8th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV San Francisco, California - September 24 - 26, 2006

ADIPOSE TISSUE AND INFLAMMATION

Antiviral Therapy 2006; 11:L1 (abstract no. P1)

K Clément
Inserm U755, University Hôtel-Dieu Hospital, Paris, France

The discovery in the mid-nineties, that adipose tissue releases specific proteins into the blood stream, was a breakthrough in the field of metabolic diseases. Among various cell types that compose adipose tissue, adipocytes themselves produce two major proteins: leptin and adiponectin. By acting on distant organs through specific receptors, leptin and adiponectin qualify as hormones. Furthermore, in metabolic diseases a moderate increase of inflammatory factors has been well described. Accompanying this so called ‘low-grade systemic inflammation’, it was recently discovered that inflammatory cells (macrophage, lymphocytes) can infiltrate the white adipose tissue (WAT) in proportion to the level of adiposity. These adipose tissue cells produce a wide panel of inflammatory and immune molecules, some of them being secreted. Adipose-produced molecules play distinct and sometimes overlapping roles in a variety of functions, including energy homeostasis, glucose and lipid metabolism, inflammation and vascular function. Large scale transcriptomic investigation of the adipose tissue also led to the target of new adipose synthesized actors that could link adipose tissue to its metabolic and vascular complications (cathepsin S, serum amyloid). On one hand, adipose tissue loss, in the obesity context, is able to improve the inflammatory state by both significantly decreasing inflammatory molecules and macrophage cell infiltration in WAT. On the other hand, peripheral fat wasting and visceral fat redistribution observed in HIV-1 infected subjects associate with increased inflammatory factors in adipose tissue and with macrophage infiltration. The mechanisms of WAT macrophage recruitment into the adipose tissue, macrophage phenotype and role in metabolic complications have not been clearly defined. In vitro studies highlighted possible adipocyte-macrophage interactions via paracrine effectors that could profoundly modify the adipocyte biology.

This conference reviews the knowledge on inflammatory cytokines associated with adipose tissue and notably focuses on macrophage infiltration in human WAT, discussing their possible recruitment mechanism and role. The interactions of macrophages with adipocyte biology will certainly be the subject of intense investigations in the future and to some redefinition of the physiopathology of common metabolic diseases.

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2006-09-24
P1

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