The Effects of Air Pollution on the Intestinal Microbiota: A Novel Approach to Assess How Gut Microbe Interactions with the Environment Affect Human Health

• Main Author: Fitch, Megan N.
• Other Authors: Lund, Amie K.
• Format: Others
• Language: English
• Published: University of North Texas 2017
• Subjects: intestinal microbiome; air pollution; inhaled air pollution; microbiome; microbiota; intestinal bacteria; SIBO; small intestinal bacterial overgrowth; dysbiosis; atherosclerosis; systemic inflammation; intestinal inflammation; metabolic syndrome; autoimmune disease; IBD; irritable bowel disease; irritable bowel syndrome; gut bacteria; Air > Pollution > Physiological effect.; Intestines > Microbiology.; Intestines > Diseases.
• Online Access: https://digital.library.unt.edu/ark:/67531/metadc984173/

This thesis investigates how air pollution, both natural and anthropogenic, affects changes in the proximal small intestine and ileum microbiota profile, as well as intestinal barrier integrity, histological changes, and inflammation. APO-E KO mice on a high fat diet were randomly selected to be exposed by whole body inhalation to either wood smoke (WS) or mixed vehicular exhaust (MVE), with filtered air (FA) acting as the control. Intestinal integrity and histology were assessed by observing expression of well- known structural components tight junction proteins (TJPs), matrix metallopeptidase-9 (MMP-9), and gel-forming mucin (MUC2), as well known inflammatory related factors: TNF-α, IL-1β, and toll-like receptor (TLR)-4. Bacterial profiling was done using DNA analysis of microbiota within the ileum, utilizing 16S metagenomics sequencing (Illumina miSeq) technique. Overall results of this experiment suggest that air pollution, both anthropogenic and natural, cause a breach in the intestinal barrier with an increase in inflammatory factors and a decrease in beneficial bacteria. This evidence suggests the possibility of air pollution being a potential causative agent of intestinal disease as well as a possible contributing mechanism for induction of systemic inflammation.