title: Gut ischemia-reperfusion affects gut mucosal immunity: a possible mechanism for infectious complications after severe surgical insults.
abstract: OBJECTIVE
  To examine influences of gut ischemia/reperfusion (I/R) on gut-associated lymphoid tissue (GALT) mass and function.
  
  
  METHODS
  Prospective, randomized controlled study.
  
  
  METHODS
  Research laboratory.
  
  
  METHODS
  Male Institute of Cancer Research mice.
  
  
  METHODS
  Ninety mice were randomized to three groups: I/R (60-min gut ischemia), sham (laparotomy only), and control (no operation). On days 1, 2, 4, 7, and 10, mice were killed to harvest lymphocytes from Peyer patches, the intraepithelial space, and the lamina propria (LP) of the small intestine. Respiratory tract and small intestinal washings were also obtained.
  
  
  RESULTS
  Gut I/R significantly reduced lymphocyte numbers in Peyer patches, the intraepithelial space, and the LP. The reduction was prominent in GALT effector sites, that is, the intraepithelial space and LP, but numbers recovered quickly in LP. Changes in cell numbers in Peyer patches, GALT inductive sites, were subtle but persistent. Gut I/R reduced B cell numbers in Peyer patches; alphabeta T cell receptor (TCR)+, gammadeltaTCR+, CD8+, and B cell numbers in the intraepithelial space; and gammadeltaTCR+, CD8+, and B cell numbers in the LP, in comparison with the sham or control group. There were no significant differences in respiratory tract immunoglobulin A levels between the I/R and sham groups. Intestinal immunoglobulin A was elevated on day 1 in the I/R group, with no significant difference after day 2 in comparison with the sham group.
  
  
  CONCLUSIONS
  Despite the maintained mucosal immunoglobulin A level, gut I/R markedly reduces GALT cell numbers, with changes in lymphocyte phenotypes. These alterations may be associated with increased morbidity due to infectious complications after severe surgical insults.
authors.affiliation: Division of Basic Traumatology, National Defense Medical College Research Institute, Tokyo, Japan.
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Fukatsu
authors.forename: Shuri
authors.initials: S
authors.lastname: Sakamoto
authors.forename: Etsuko
authors.initials: E
authors.lastname: Hara
authors.forename: Chikara
authors.initials: C
authors.lastname: Ueno
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Maeshima
authors.forename: Isamu
authors.initials: I
authors.lastname: Matsumoto
authors.forename: Hidetaka
authors.initials: H
authors.lastname: Mochizuki
authors.forename: Hoshio
authors.initials: H
authors.lastname: Hiraide
mesh_terms: D000818:Animals; D001424:Bacterial Infections / Q000276:immunology / Q000503:physiopathology; D002478:Cells, Cultured; D004195:Disease Models, Animal; D005434:Flow Cytometry; D007070:Immunoglobulin A / Q000276:immunology; D007413:Intestinal Mucosa / Q000276:immunology* / Q000503:physiopathology; D007421:Intestine, Small / Q000098:blood supply* / Q000276:immunology* / Q000473:pathology; D007813:Laparotomy / Q000009:adverse effects; D018655:Lymphocyte Count; D008221:Lymphoid Tissue / Q000276:immunology* / Q000473:pathology; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D010581:Peyer's Patches / Q000276:immunology / Q000473:pathology; D011183:Postoperative Complications / Q000276:immunology / Q000382:microbiology; D011336:Probability; D011897:Random Allocation; D012016:Reference Values; D015427:Reperfusion Injury / Q000276:immunology* / Q000503:physiopathology
chemical_list: D007070:Immunoglobulin A