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The Lard Legacy: Pre and Perinatal Dietary Fat Exposure Alters Offspring Immunity

Thursday, October 11, 2012 — Poster Session IV

2:00 p.m. – 4:00 p.m.

Natcher Conference Center, Building 45




  • IA Myles
  • N Fontecilla
  • B Janelsins
  • P Vithayathil
  • M Lu
  • SK Datta


Rates of sepsis, auto-immunity, and allergies are increasing in Western societies. Response to lipopolysaccharide (LPS) is central in these diseases; LPS-tolerant mice are more susceptible to infections and allergies. Fatty acids modulate LPS signaling though their interaction with TLR4. Because LPS signaling is related to the development of Western disease and because fatty acids can modulate LPS signaling, we hypothesized that fatty acid intake could impact these disease states. We focused on exposures during the peri-natal timeframe. We placed breeding mice on diets high in Omega-6 (O6), high in both saturated fat and Omega-6 (reflective of the Western Diet, WD), or a low-fat/control diet (LF). Pups from all breeders were weaned onto the LF diet for several weeks before being challenged in models of sepsis, MRSA skin infection, peanut allergy, and EAE. Pups from WD breeders had significantly more fatalities after E. coli challenge, had larger MRSA skin infection lesion sizes, greater allergic reactivity to peanut challenge, and had greater EAE susceptibility. Weight, glucose levels, and systemic LPS responses did not explain the differences. WD pups had altered epi-genetic histone methylation at LPS-associated genes such as AOAH, marketed differences in the colonic response to LPS, and an altered gut microbiome.

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