title: Impaired Immune Response in Old Mice Suffering from Obesity and Premature Immunosenescence in Adulthood.
abstract: Obesity and aging share an impaired immune system and oxidative and inflammatory stress. Therefore, the hypothesis of obesity as a possible model of premature immunosenescence has been proposed. In this study, we investigated whether adult obese mice, as a consequence of being fed with a fat-rich diet during their adolescence, showed premature immunosenescence and if this was aggravated with aging. Peritoneal cell suspensions were obtained when ICR/CD1 obese female mice were adults (28 weeks) and old (72 weeks), and several functions and antioxidant defenses were evaluated. The results showed that the chemotaxis of both macrophages and lymphocytes, phagocytosis of macrophages, activity of natural killer cells, proliferative response of lymphocytes, interleukin-1β, tumor necrosis factor-alpha, interleukin-6, interleukin-2, and interleukin-10 released in leukocyte cultures, as well as antioxidant and oxidant capacity were significantly impaired in adult obese mice with respect to adult nonobese mice, with values similar to those in chronologically old mice. When these obese animals grew older, although having been fed with a standard diet, they showed a higher deterioration of their immune functions in comparison with the old control group. In conclusion, these results demonstrate that a high fat intake during adolescence can produce an obesity state in adult age associated with a premature immunosenescence, which is aggravated through aging.
authors.affiliation: Department of Animal Physiology II, Faculty of Biology, Complutense University of Madrid and Research Institute of Hospital 12 de Octubre, Madrid, Spain.
authors.forename: Caroline
authors.initials: C
authors.lastname: Hunsche
authors.affiliation: Department of Animal Physiology II, Faculty of Biology, Complutense University of Madrid and Research Institute of Hospital 12 de Octubre, Madrid, Spain.
authors.forename: Oskarina
authors.initials: O
authors.lastname: Hernandez
authors.affiliation: Department of Animal Physiology II, Faculty of Biology, Complutense University of Madrid and Research Institute of Hospital 12 de Octubre, Madrid, Spain. mondelaf@bio.ucm.es.
authors.forename: Monica
authors.initials: M
authors.lastname: De la Fuente
mesh_terms: D000375:Aging / Q000276:immunology*; D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D000068884:Immunosenescence; D016753:Interleukin-10 / Q000276:immunology; D053583:Interleukin-1beta; D007376:Interleukin-2 / Q000276:immunology; D015850:Interleukin-6 / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology; D008214:Lymphocytes / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008813:Mice, Inbred ICR; D055611:Natural Killer T-Cells / Q000276:immunology; D009765:Obesity / Q000276:immunology*; D010537:Peritoneum / Q000166:cytology; D010587:Phagocytosis / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha
chemical_list: D053583:Interleukin-1beta; D007376:Interleukin-2; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10
keywords: Immune function; Obesity; Oxidative stress; Premature immunosenescence