Abstract
Numerous epidemiological studies have shown that a high dietary fiber intake is associated inversely with the incidence of asthma in the population. There have been many studies on the role of soluble dietary fiber, but the mechanism of action for insoluble dietary fiber, such as cellulose-the most widely existing dietary fiber, in asthma is still unclear. The current study investigated the outcomes of a high-cellulose diet in a mouse model of asthma and detected pathological manifestations within the lungs, changes in the intestinal microbiome, and changes in intestinal short-chain fatty acids (SCFAs) in mice. A high-cellulose diet can reduce lung inflammation and asthma symptoms in asthmatic mice. Furthermore, it dramatically changes the composition of the intestinal microbiome. At the family level, a new dominant fungus family Peptostreptococcaceae is produced, and at the genus level, the unique genus Romboutsla, [Ruminococcus]_torques_group was generated. These genera and families of bacteria are closely correlated with lipid metabolism in vivo. Many studies have proposed that the mechanism of dietary fiber regulating asthma may involve the intestinal microbiome producing SCFAs, but the current research shows that a high-cellulose diet cannot increase the content of SCFAs in the intestine. These data suggest that a high-cellulose diet decreases asthma symptoms by altering the composition of the intestinal microbiome, however, this mechanism is thought to be independent of SCFAs and may involve the regulation of lipid metabolism.
Highlights
It is currently believed that most soluble dietary fiber is fermented and broken down by intestinal bacteria to produce short-chain fatty acids (SCFAs), which can participate in the initiation and development of asthma by reducing inflammation within the respiratory tract in asthmatic mice [21] and inhibit the migration of eosinophils [22]
The results showed that the lung inflammation symptoms of asthmatic mice treated with high cellulose diet were significantly improved, and different dominant intestinal microbiome concerning lipid metabolism was produced, but this change may not be achieved by increasing the amount of short-chain fatty acids
Feeds containing different concentrations of cellulose were fed to asthmatic mice to study the effect of a highfiber diet on lung inflammation in asthmatic mouse models
Summary
Allergic asthma is a disease caused by allergens entering the respiratory tract and stimulating B lymphocytes to produce specific antibodies, mainly IgE, and stimulate mast cells, basophils, and other immune cells to release inflammatory mediators [1]. The grantees were Song Wen, Guifang Yuan and Cunya Li, I am the instructor of this project This program was established by Chongqing Medical University to encourage undergraduate students to conduct clinical or basic scientific research and to exercise scientific thinking and research skills. It is currently believed that most soluble dietary fiber is fermented and broken down by intestinal bacteria to produce short-chain fatty acids (SCFAs), which can participate in the initiation and development of asthma by reducing inflammation within the respiratory tract in asthmatic mice [21] and inhibit the migration of eosinophils [22]. The results showed that the lung inflammation symptoms of asthmatic mice treated with high cellulose diet were significantly improved, and different dominant intestinal microbiome concerning lipid metabolism was produced, but this change may not be achieved by increasing the amount of short-chain fatty acids
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: 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.