May prior Chlamydia pneumoniae infection may determine the development of chronic inflamation in obesity?

Monika Koziołek; Barbara Krzyżanowska-Świniarska; Tomasz Miazgowski; Krystyna Pilarska

Vol 2, No 4 (2006)

Prace poglądowe

Published online: 2007-01-25

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May prior Chlamydia pneumoniae infection may determine the development of chronic inflamation in obesity?

Monika Koziołek, Barbara Krzyżanowska-Świniarska, Tomasz Miazgowski, Krystyna Pilarska

Endokrynol. Otył. Zab. Przem. Mat 2006;2(4):129-133.

Vol 2, No 4 (2006)

Prace poglądowe

Published online: 2007-01-25

Abstract

Obesity is associated with a mild and chronic inflammatory process. There is increasing evidence that in obesity the adipocytes secrete numerous bioactive substances, such as CRP, IL-6, TNF-α, leptin and adiponectin. Thus, adipose tissue actively contributes in the development of inflammatory response. Among many theories elucidating subclinical, chronic inflammatory process in obesity, relatively less is known about possible bacterial infection in the initiation of this process and in modulation of its course. Does intracellular bacteria Chlamydia pneumonia, associated with the progression of atheromatosis which has been considered recently as a vascular inflammatory disease, might be a factor initiating the cytokine cascade in obesity? This bacterium may infect and live in number of the host cells (including circulating monocytes, tissue macrophages, or endothelial cells). If human immune system is unable to eliminate Chlamydia pneumoniae, the inflammation progresses to a self-supporting chronic process, in which are essentially involved macrophages infiltrating fat tissue, increased synthesis of the pro-inflammatory cytokines, and C-reactive protein in adipose cells as a reaction of the body for prolonged antigen stimulation.