Accession Number : AD1050351


Title :   Control of Lung Inflammation by Microbiome and Peptidoglycan Recognition Protein


Descriptive Note : Technical Report,01 Jul 2016,30 Jun 2017


Corporate Author : TRUSTEES OF INDIANA UNIVERSITY INDIANAPOLIS United States


Personal Author(s) : Dziarski, Roman


Full Text : https://apps.dtic.mil/dtic/tr/fulltext/u2/1050351.pdf


Report Date : 01 Jul 2017


Pagination or Media Count : 16


Abstract : This project is using a mouse model of experimentally-induced asthma to test two hypotheses: (i) that respiratory and intestinal microbiomes control sensitivity to asthma; and (ii) that this microbiome is controlled by antibacterial innate immunity protein, Peptidoglycan Recognition Protein 1 (Pglyrp1). Microflora was depleted in mice with antibiotics and pregnant females and their pups were colonized with microfloras from wild-type mice or from Pglyrp1-deficient mice. These pups were then sensitized with house dust mite allergen to induce asthma. Mice colonized with microfloras from wild-type or Pglyrp-deficient mice had similar severity of asthma and lung inflammation, as measured by lung resistance test and extent of infiltration with inflammatory cells. By contrast, germ-free mice (completely devoid of microflora), similarly colonized with microbiomes from Pglyrp1-/- mice and sensitized, had significantly less severe asthma and lung inflammation than germ-free mice colonized with microbiomes from wild-type mice, as measured by lung resistance test and extent of infiltration with inflammatory cells. These results indicate that microbiome significantly affects sensitivity to asthma and lung inflammation and that microbiome from Pglyrp1-deficient mice reduces allergic inflammatory response in the lungs compared with microbiome from wild-type mice.


Descriptors :   inflammation , lungs , proteins , sensitivity , asthma , allergens , lung injuries , intestines , immunity


Subject Categories : Medicine and Medical Research
      Anatomy and Physiology
      Biochemistry


Distribution Statement : APPROVED FOR PUBLIC RELEASE