title: Route and type of nutrition and surgical stress influence secretory phospholipase A2 secretion of the murine small intestine.
abstract: BACKGROUND
  The function of secretory phospholipase A2 (sPLA2) is site dependent. In tissue, sPLA2 regulates eicosanoid production; in circulation, sPLA2 primes neutrophils; and in the intestinal lumen, sPLA2 provides innate bactericidal immunity as a defensin-related protein. Since parenteral nutrition (PN) primes leukocytes while suppressing intraluminal mucosal immunity, the authors hypothesized that (1) PN would diminish luminal sPLA2 activity but increase activity in intestinal tissue and serum and (2) stress would accentuate these changes.
  
  
  METHODS
  Mice received chow, a complex enteral diet (CED), intragastric PN (IG-PN), or PN in experiment 1 and chow, chow+stress, PN, or PN+stress in experiment 2.
  
  
  RESULTS
  In experiment 1, luminal sPLA2 activity was greatest in chow and decreased in CED, IG-PN, and PN, with PN lower than CED and IG-PN. Compared to that after chow, serum sPLA2 activity dropped after CED, IG-PN, and PN. Serum sPLA2 was higher in portal than systemic serum. In experiment 2, PN lowered luminal sPLA2 activity vs chow. Stress lowered luminal sPLA2 activity in chow, without change in PN. Following stress, luminal immunoglobulin A increased in chow but not PN. Serum sPLA2 activity increased in PN.
  
  
  CONCLUSIONS
  PN attenuates sPLA2 activity in intestinal fluid, consistent with suppressed innate mucosal defense. Stress suppresses luminal fluid sPLA2 activity in chow but not the immunoglobulin A response; PN impairs both. Stress significantly elevates serum sPLA2 in PN-fed mice, consistent with known increased neutrophil priming with PN. PN reduces innate bactericidal immunity of the gut but upregulates serum proinflammatory products poststress.
authors: Department of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
authors: Joseph F
authors: JF
authors: Pierre
authors: Aaron F
authors: AF
authors: Heneghan
authors: Francis H C
authors: FH
authors: Tsao
authors: Yoshifumi
authors: Y
authors: Sano
authors: Mark A
authors: MA
authors: Jonker
authors: Jiro
authors: J
authors: Omata
authors: Jinggang
authors: J
authors: Lan
authors: Kenneth A
authors: KA
authors: Kudsk
mesh_terms: D000818:Animals; D001419:Bacteria; D004750:Enteral Nutrition; D007113:Immunity, Innate / Q000502:physiology*; D018928:Immunity, Mucosal; D007070:Immunoglobulin A / Q000378:metabolism; D018836:Inflammation Mediators / Q000097:blood; D007413:Intestinal Mucosa / Q000201:enzymology* / Q000276:immunology; D007421:Intestine, Small / Q000201:enzymology* / Q000276:immunology; D051379:Mice; D010288:Parenteral Nutrition / Q000009:adverse effects; D054497:Phospholipases A2, Secretory / Q000097:blood / Q000276:immunology / Q000378:metabolism*; D011168:Portal System / Q000276:immunology* / Q000378:metabolism; D013312:Stress, Physiological / Q000276:immunology*
chemical_list: D007070:Immunoglobulin A; D018836:Inflammation Mediators; D054497:Phospholipases A2, Secretory