title: Inflammation, genes and zinc in ageing and age-related diseases.
abstract: Lifelong antigenic burden determines a condition of chronic inflammation, with increased lymphocyte activation and pro-inflammatory cytokine production. A large number of studies have documented changes in Zn metabolism in experimental animal models of acute and chronic inflammation and in human chronic inflammatory diseases. In particular, modification of zinc plasma concentration as well as intracellular disturbance of antioxidant intracellular pathways have been found associated to age-related inflammatory diseases, like atherosclerosis. Zinc deficiency is extremely diffused in aged people that are educated to avoid meat and other high Zn-content foods due to fear of cholesterol. Rather, they increase consumption of refined wheat products that lack of Zn, magnesium and other critical nutrients in consequence of refining process. On the other hand, plasma concentration of metallic ions like Zn is influenced by pro-inflammatory cytokines production. A major target of Zn may be NF-kB, a transcription factor critical for the expression of many pro-inflammatory cytokines whose production is finely regulated by extra- and intracellular activating and inhibiting factors interacting with regulatory elements on cytokine genes. Moreover, this factor is regulated by the expression of specific cellular genes involved in inflammation. So it is not surprising that Zn deficiency is constantly observed in aged patients affected by infectious diseases. On the other hand, cytokine genes are highly polymorphic and some of these polymorphisms have been found associated to age-related diseases as atherosclerosis. Therefore, Zn deficiency in individuals genetically predisposed to a dis-regulation of inflammation response, may play a crucial role, in causing adverse events and in reducing the probability of a successful aging.
authors.affiliation: Department of Pathobiology and Biomedical Methodology, Palermo University, Corso Tukory 211, 90134, Palermo , Italy.
authors.forename: Sonya
authors.initials: S
authors.lastname: Vasto
authors.forename: Eugenio
authors.initials: E
authors.lastname: Mocchegiani
authors.forename: Giuseppina
authors.initials: G
authors.lastname: Candore
authors.forename: Florinda
authors.initials: F
authors.lastname: Listì
authors.forename: Giuseppina
authors.initials: G
authors.lastname: Colonna-Romano
authors.forename: Domenico
authors.initials: D
authors.lastname: Lio
authors.forename: Marco
authors.initials: M
authors.lastname: Malavolta
authors.forename: Robertina
authors.initials: R
authors.lastname: Giacconi
authors.forename: Catia
authors.initials: C
authors.lastname: Cipriano
authors.forename: Calogero
authors.initials: C
authors.lastname: Caruso
mesh_terms: D000375:Aging / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D000818:Animals; D050197:Atherosclerosis / Q000235:genetics / Q000378:metabolism; D016922:Cellular Senescence / Q000235:genetics; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D015870:Gene Expression; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics; D007249:Inflammation / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D015850:Interleukin-6 / Q000378:metabolism; D008136:Longevity / Q000235:genetics*; D008668:Metallothionein / Q000378:metabolism; D011110:Polymorphism, Genetic; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015032:Zinc / Q000172:deficiency / Q000378:metabolism*
chemical_list: D016207:Cytokines; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D008668:Metallothionein; D015032:Zinc