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Microbial Reprogramming Inhibits Western Diet-Associated Obesity
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Book Chapter
Microbial Reprogramming Inhibits Western Diet-Associated Obesity
2014
Overview
THEOFILOS POUTAHIDIS, MARKUS KLEINEWIETFELD,
CHRISTOPHER SMILLIE, TATIANA LEVKOVICH,
ALISON PERROTTA, SIDDHESHVAR BHELA,
BERNARD J. VARIAN,YASSIN M. IBRAHIM, JESSICA R. LAKRITZ,
SEAN M. KEARNEY, ANTONIS CHATZIGIAGKOS,
DAVID A. HAFLER, ERIC J. ALM MAIL, AND SUSAN E. ERDMAN3.1 INTRODUCTIONThe risk of developing obesity rises with a Westernized lifestyle. In industrialized and developing countries obesity contributes to increased mortality by predisposing to serious pathological conditions such as type 2
diabetes, cardiovascular disease, fatty liver, arthritis, asthma, and neoplasia [1]–[2]. Clinical and experimental data suggest that the white adipose
tissue of obese organisms is in a low-grade, persistent state of chronic inflammation that exerts adverse systemic effects [2]–[3]. The most prominent inflammatory cell type of the obesity-associated inflammation is theadipose tissue macrophage. Macrophages are recruited and surround dead
adipocytes, thus creating the so-called crown-like structures (CLS). These
cells along with hypertrophic adipocytes are thought to be the key cells
initiating the unique subclinical pro-inflammatory signaling cascade encountered in obesity [2], [4]–[5]. Macrophages, B and T lymphocytes, and
up-regulated pro-inflammatory cytokines including TNF-α, IL-1, IL-6,
IL-17, and monocyte chemoattractant protein-1 (MCP-1) have been reported to contribute to obesity-associated pathologies. In parallel, regulatory T cells down-regulate host inflammatory responses [2]–[3], [6]–[10].
Publisher
Apple Academic Press,Apple Academic Press, Incorporated
Subject
ISBN
9781771880725, 1771880724
