Is A High-fiber Diet able to Influence Ovalbumin-induced Allergic Airway Inflammation in a Mouse Model?

• Main Authors: Zhiyu Zhang M.S., Lei Shi Ph.D., Wenhui Pang Ph.D., Xiaoting Wang Ph.D., Jianfeng Li Ph.D., Haibo Wang Ph.D., Guanggang Shi Ph.D.
• Format: Article
• Language: English
• Published: SAGE Publishing 2016-10-01
• Series: Allergy & Rhinology
• Online Access: https://doi.org/10.2500/ar.2016.7.0186

Background More recently, a large amount of experimental and clinical discovered that dietary-fiber intake would decrease the susceptibility to allergic airway disease (AAD) and respiratory inflammation. Objective To investigate whether a fiber-intake supplement is able to influence the induction of AAD and to elucidate the interactive relationship. Methods AAD model mice and control mice were raised on a fundamental diet with standard 4% fiber content, whereas other mice were fed a 10% fiber-content diet in the high fiber-content group, along with a 25% fiber-content diet instead in very-high fiber-content group. All experimental mice were sensitized and challenged with ovalbumin to induce allergic inflammation in both the upper and lower airways. Hallmarks of AAD were examined in terms of eosinophil infiltration and goblet cell metaplasia in subepithelial mucosa, T-helper type 1 (Th1) to Th2 skewing of the immune response. Furthermore, to elucidate the interrelations, we generated 16S ribosomal DNA from fecal samples and further validated the variation of colony composition in each group. Results The excessive high-fiber supplement induced a promoting effect rather than a suppressive effect, including a rise in nasal rubbing and sneezing, an increase in eosinophil inflammation and goblet cell metaplasia in subepithelial mucosa, and promoted Th1 skewing of the immune response as well as the production of serum levels of ovalbumin-specific immunoglobulin E. Moreover, overconsumption of dietary fiber greatly altered the construction of bacterial flora in the intestinal tract, including an increased proportion of Firmicutes, Actinobacteria, and Proteobacteria, and a decreased proportion of Bacteroidetes. Conclusion Our work indicated that, instead of a protecting impact, excessive fiber intake preformed a negative influence on the induction of AAD. Therefore, we suspected that an excessive supplement of dietary fiber might not be an advisable method for the prevention and treatment of AADs.