviations used in this paper: IR, insulin receptor; PBEF, pre-B cell-enhancing factor; IL-1Ra, IL-1 receptor antagonist; DC, dendritic cell; GUSB, glucuronidase ; qPCR, quantitative PCR; IBD, inflammatory bowel disease; CD, Crohn’s disease; UC, ulcerative colitis; SGBS, Simpson Golabi Behmel syndrome; CDAI, CD activity index; CAI, clinical activity score.

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