title: Effects of feeding fish oil on mesenteric lymph node cytokine responses in obese leptin receptor-deficient JCR:LA-cp rats.
abstract: OBJECTIVE
  berrant immune responses have been identified in obesity; however, immune cells of lymph nodes residing in the inflammatory environment of visceral adipose tissue have been largely overlooked. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) can reduce inflammation and modify T-cell function and therefore may improve immune function in obesity. Thus, we determined the effects of feeding fish oil (FO) containing EPA and DHA on mesenteric lymph node (MLN) immune cell function.
  
  
  METHODS
  In this study, 14-week-old obese, leptin receptor-deficient JCR:LA-cp rats (cp/cp) (n=10 per group) were randomized to one of three nutritionally adequate diets for 3 weeks: control (ctl, 0% EPA+DHA), low FO (LFO, 0.8% w/w EPA+DHA) or high FO (HFO, 1.4% w/w EPA+DHA). Lean JCR:LA-cp (Cp/cp or Cp/Cp) rats (n=5) were fed ctl diet. MLN cell phospholipid (PL) fatty acid composition, phenotypes and cytokine production were measured.
  
  
  RESULTS
  Obese ctl rats produced more IL-1beta, IL-4 and IL-10, despite a higher proportion of (n-3) polyunsaturated fatty acids (PUFAs) and a lower (n-6):(n-3) PUFA ratio in MLN PL compared with lean ctl rats (P<0.05). Concanavalin A-stimulated IL-2 production did not differ from lean rats even though obese ctl rats had a lower proportion of CD4(+)CD25(+) cells (P<0.05). Feeding FO to obese rats increased the incorporation of (n-3) PUFA into MLN PL and normalized production of IL-1beta (HFO only), IL-4 and IL-10 to the levels similar to lean ctl rats (P<0.05).
  
  
  CONCLUSIONS
  We demonstrate for the first time that obese JCR:LA-cp rats have impaired responses of MLN immune cells to mitogen stimulation and altered PL fatty acid composition. Feeding FO lowered the ex vivo inflammatory response (HFO only) and production of Th2 cytokines, without changing IL-2 production from ConA-stimulated splenocytes, which may occur independent of leptin signalling.
authors.affiliation: Department of Agricultural Food and Nutritional Science, Alberta Institute for Human Nutrition, University of Alberta, Edmonton, Alberta, Canada.
authors.forename: M R
authors.initials: MR
authors.lastname: Ruth
authors.forename: S D
authors.initials: SD
authors.lastname: Proctor
authors.forename: C J
authors.initials: CJ
authors.lastname: Field
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D016207:Cytokines / Q000096:biosynthesis*; D004281:Docosahexaenoic Acids / Q000494:pharmacology; D015118:Eicosapentaenoic Acid / Q000494:pharmacology; D015525:Fatty Acids, Omega-3 / Q000494:pharmacology*; D005395:Fish Oils; D006242:Haptoglobins / Q000032:analysis; D016130:Immunophenotyping; D008198:Lymph Nodes / Q000276:immunology* / Q000473:pathology; D008643:Mesentery; D009765:Obesity / Q000378:metabolism* / Q000473:pathology; D010743:Phospholipids / Q000032:analysis; D011897:Random Allocation; D051381:Rats; D011922:Rats, Mutant Strains; D054411:Receptors, Leptin / Q000172:deficiency*
chemical_list: D016207:Cytokines; D015525:Fatty Acids, Omega-3; D005395:Fish Oils; D006242:Haptoglobins; D010743:Phospholipids; D054411:Receptors, Leptin; D004281:Docosahexaenoic Acids; D015118:Eicosapentaenoic Acid