Obesity, inflammation and the immune system

• Published in: Proceedings of the Nutrition Society Vol. 71; no. 2; pp. 332 - 338
• Main Authors: de Heredia, Fátima Pérez, Gómez-Martínez, Sonia, Marcos, Ascensión
• Format: Journal Article
• Language: English
• Published: Cambridge, UK Cambridge University Press 01-05-2012
• Subjects: Abdomen; Adipocytes; Adipokines - metabolism; Adiponectin; Adipose tissue; Adipose Tissue - cytology; Adipose Tissue - immunology; Adolescence; Alzheimer's disease; Body fat; Children; Chronic and degenerative diseases; Chronic illnesses; Conferences; Data processing; Endoplasmic reticulum; Endoplasmic Reticulum - metabolism; Endoplasmic Reticulum Stress; Exercise; Fatty Acids - adverse effects; Fatty Acids - metabolism; Feedback; Health care; Humans; Hypoxia; Immune response; Immune response (cell-mediated); Immune system; Immune System - drug effects; Immune System - metabolism; Infections; Inflammation; Inflammation - etiology; Inflammation - immunology; Inflammation - metabolism; Insulin resistance; Leptin; Leukocytes; Malnutrition; Metabolic disorders; Metabolism; Nutrients; Nutrition; Obesity; Obesity - complications; Obesity - immunology; Obesity - metabolism; Overnutrition - immunology; Overweight; Physical fitness; Proteins; Stress; Teenagers; TLR3 protein; Toll-like receptors; Obesity; Inflammation; Immunonutrition; Immune response; Adipose tissue
• ISSN: 0029-6651; 1475-2719
• DOI: 10.1017/S0029665112000092

Obesity shares with most chronic diseases the presence of an inflammatory component, which accounts for the development of metabolic disease and other associated health alterations. This inflammatory state is reflected in increased circulating levels of pro-inflammatory proteins, and it occurs not only in adults but also in adolescents and children. The chronic inflammatory response has its origin in the links existing between the adipose tissue and the immune system. Obesity, like other states of malnutrition, is known to impair the immune function, altering leucocyte counts as well as cell-mediated immune responses. In addition, evidence has arisen that an altered immune function contributes to the pathogenesis of obesity. This review attempts to briefly comment on the various plausible explanations that have been proposed for the phenomenon: (1) the obesity-associated increase in the production of leptin (pro-inflammatory) and the reduction in adiponectin (anti-inflammatory) seem to affect the activation of immune cells; (2) NEFA can induce inflammation through various mechanisms (such as modulation of adipokine production or activation of Toll-like receptors); (3) nutrient excess and adipocyte expansion trigger endoplasmic reticulum stress; and (4) hypoxia occurring in hypertrophied adipose tissue stimulates the expression of inflammatory genes and activates immune cells. Interestingly, data suggest a greater impact of visceral adipose tissue and central obesity, rather than total body fat, on the inflammatory process. In summary, there is a positive feedback loop between local inflammation in adipose tissue and altered immune response in obesity, both contributing to the development of related metabolic complications.