Lv Jian, Zhang Yu, Liu Shuang, Wang Ruoyu, Zhao Jianan
Graduate School, Heilongjiang University of Chinese Medicine, Harbin, China.
The Affiliated Traditional Chinese Medicine Hospital, Guangzhou Medical University, Guangzhou, China.
Front Pharmacol. 2025 Jul 31;16:1617546. doi: 10.3389/fphar.2025.1617546. eCollection 2025.
Allergic asthma, a chronic respiratory disorder, is intricately linked to gut microbiota dysbiosis and metabolite perturbations through the gut-lung axis.
This review the relationship between microbial immune crosstalk and the onset of asthma, with the aim of determining the mechanism by which gut microbiota drives the onset of asthma and providing evidence for therapeutic interventions.
Literature search was conducted on PubMed using keywords ("gut microbiota" or "gut microbiota" or "gut microbiota metabolites" or "lung gut axis"), ("allergic asthma" or "asthma"), and ("immune regulation"), without date restrictions. Including peer-reviewed studies on human/animal models, articles that do not meet the requirements are excluded.
Microbial imbalance in asthma patients-marked by reduced α-diversity, depletion of immunomodulatory taxa (e.g., Bifidobacterium, Faecalibacterium), and enrichment of pathobionts-disrupts short-chain fatty acid (SCFA) and tryptophan metabolism, skewing Th17/Treg balance toward Th2-dominated inflammation and airway hyperresponsiveness. SCFAs, particularly butyrate, activate GPR41/43 receptors and inhibit histone deacetylases (HDACs), enhancing Treg differentiation while suppressing Th2/Th17 responses. Tryptophan metabolites, such as indole derivatives, alleviate pulmonary inflammation via aryl hydrocarbon receptor (AhR)-dependent IL-22 production. Clinically, diminished SCFA levels correlate with impaired immune tolerance and airway remodeling, while probiotics (, Bifidobacterium), prebiotics, and high-fiber diets restore microbial equilibrium, attenuating asthma severity.
Future research must integrate multi-omics data to delineate strain-specific functions, host-microbe interactions, and individualized responses influenced by genetics, diet, and environmental factors. This review underscores the gut microbiota's dual role as a biomarker and therapeutic target, advocating for microbiota-directed strategies in asthma prevention and precision medicine.
过敏性哮喘是一种慢性呼吸系统疾病,通过肠-肺轴与肠道微生物群失调和代谢物紊乱密切相关。
本综述探讨微生物免疫相互作用与哮喘发病之间的关系,旨在确定肠道微生物群驱动哮喘发病的机制,并为治疗干预提供证据。
在PubMed上进行文献检索,关键词为(“肠道微生物群”或“肠道微生物群”或“肠道微生物群代谢物”或“肠-肺轴”)、(“过敏性哮喘”或“哮喘”)和(“免疫调节”),无日期限制。纳入关于人类/动物模型的同行评审研究,排除不符合要求的文章。
哮喘患者的微生物失衡表现为α多样性降低、免疫调节类群(如双歧杆菌、粪杆菌)减少以及致病共生菌富集,这会破坏短链脂肪酸(SCFA)和色氨酸代谢,使Th17/Treg平衡向以Th2为主的炎症和气道高反应性倾斜。SCFA,尤其是丁酸盐,可激活GPR41/43受体并抑制组蛋白脱乙酰酶(HDAC),增强Treg分化,同时抑制Th2/Th17反应。色氨酸代谢物,如吲哚衍生物,通过芳烃受体(AhR)依赖性白细胞介素-22的产生减轻肺部炎症。临床上,SCFA水平降低与免疫耐受受损和气道重塑相关,而益生菌(如双歧杆菌)、益生元和高纤维饮食可恢复微生物平衡,减轻哮喘严重程度。
未来的研究必须整合多组学数据,以描述菌株特异性功能、宿主-微生物相互作用以及受遗传、饮食和环境因素影响的个体反应。本综述强调了肠道微生物群作为生物标志物和治疗靶点的双重作用,提倡在哮喘预防和精准医学中采用以微生物群为导向的策略。