Zhang Zhiyu, Shi Lei, Pang Wenhui, Wang Xiaoting, Li Jianfeng, Wang Haibo, Shi Guanggang
Department of Otolaryngology-Head and Neck Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, P.R. China.
Allergy Rhinol (Providence). 2016 Jan 1;7(4):213-222. doi: 10.2500/ar.2016.7.0186.
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.
To investigate whether a fiber-intake supplement is able to influence the induction of AAD and to elucidate the interactive relationship.
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.
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 Th2 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.
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.
最近，大量实验和临床研究发现，膳食纤维摄入可降低过敏性气道疾病（AAD）易感性和呼吸道炎症。
研究膳食纤维补充剂是否会影响AAD的诱发，并阐明其相互作用关系。
将AAD模型小鼠和对照小鼠饲养在纤维含量为标准4%的基础饮食中，而高纤维含量组的其他小鼠喂食纤维含量为10%的饮食，极高纤维含量组则喂食纤维含量为25%的饮食。所有实验小鼠均用卵清蛋白致敏并激发，以诱导上、下呼吸道的过敏性炎症。从嗜酸性粒细胞浸润、上皮下黏膜杯状细胞化生、免疫反应从1型辅助性T细胞（Th1）向2型辅助性T细胞（Th2）偏移等方面检查AAD的特征。此外，为阐明相互关系，我们从粪便样本中提取16S核糖体DNA，并进一步验证每组菌落组成的变化。
过高的膳食纤维补充产生了促进而非抑制作用，包括鼻擦和打喷嚏次数增加、上皮下黏膜嗜酸性粒细胞炎症和杯状细胞化生增加、免疫反应向Th2偏移以及血清中卵清蛋白特异性免疫球蛋白E水平升高。此外，膳食纤维摄入过量极大地改变了肠道菌群结构，包括厚壁菌门、放线菌门和变形菌门比例增加，拟杆菌门比例降低。
我们的研究表明过量摄入膳食纤维对AAD的诱发产生负面影响，而非保护作用。因此，我们怀疑过量补充膳食纤维可能不是预防和治疗AAD的明智方法。
