title: Effect of proinflammatory interleukins on jejunal nutrient transport.
abstract: OBJECTIVE
  We examined the effect of proinflammatory and anti-inflammatory interleukins on jejunal nutrient transport and expression of the sodium-glucose linked cotransporter (SGLT-1).
  
  
  METHODS
  3-O-methyl glucose and L-proline transport rates were examined in New Zealand White rabbit stripped, short circuited jejunal tissue. The effects of the proinflammatory cytokines interleukin (IL)-1alpha, IL-6, and IL-8, IL-1alpha plus the specific IL-1 antagonist, IL-1ra, and the anti-inflammatory cytokine IL-10 were investigated. In separate experiments, passive tissue permeability was assessed and brush border SGLT-1 expression was measured by western blot in tissues exposed to proinflammatory interleukins.
  
  
  RESULTS
  The proinflammatory interleukins IL-6, IL-1alpha, and IL-8 significantly increased glucose absorption compared with control levels. This increase in glucose absorption was due to an increase in mucosal to serosal flux. IL-1alpha and IL-8 also significantly increased L-proline absorption due to an increase in absorptive flux. The anti-inflammatory IL-10 had no effect on glucose transport. The receptor antagonist IL-1ra blocked the ability of IL-1alpha to stimulate glucose transport. IL-8 had no effect on passive tissue permeability. SGLT-1 content did not differ in brush border membrane vesicles (BBMV) from control or interleukin treated tissue.
  
  
  CONCLUSIONS
  These findings suggest that intestinal inflammation and release of inflammatory mediators such as interleukins increase nutrient absorption in the gut. The increase in glucose transport does not appear to be due to changes in BBMV SGLT-1 content.
authors.affiliation: Gastrointestinal Research Group, University of Calgary, Alberta, Canada.
authors.forename: J
authors.initials: J
authors.lastname: Hardin
authors.forename: K
authors.initials: K
authors.lastname: Kroeker
authors.forename: B
authors.initials: B
authors.lastname: Chung
authors.forename: D G
authors.initials: DG
authors.lastname: Gall
mesh_terms: D019325:3-O-Methylglucose / Q000378:metabolism*; D000818:Animals; D015153:Blotting, Western; D004751:Enteritis / Q000503:physiopathology; D007375:Interleukin-1 / Q000037:antagonists & inhibitors / Q000494:pharmacology; D016753:Interleukin-10 / Q000494:pharmacology; D015850:Interleukin-6 / Q000494:pharmacology; D016209:Interleukin-8 / Q000494:pharmacology; D007378:Interleukins / Q000494:pharmacology*; D007408:Intestinal Absorption / Q000187:drug effects / Q000502:physiology; D007579:Jejunal Diseases / Q000503:physiopathology; D007583:Jejunum / Q000187:drug effects* / Q000502:physiology; D008562:Membrane Glycoproteins / Q000378:metabolism*; D008871:Microvilli / Q000187:drug effects / Q000502:physiology; D009004:Monosaccharide Transport Proteins / Q000378:metabolism*; D011392:Proline / Q000378:metabolism; D011817:Rabbits; D051269:Sodium-Glucose Transporter 1
chemical_list: D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D007378:Interleukins; D008562:Membrane Glycoproteins; D009004:Monosaccharide Transport Proteins; D051269:Sodium-Glucose Transporter 1; D016753:Interleukin-10; D019325:3-O-Methylglucose; D011392:Proline