ena-STUDY-HARVARD SCHOOL OF PUBLIC HEALTH-10-01-2019-18:41:43:368-7
The microbiome contributes to obesity-related increases in the pulmonary response to ozone
Obesity is a risk factor for asthma, especially non-atopic asthma. Established asthma therapeutics like corticosteroids are less effective in obese than lean subjects which associated with severe asthma. In human and mice studies, obesity augments pulmonary responses to ozone, a non-atopic asthma trigger. Obesity related gut microbiome alternation contributes to obesity related condition such as glucose tolerance and systemic inflammation however, still unclear the association between obesity related augmentation of pulmonary responses to ozone and gut microbiome.We find that intact obese gut microbiome contributes to augment ozone induced airway hyperresponsiveness by antibiotics treatment in mice.  Gnotobiotic experiment using germ free mice also indicates obese gut microbiome is sufficient to increase ozone induced pulmonary response to ozone.Additionally, we clarify that prebiotics treatment of fermentable (pectin) but not non-fermentable (cellulose) fiber has beneficial effects to obesity related increases in pulmonary response to ozone with greater manipulation of gut microbiome in obese than lean individual, likely by a mechanisms involving microbial modulation of the immune system rather than changes in short chain fatty acids.Thus, development of these strategies will make greater understanding of the mechanistic basis for the role of the microbiome in the effect of obesity on the lung.
Obesity is a risk factor for asthma, especially non-atopic asthma. Established asthma therapeutics like corticosteroids are less effective in obese than lean subjects which associated with severe asthma. In human and mice studies, obesity augments pulmonary responses to ozone, a non-atopic asthma trigger. Obesity related gut microbiome alternation contributes to obesity related condition such as glucose tolerance and systemic inflammation however, still unclear the association between obesity related augmentation of pulmonary responses to ozone and gut microbiome.We find that intact obese gut microbiome contributes to augment ozone induced airway hyperresponsiveness by antibiotics treatment in mice.  Gnotobiotic experiment using germ free mice also indicates obese gut microbiome is sufficient to increase ozone induced pulmonary response to ozone.Additionally, we clarify that prebiotics treatment of fermentable (pectin) but not non-fermentable (cellulose) fiber has beneficial effects to obesity related increases in pulmonary response to ozone with greater manipulation of gut microbiome in obese than lean individual, likely by a mechanisms involving microbial modulation of the immune system rather than changes in short chain fatty acids.Thus, development of these strategies will make greater understanding of the mechanistic basis for the role of the microbiome in the effect of obesity on the lung.