色氨酸及其代谢产物在过敏性哮喘发病机制中的研究进展  

Progress of tryptophan and its metabolites in pathogenesis of allergic asthma

作　　者：王菲(综述)[1] 尚云晓(审校)[1] Wang Fei;Shang Yunxiao(Department of Pediatric Respiratory Medicine,Shengjing Hospital of China Medical University,Shenyang 110004,China)

机构地区：[1]中国医科大学附属盛京医院小儿呼吸内科,沈阳110004

出　　处：《国际儿科学杂志》2022年第1期24-28,共5页International Journal of Pediatrics

基　　金：辽宁省教育厅辽宁省高等学校创新团队支持计划(辽教函(2018)479号)。

摘　　要：气道上皮损害、Th2炎症反应增强、免疫调节性T细胞功能受损是哮喘发生的重要机制。吲哚胺2,3-双加氧酶(indoleamine 2,3-dioxygenase,IDO)由脂多糖、干扰素-γ诱导表达,调控幼稚T细胞分化成CD4+CD25+调节性T细胞(T regulatory cell,Treg),诱导免疫耐受,可抑制嗜酸粒细胞性气道炎症;IDO活性下降可能会促进哮喘的发生。色氨酸代谢产物与芳烃受体作用,促进IL-22的产生,增强上皮的完整性及抗感染性;可改变特异性免疫治疗诱导的Th17/Treg平衡,Treg细胞增多;降低气道炎症,减少炎症细胞因子浸润。D-色氨酸可促进肠道菌群的多样性,增加肺和结肠中Treg的数量,降低Th2炎症反应,降低气道高反应性。色氨酸及其代谢产物、IDO、D-色氨酸等在哮喘发生、发展及特异性免疫治疗中有重要作用。Airway epithelial damage,increased Th2 inflammatory response,and impaired immune regulatory T cell function are important mechanisms for the development of asthma.Indoleamine 2,3-dioxygenase(IDO)is induced by LPS and IFN-γ,which regulates the differentiation of naive T cells into CD4+CD25+regulatory T cells(Treg)and induces immune tolerance.It can inhibit eosinophilic airway inflammation.Decreased IDO activity may promote the development of asthma.Tryptophan metabolites act on AhR receptors to promote the production of IL-22 and enhance the integrity of the epithelium and its resistance to infection.The Th17/Treg balance induced by specific immunotherapy could be altered,and Treg cell proliferation was observed.Tryptophan metabolites can reduce airway inflammation and inflammatory cytokine infiltration.D-tryptophan can promote the diversity of intestinal flora,increase the number of Treg in lung and colon,reduce Th2 reaction,and reduce airway hyperresponsiveness.Tryptophan and its metabolites,IDO and D-tryptophan play an important role in the occurrence,development and specific immunotherapy of asthma.

关 键 词：哮喘 色氨酸 吲哚胺2 3-双加氧酶 D-色氨酸 

分 类 号：R73[医药卫生—肿瘤]