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.

Technically, symptom of offspring asthma is also closely reliant on its maternal high-fiber diet as well as the intestinal microbiome. Fruits and vegetables are abundant in inulin, and this naturally soluble dietary fiber is endowed with a potential value on offspring asthma control through the maternal intake, but the mechanism now remains less studied. In this study, rats were given with inulin-included drinking water, whereas in normal group rats were allowed with normal water. Afterwards, we analyzed both the formations of the offspring intestinal microbiome ahead of asthma model establishment and of the maternal intestinal microbiome through high throughput sequence and the short-chain fatty acids (SCFAs) by metabolomic analysis. Subsequently, lung inflammation indexes were detected by Elisa, and the expression of short-chain fatty acid receptors (GPR41, GPR43) in the offspring of asthma models were evaluated through qPCR assay. Inulin intake resulted in altered maternal intestinal microbiome composition, with a significant increase in SCFAs-producing bacteria (mainly Bifidobacterium), attenuating the asthmatic inflammatory response in the offspring. Meanwhile, inulin intake during pregnancy modulates the composition of the intestinal microbiome of the offspring, and this alteration appears before the onset of asthma, hence, there should be further studies onto the impacts of offspring’s intestinal microbiome on asthma procession.