title: T lymphocyte responses to antigens of gram-negative bacteria in pyelonephritis.
abstract: We showed previously that large numbers of T lymphocytes accumulate within a few days in the kidneys of rats with ascending pyelonephritis induced with Escherichia coli or Pseudomonas aeruginosa. CD4+ T cells propagated from the lesions exhibited MHC-restricted proliferative responses to formalin-fixed bacteria of the species used to induce infection. In the present study we investigated further the nature of the antigens responsible for the T cell proliferation and studied the ability of different bacterial strains and species to produce proliferative responses. We found that heat-killed bacteria were more stimulatory than formalin-fixed bacteria, and that soluble supernatants of heat-killed organism were also effective. The stimulatory effects of supernatants were destroyed by trypsin and the responses were MHC-restricted. Twelve different E. coli strains, with or without characteristics of uropathogenicity in humans, were all highly stimulatory to T cells derived from a kidney infected with a single E. coli strain. Strains of Klebsiella pneumoniae, Enterobacter aerogenes, and Serratia marcescens--species of Enterobacteriaceae closely related to E. coli--were also stimulatory, whereas more distantly related bacteria--Proteus, Morganella, and P. aeruginosa--were not. T cells propagated from kidneys infected with P. aeruginosa responded to supernatants of this organism, but not to E. coli supernatants. We conclude that a protein antigen (or antigens) shared by strains of E. coli and related Enterobacteriaceae, but not by other gram-negative bacteria, produce MHC-restricted proliferative responses of CD4+ T cells that infiltrate rat kidneys infected with E. coli.
authors.affiliation: Department of Pathology, Harvard Medical School, Massachusetts General Hospital, Charlestown 02129.
authors.forename: S W
authors.initials: SW
authors.lastname: Wilz
authors.forename: J T
authors.initials: JT
authors.lastname: Kurnick
authors.forename: F
authors.initials: F
authors.lastname: Pandolfi
authors.forename: R H
authors.initials: RH
authors.lastname: Rubin
authors.forename: H S
authors.initials: HS
authors.lastname: Warren
authors.forename: R
authors.initials: R
authors.lastname: Goldstein
authors.forename: C M
authors.initials: CM
authors.lastname: Kersten
authors.forename: R T
authors.initials: RT
authors.lastname: McCluskey
mesh_terms: D000818:Animals; D000942:Antigens, Bacterial / Q000276:immunology*; D004195:Disease Models, Animal; D004926:Escherichia coli / Q000276:immunology; D004927:Escherichia coli Infections; D005260:Female; D006090:Gram-Negative Bacteria / Q000276:immunology* / Q000472:pathogenicity; D006358:Hot Temperature; D007124:Immunoenzyme Techniques; D007668:Kidney / Q000382:microbiology / Q000473:pathology; D008213:Lymphocyte Activation / Q000276:immunology; D008285:Major Histocompatibility Complex / Q000276:immunology; D011552:Pseudomonas Infections; D011550:Pseudomonas aeruginosa / Q000276:immunology; D011704:Pyelonephritis / Q000276:immunology* / Q000382:microbiology*; D051381:Rats; D011917:Rats, Inbred Lew; D013268:Stimulation, Chemical; D013601:T-Lymphocytes / Q000276:immunology*; D014357:Trypsin / Q000494:pharmacology; D014774:Virulence
chemical_list: D000942:Antigens, Bacterial; D014357:Trypsin