title: Experimental inflammatory bowel disease--role of T cells.
abstract: BACKGROUND
  Our experiments were aimed to test: 1. which lymphocyte subpopulations participate in mouse colitis, produced by intrarectal (i.r.) deposition of trinitrobenzene sulphonic acid (TNBSA, TNP hapten); 2. the expression of cell adhesion molecules on lymphocytes draining the site of reaction; 3. the influence of mouse haplotype on the development of colitis.
  
  
  METHODS
  CBA/J, BALB/c and C57BI/6 inbred and outbred Swiss Webster strains were used. Mesentheric lymph node (MLN) cells of immunized animals, unseparated or separated into CD4+, CD8+ or gammadelta+ and alphabeta+ T cell subpopulations or depleted of B lymphocytes, were transferred into recipients which were challenged i.r. with TNBSA. Inflammatory reaction in the colon was confirmed macro- and microscopically and by myeloperoxidase (MPO) level. MLN lymphocyte surface markers were tested cytofluorimetrically using appropriate antibodies.
  
  
  RESULTS
  Sensitization with TNP results in chronic colitis (hapten dose-dependent colon weight gain and cellular infiltrate, significant increase of MPO level) only in CBA/J and BALB/c strains and can be adoptively transferred in a cell-dose dependent manner into syngeneic recipients by T alphabeta+ cells of both CD4+ and CD8+ subpopulations. T gammadelta+ cells were ineffective and B lymphocytes do not participate in the passive transfer reaction. In MLN the number of T lymphocytes positive for cell adhesion molecules particularly LPAM-1 (V-CAM1) and LPAM-2 increases significantly.
  
  
  CONCLUSIONS
  Both CD4+ and CD8+ lymphocytes participate in the development of TNP-induced colitis. High MPO level may suggests that both Th1 and Th2 cells are involved. Colitis is accompanied by a significant accumulation in MLN of T lymphocytes positive for several cell surface adhesion molecules characteristic for memory T cells. Significant differences in susceptibility to develop colitis were found between different strains of mice.
authors.affiliation: Department of Immunology, Jagiellonian University College of Medicine, Cracow, Poland.
authors.forename: M
authors.initials: M
authors.lastname: Szczepanik
authors.forename: A
authors.initials: A
authors.lastname: Gryglewski
authors.forename: K
authors.initials: K
authors.lastname: Bryniarski
authors.forename: J
authors.initials: J
authors.lastname: Stachura
authors.forename: W
authors.initials: W
authors.lastname: Ptak
mesh_terms: D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000502:physiology; D018414:CD8-Positive T-Lymphocytes / Q000502:physiology; D017690:Cell Transplantation; D003092:Colitis / Q000139:chemically induced / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D004305:Dose-Response Relationship, Drug; D020022:Genetic Predisposition to Disease; D008198:Lymph Nodes / Q000166:cytology / Q000276:immunology; D016131:Lymphocyte Subsets / Q000276:immunology; D008297:Male; D008643:Mesentery; D051379:Mice; D008815:Mice, Inbred Strains / Q000235:genetics / Q000276:immunology; D013045:Species Specificity; D013601:T-Lymphocytes / Q000276:immunology*; D014302:Trinitrobenzenesulfonic Acid
chemical_list: D014302:Trinitrobenzenesulfonic Acid