ena-STUDY-Harvard T.H. Chan School of Public Health-16-01-2019-19:33:51:343-671
Male ST2 deficient mice and control WT mice were same-genotype housed or cohoused with the other genotype and place under chow or high fat diet for 12 wks. Gut microbiota were determined in the fecal samples harvested from those mice at end of 12 wks of diet and just before mice being exposed to air or ozone.
Exposure to environmental toxicants can injury the epithelium and release IL-33, and alarmin molecule capable to activate many innate immune cells including ILC2, mast-cells, T-cells, epithelium, etc. IL-33 acts directly on its receptor ST2 and promote secretion of type2 cytokines. The objective of this study was to determine the impact of IL-33 in the ozone-induced airway hyper responsiveness via its contribution in altering the gut microbiota. Age matched mice deficient for IL-33 receptor (ST2-/-) and littermate WT mice were fed with chow (pico 5053) or High Fat Diet (60% caloric intake in fat, Research Diet) for 12-13 weeks. At end of this period, fecal pellets were collected, fecal DNA extracted, and amplified by PCR for bacterial V1-V3 region of 16S rRNA gene and barcoded. The amplicon were sequenced via MiSeq.
Exposure to environmental toxicants can injury the epithelium and release IL-33, and alarmin molecule capable to activate many innate immune cells including ILC2, mast-cells, T-cells, epithelium, etc. IL-33 acts directly on its receptor ST2 and promote secretion of type2 cytokines. The objective of this study was to determine the impact of IL-33 in the ozone-induced airway hyper responsiveness via its contribution in altering the gut microbiota. Age matched mice deficient for IL-33 receptor (ST2-/-) and littermate WT mice were fed with chow (pico 5053) or High Fat Diet (60% caloric intake in fat, Research Diet) for 12-13 weeks. At end of this period, fecal pellets were collected, fecal DNA extracted, and amplified by PCR for bacterial V1-V3 region of 16S rRNA gene and barcoded. The amplicon were sequenced via MiSeq.