title: The role of experimental chronic renal failure and aluminium intoxication in cellular immune response.
abstract: BACKGROUND
  A positive correlation between successful kidney transplantation, few rejection episodes, greater susceptibility to infection and morbidity in patients with high tissue levels of aluminium (Al) indicate that the metal may play a role in the immune response. The aim of this study was to determine if experimental aluminium intoxication could result in significant changes in lymphocyte activity in uraemic and nonuraemic rats.
  
  
  METHODS
  Lewis rats were divided into four groups: normals (N), nephrectomized control (U), and Al-treated (N + Al) and nephrectomized Al-treated (U + Al), which received a cumulative dose of 30 mg Al over a 4-week period. Al quantification, histology, histochemical analysis and immunological assays were performed after Al intoxication.
  
  
  RESULTS
  High tissue levels of Al and positive histochemical staining in bones were seen in Al-treated rats. Bone histology revealed osteomalacia in U + Al rats. No statistical differences were observed in mixed lymphocyte cultures from controls and Al-treated rats, whereas U and Al-treated rats showed a decrease in lymphoproliferative response to mitogen and natural killer cell cytotoxic activity. A decreased helper T lymphocyte: cytotoxic T lymphocyte cell ratio and a reduction in interleukin-2 production were observed only in the U + Al group. A reduced number of total T lymphocytes was detected in the spleens of all Al-treated rats.
  
  
  CONCLUSIONS
  These findings suggest that aluminium toxicity may contribute to immunological impairment in chronic renal failure.
authors.affiliation: Immunology Division, University of São Paulo Medical School, Brazil.
authors.forename: C
authors.initials: C
authors.lastname: Tzanno-Martins
authors.forename: L S
authors.initials: LS
authors.lastname: Azevedo
authors.forename: N
authors.initials: N
authors.lastname: Orii
authors.forename: E
authors.initials: E
authors.lastname: Futata
authors.forename: V
authors.initials: V
authors.lastname: Jorgetti
authors.forename: M
authors.initials: M
authors.lastname: Marcondes
authors.forename: A J
authors.initials: AJ
authors.lastname: Duarte
mesh_terms: D000535:Aluminum / Q000633:toxicity*; D000818:Animals; D001842:Bone and Bones / Q000473:pathology; D002455:Cell Division; D002478:Cells, Cultured; D003208:Concanavalin A / Q000494:pharmacology; D003602:Cytotoxicity, Immunologic / Q000276:immunology; D007111:Immunity, Cellular; D007376:Interleukin-2 / Q000096:biosynthesis; D007676:Kidney Failure, Chronic / Q000139:chemically induced / Q000276:immunology*; D008213:Lymphocyte Activation / Q000187:drug effects / Q000276:immunology; D018655:Lymphocyte Count; D008297:Male; D009392:Nephrectomy; D010018:Osteomalacia / Q000139:chemically induced / Q000473:pathology; D051381:Rats; D011917:Rats, Inbred Lew; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*; D013602:T-Lymphocytes, Cytotoxic / Q000187:drug effects / Q000276:immunology; D006377:T-Lymphocytes, Helper-Inducer / Q000187:drug effects / Q000276:immunology; D014511:Uremia / Q000139:chemically induced / Q000276:immunology
chemical_list: D007376:Interleukin-2; D003208:Concanavalin A; D000535:Aluminum