title: Intraluminal nonbacterial intestinal components control gut and lung injury after trauma hemorrhagic shock.
abstract: OBJECTIVE
  To test whether the mucus layer, luminal digestive enzymes, and intestinal mast cells are critical components in the pathogenesis of trauma shock-induced gut and lung injury.
  
  
  BACKGROUND
  Gut origin sepsis studies have highlighted the importance of the systemic component (ischemia-reperfusion) of gut injury, whereas the intraluminal component is less well studied.
  
  
  METHODS
  In rats subjected to trauma hemorrhagic shock (T/HS) or sham shock, the role of pancreatic enzymes in gut injury was tested by diversion of pancreatic enzymes via pancreatic duct exteriorization whereas the role of the mucus layer was tested via the enteral administration of a mucus surrogate. In addition, the role of mast cells was assessed by measuring mast cell activation and the ability of pharmacologic inhibition of mast cells to abrogate gut and lung injury. Gut and mucus injury was characterized functionally, morphologically, and chemically.
  
  
  RESULTS
  Pancreatic duct exteriorization abrogated T/HS-induced gut barrier loss and limited chemical mucus changes. The mucus surrogate prevented T/HS-induced gut and lung injury. Finally, pancreatic enzyme-induced gut and lung injury seems to involve mast cell activation because T/HS activates mast cells and pharmacologic inhibition of intestinal mast cells prevented T/HS-induced gut and lung injury.
  
  
  CONCLUSIONS
  These results indicate that gut and gut-induced lung injury after T/HS involves a complex process consisting of intraluminal digestive enzymes, the unstirred mucus layer, and a systemic ischemic-reperfusion injury. This suggests the possibility of intraluminal therapeutic strategies.
authors.affiliation: From the Department of Surgery, UMDNJ-NJMS, Newark, NJ.
authors.forename: Jordan E
authors.initials: JE
authors.lastname: Fishman
authors.forename: Sharvil U
authors.initials: SU
authors.lastname: Sheth
authors.forename: Gal
authors.initials: G
authors.lastname: Levy
authors.forename: Vamsi
authors.initials: V
authors.lastname: Alli
authors.forename: Qu
authors.initials: Q
authors.lastname: Lu
authors.forename: Dazhong
authors.initials: D
authors.lastname: Xu
authors.forename: Yung
authors.initials: Y
authors.lastname: Qin
authors.forename: Xiaofa
authors.initials: X
authors.lastname: Qin
authors.forename: Edwin A
authors.initials: EA
authors.lastname: Deitch
mesh_terms: D055371:Acute Lung Injury / Q000209:etiology / Q000628:therapy*; D000818:Animals; D004195:Disease Models, Animal; D004798:Enzymes / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000201:enzymology; D007422:Intestines / Q000201:enzymology*; D008297:Male; D010196:Pancreatic Elastase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012771:Shock, Hemorrhagic / Q000209:etiology / Q000628:therapy*; D014947:Wounds and Injuries / Q000150:complications*
chemical_list: D004798:Enzymes; D010196:Pancreatic Elastase