Lin, Tzu-LungTzu-LungLinKuo, Yen-LiangYen-LiangKuoLai, Juo-HsinJuo-HsinLaiLu, Chia-ChenChia-ChenLuCHANG-TSU YUANHsu, Chi-YuChi-YuHsuBO-SHIUN YANWu, Lawrence Shih-HsinLawrence Shih-HsinWuWu, Ting-ShuTing-ShuWuJANN-YUAN WANGCHONG-JEN YUShu, Jwu-ChingJwu-ChingShuHSIN-CHIH LAICHIN-CHUNG SHU2024-08-062024-08-062024https://pubmed.ncbi.nlm.nih.gov/38860456/https://scholars.lib.ntu.edu.tw/handle/123456789/720115The role of gut microbiota in host defense against nontuberculous mycobacterial lung disease (NTM-LD) was poorly understood. Here, we showed significant gut microbiota dysbiosis in patients with NTM-LD. Reduced abundance of was significantly associated with NTM-LD and its disease severity. Compromised TLR2 activation activity in feces and plasma in the NTM-LD patients was highlighted. In the antibiotics-treated mice as a study model, gut microbiota dysbiosis with reduction of TLR2 activation activity in feces, sera, and lung tissue occurred. Transcriptomic analysis demonstrated immunocompromised in lung which were closely associated with increased NTM-LD susceptibility. Oral administration of or its capsular polysaccharides enhanced TLR2 signaling, restored immune response, and ameliorated NTM-LD susceptibility. Our data highlighted the association of gut microbiota dysbiosis, systematically compromised immunity and NTM-LD development. TLR2 activation by or its capsular polysaccharides might help prevent NTM-LD.enGut microbiota dysbiosisTLR2 activationcapsular polysaccharidenontuberculous mycobacterial lung diseaseprevotella copri[SDGs]SDG3journal article10.1080/19490976.2024.236149038860456