Abstract
BackgroundParticulate matter (PM) is a key pollutant in ambient air that has been associated with negative health conditions in urban environments. The aim of this study was to examine the effects of orally administered PM on the gut microbiome and immune function under normal and inflammatory conditions.MethodsWild-type 129/SvEv mice were gavaged with Ottawa urban PM10 (EHC-93) for 7–14 days and mucosal gene expression analyzed using Ingenuity Pathways software. Intestinal permeability was measured by lactulose/mannitol excretion in urine. At sacrifice, segments of small and large intestine were cultured and cytokine secretion measured. Splenocytes were isolated and incubated with PM10 for measurement of proliferation. Long-term effects of exposure (35 days) on intestinal cytokine expression were measured in wild-type and IL-10 deficient (IL-10−/−) mice. Microbial composition of stool samples was assessed using terminal restriction fragment length polymorphism. Short chain fatty acids were measured in caecum.ResultsShort-term treatment of wild-type mice with PM10 altered immune gene expression, enhanced pro-inflammatory cytokine secretion in the small intestine, increased gut permeability, and induced hyporesponsiveness in splenocytes. Long-term treatment of wild-type and IL-10−/− mice increased pro-inflammatory cytokine expression in the colon and altered short chain fatty acid concentrations and microbial composition. IL-10−/− mice had increased disease as evidenced by enhanced histological damage.ConclusionsIngestion of airborne particulate matter alters the gut microbiome and induces acute and chronic inflammatory responses in the intestine.
Highlights
Particulate matter (PM) is a key pollutant in ambient air that has been associated with negative health conditions in urban environments [1,2]
Emerging evidence suggests PM exposure can have adverse consequences on the gastrointestinal tract [11], with associations shown between air pollution exposure and an increased risk of appendicitis [12], gastroenteritis [13], Crohn’s Disease (CD) in younger individuals [14], hospitalizations in patients with inflammatory bowel disease (IBD) [15], and colon and liver cancer [16]
Genes down-regulated at 7 days in PM10 treated mice included cytokines (Il13, Il12a, Il5, IFNg), Ccl19, a chemokine involved in T cell trafficking to secondary lymph nodes, and Cd19, a cell marker for B cells
Summary
Particulate matter (PM) is a key pollutant in ambient air that has been associated with negative health conditions in urban environments [1,2]. Epidemiological studies have shown a strong association between PM exposure and adverse health effects, including stroke, myocardial infarction, arrhythmia, cardiac arrest, venous thrombosis, and lung cancer [2,3,4,7,8,9]. Emerging evidence suggests PM exposure can have adverse consequences on the gastrointestinal tract [11], with associations shown between air pollution exposure and an increased risk of appendicitis [12], gastroenteritis [13], Crohn’s Disease (CD) in younger individuals [14], hospitalizations in patients with inflammatory bowel disease (IBD) [15], and colon and liver cancer [16]. Particulate matter (PM) is a key pollutant in ambient air that has been associated with negative health conditions in urban environments. The aim of this study was to examine the effects of orally administered PM on the gut microbiome and immune function under normal and inflammatory conditions
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
