title: Defective bronchus-associated lymphoid tissue in long-term surviving rat lung allografts.
abstract: In a previous study we found that a local immune response did not develop in the bronchus-associated lymphoid tissue (BALT) of infected rat allografts. We hypothesized that the BALT in rat lung allografts was damaged after allotransplantation. Therefore, we investigated three prerequisites for a normal function of the BALT, i.e., its structure, the uptake of antigens, and the lymphocyte migration to the BALT in three groups of rats (n = 10 each): (1) Brown Norway(BN)-to-Lewis (LEW) allografts; (2) LEW-to-LEW isografts; and (3) normal LEW rats. All rats were immunosuppressed with CsA (injected on days 2 and 3). Six mo after transplantation the structure of the BALT and the uptake of intrabronchially injected carbon particles in the BALT were determined histologically; the migration of intravenously injected, fluoroscein-isothiocyanate labeled lymphocytes to the BALT was determined immunohistochemically. In the allografts the BALT was defective in all three investigated aspects. It was reduced in size and lymphocyte density and was largely replaced by fibrous tissue. Twenty-four h after administration no carbon particles and only a few labeled lymphocytes were found in the BALT. In contrast, in the syngeneically transplanted and nontransplanted lungs the BALT consisted of a large and dense collection of lymphocytes. In these BALTs large numbers of carbon particles and labeled lymphocytes were found. In conclusion, after allogeneic transplantation the BALT in the lung becomes defective in structure and function. The BALT is most likely damaged by rejection, since the BALT is syngeneic lung transplants was perfectly normal.
authors.affiliation: Cardiopulmonary Surgery Research Division, University Hospital Groningen, The Netherlands.
authors.forename: J B
authors.initials: JB
authors.lastname: Winter
authors.forename: J
authors.initials: J
authors.lastname: Prop
authors.forename: M
authors.initials: M
authors.lastname: Groen
authors.forename: A H
authors.initials: AH
authors.lastname: Petersen
authors.forename: T
authors.initials: T
authors.lastname: Uyama
authors.forename: B
authors.initials: B
authors.lastname: Meedendorp
authors.forename: C R
authors.initials: CR
authors.lastname: Wildevuur
mesh_terms: D000818:Animals; D001980:Bronchi / Q000276:immunology* / Q000473:pathology; D002465:Cell Movement; D016572:Cyclosporine / Q000627:therapeutic use; D006084:Graft Rejection / Q000276:immunology* / Q000473:pathology; D006085:Graft Survival / Q000276:immunology*; D016040:Lung Transplantation / Q000276:immunology* / Q000473:pathology; D008214:Lymphocytes / Q000502:physiology; D008221:Lymphoid Tissue / Q000276:immunology* / Q000473:pathology; D008297:Male; D051381:Rats; D011914:Rats, Inbred BN; D011917:Rats, Inbred Lew; D013047:Specific Pathogen-Free Organisms; D013997:Time Factors; D014184:Transplantation, Homologous; D014185:Transplantation, Isogeneic
chemical_list: D016572:Cyclosporine