TY - JOUR T1 - LSC 2013 abstract - Dietary fiber shapes the intestinal and airway microbiome, alters dendritic cell functionality, and leads to an environment less permissive to allergic inflammation JF - European Respiratory Journal JO - Eur Respir J VL - 42 IS - Suppl 57 SP - YI04 AU - Aurelien Trompette AU - Koshika Yadava AU - Eva Gollwitzer AU - Anke Sichelstiel AU - Nicola Harris AU - Laurent Nicod AU - Benjamin Marsland Y1 - 2013/09/01 UR - http://erj.ersjournals.com/content/42/Suppl_57/YI04.abstract N2 - Diet and dysbiosis of host-microbe mutalism has been linked with chronic diseases such as Inflammatory Bowel Disease. Less well established is whether diet and host-microbe interactions influence pulmonary inflammation. To address this we have developed an experimental model in which mice were fed diets high or low in fiber and the consequences for the intestinal and lung microbiomes, the immune system and the development of allergic asthma were determined. We found that dietary fiber content changed both the intestinal and lung microbiome constituents, most notably expanding the phylum Bacteriodetes. Constituents of the Bacteriodetes phylum are known to efficiently metabolize fiber into short-chain fatty acids, and indeed, increased levels of propionate were found in mice fed a high fiber diet. High-fiber fed mice exhibited significantly attenuated allergic airway inflammation following exposure to house dust mite allergens; a phenomenon that was similarly found when mice on regular diets were directly treated with propionate. The mechanism of action critically involved the G-protein coupled receptor, GPR41 but not its related receptor, GPR43. Propionate treatment shaped the maturation of the CD11c+CD11b+FceRa1+ inflammatory dendritic cell subpopulation such that they were capable of inducing naive T cell proliferation in the lymph node, but failed to induce full Th2 cell differentation and effector function. Our results show that diet can influence the intestinal and airway microbiomes, alter the maturation profiles of dendritic cells in the lung and consequently shape the nature of pulmonary inflammation. ER -