title: HIV-1 transgenic rats display alterations in immunophenotype and cellular responses associated with aging.
abstract: Advances in anti-retroviral therapy over the last two decades have allowed life expectancy in patients infected with the human immunodeficiency virus to approach that of the general population. The process of aging in mammalian species, including rats, results in immune response changes, alterations in immunological phenotypes, and ultimately increased susceptibility to many infectious diseases. In order to investigate the immunological pathologies associated with chronic HIV-1 disease, particularly in aging individuals, the HIV-1 transgenic (HIV-1Tg) rat model was utilized. HIV-1Tg rats were challenged with lipopolysaccharide (LPS) to determine immunological alterations during the aging process. LPS is known to cause an imbalance in cytokine and chemokine release, and provides a method to identify changes in immune responses to bacterial infection in an HIV animal model. An immune profile and accompanying cellular consequences as well as changes in inflammatory cytokine and chemokine release related to age and genotype were assessed in HIV-1Tg rats. The percentage of T cells decreased with age, particularly T cytotoxic cells, whereas T helper cells increased with age. Neutrophils and monocytes increased in HIV-1Tg rats during maturation compared to age-matched F344 control rats. Aging HIV-1Tg rats displayed a significant increase in the pro-inflammatory cytokines, IL-6 and TNF-α, along with an increase in the chemokine, KC/GRO, in comparison to age-matched controls. Our data indicate that immunophenotype and immune responses can change during aging in HIV-positive individuals. This information could be important in determining the most beneficial age-dependent therapeutic treatment for HIV patients.
authors.affiliation: Institute of NeuroImmune Pharmacology and Department of Biological Sciences, Seton Hall University, South Orange, New Jersey, United States of America.
authors.forename: Susan J
authors.initials: SJ
authors.lastname: Abbondanzo
authors.affiliation: Institute of NeuroImmune Pharmacology and Department of Biological Sciences, Seton Hall University, South Orange, New Jersey, United States of America.
authors.forename: Sulie L
authors.initials: SL
authors.lastname: Chang
mesh_terms: D000375:Aging / Q000276:immunology*; D000818:Animals; D018925:Chemokines / Q000097:blood; D015658:HIV Infections / Q000097:blood / Q000188:drug therapy / Q000276:immunology*; D015497:HIV-1 / Q000276:immunology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008198:Lymph Nodes / Q000276:immunology / Q000378:metabolism; D008297:Male; D010641:Phenotype; D011916:Rats, Inbred F344; D055647:Rats, Transgenic; D013154:Spleen / Q000276:immunology / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology / Q000821:virology
chemical_list: D018925:Chemokines; D008070:Lipopolysaccharides