title: Hemorrhagic shock induces a proinflammatory milieu in the gut lumen.
abstract: BACKGROUND
  Intestinal injury is a consequence of hemorrhagic shock and resuscitation. The intestinal mucosa has been shown to respond to ischemia/reperfusion injury with production of inflammatory mediators. Previous work in our laboratory indicates that intestinal epithelial cells secrete proinflammatory cytokines in the direction of both the lamina propria and intestinal lumen. The ability of the intestinal mucosa to transmit inflammatory signals into the gut lumen after hemorrhagic shock is unknown. We hypothesized that hemorrhagic shock results in secretion of proinflammatory cytokines into the gut lumen.
  
  
  METHODS
  Male C57/Bl6 mice underwent femoral artery cannulation and hemorrhage to a systolic blood pressure of 20 mmHg for 1 h, then resuscitation with lactated Ringer's (LR) solution. Sham animals were cannulated only. Mice were decannulated and sacrificed at intervals. Stool and succus were removed from intestinal segments, weighed, and placed into buffer solution. Specimens were analyzed via enzyme-linked immunosorbent assay (ELISA).
  
  
  RESULTS
  Compared with sham-injured mice, hemorrhagic shock resulted in increased intestinal luminal cytokines. At 3 h after injury, elevated levels of IL-6 were found in the cecal stool. At 6 h after injury, TNFα, IL-6, and MIP-2 were significantly elevated in the cecal stool, and IL-6 and MIP-2 were significantly elevated in the distal colonic stool.
  
  
  CONCLUSIONS
  Hemorrhagic shock results in secretion of proinflammatory cytokines into the intestinal lumen. These findings suggest that the intestinal mucosa may transmit and receive signals in a paracrine fashion via the gut lumen.
authors.affiliation: Department of Surgery, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. sonnieds@ucmail.uc.edu
authors.forename: Dennis I
authors.initials: DI
authors.lastname: Sonnier
authors.forename: Amy T
authors.initials: AT
authors.lastname: Makley
authors.forename: Lou Ann W
authors.initials: LA
authors.lastname: Friend
authors.forename: Stephanie R
authors.initials: SR
authors.lastname: Bailey
authors.forename: Alex B
authors.initials: AB
authors.lastname: Lentsch
authors.forename: Timothy A
authors.initials: TA
authors.lastname: Pritts
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000276:immunology; D001810:Blood Volume / Q000276:immunology; D054426:Chemokine CXCL2 / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism*; D004751:Enteritis / Q000276:immunology*; D005243:Feces; D015850:Interleukin-6 / Q000378:metabolism; D007413:Intestinal Mucosa / Q000276:immunology* / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D019899:Paracrine Communication / Q000276:immunology; D012151:Resuscitation; D012771:Shock, Hemorrhagic / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D054426:Chemokine CXCL2; C404915:Cxcl2 protein, mouse; D016207:Cytokines; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha