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益生菌补充剂对肠道微生物结构在管理中的双刃剑作用。

The double-edged sword of probiotic supplementation on gut microbiota structure in management.

机构信息

Foodborne and Waterborne Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

出版信息

Gut Microbes. 2022 Jan-Dec;14(1):2108655. doi: 10.1080/19490976.2022.2108655.

Abstract

As management has become more challenging and less efficient over the last decade, the interest in innovative interventions is growing by the day. Probiotic co-supplementation to antibiotic therapies is reported in several studies, presenting a moderate reduction in drug-related side effects and a promotion in positive treatment outcomes. However, the significance of gut microbiota involvement in the competence of probiotic co-supplementation is emphasized by a few researchers, indicating the alteration in the host gastrointestinal microbiota following probiotic and drug uptake. Due to the lack of long-term follow-up studies to determine the efficiency of probiotic intervention in eradication, and the delicate interaction of the gut microbiota with the host wellness, this review aims to discuss the gut microbiota alteration by probiotic co-supplementation in management to predict the comprehensive effectiveness of probiotic oral administration.: acyl-CoA- acyl-coenzyme A; AMP- antimicrobial peptide; AMPK- AMP-activated protein kinase; AP-1- activator protein 1; BA- bile acid; BAR- bile acid receptor; BCAA- branched-chain amino acid; C2- acetate; C3- propionate; C4- butyrate; C5- valeric acid; CagA- Cytotoxin-associated gene A; cAMP- cyclic adenosine monophosphate; CD- Crohn's disease; CDI- C. difficile infection; COX-2- cyclooxygenase-2; DC- dendritic cell; EMT- epithelial-mesenchymal transition; FMO- flavin monooxygenases; FXR- farnesoid X receptor; GPBAR1- G-protein-coupled bile acid receptor 1; GPR4- G protein-coupled receptor 4; H2O2- hydrogen peroxide; HCC- hepatocellular carcinoma; HSC- hepatic stellate cell; IBD- inflammatory bowel disease; IBS- irritable bowel syndrome; IFN-γ- interferon-gamma; IgA immunoglobulin A; IL- interleukin; iNOS- induced nitric oxide synthase; JAK1- janus kinase 1; JAM-A- junctional adhesion molecule A; LAB- lactic acid bacteria; LPS- lipopolysaccharide; MALT- mucosa-associated lymphoid tissue; MAMP- microbe-associated molecular pattern; MCP-1- monocyte chemoattractant protein-1; MDR- multiple drug resistance; mTOR- mammalian target of rapamycin; MUC- mucin; NAFLD- nonalcoholic fatty liver disease; NF-κB- nuclear factor kappa B; NK- natural killer; NLRP3- NLR family pyrin domain containing 3; NOC- N-nitroso compounds; NOD- nucleotide-binding oligomerization domain; PICRUSt- phylogenetic investigation of communities by reconstruction of unobserved states; PRR- pattern recognition receptor; RA- retinoic acid; RNS- reactive nitrogen species; ROS- reactive oxygen species; rRNA- ribosomal RNA; SCFA- short-chain fatty acids; SDR- single drug resistance; SIgA- secretory immunoglobulin A; STAT3- signal transducer and activator of transcription 3; T1D- type 1 diabetes; T2D- type 2 diabetes; Th17- T helper 17; TLR- toll-like receptor; TMAO- trimethylamine N-oxide; TML- trimethyllysine; TNF-α- tumor necrosis factor-alpha; Tr1- type 1 regulatory T cell; Treg- regulatory T cell; UC- ulcerative colitis; VacA- Vacuolating toxin A.

摘要

由于过去十年管理变得更加具有挑战性且效率更低,人们对创新干预措施的兴趣与日俱增。在几项研究中报道了抗生素治疗的益生菌联合补充,这表明药物相关副作用的适度减少和积极治疗结果的促进。然而,一些研究人员强调了肠道微生物群在益生菌联合补充中的作用的重要性,表明益生菌和药物摄入后宿主胃肠道微生物群的改变。由于缺乏长期随访研究来确定益生菌干预在根除中的效率,以及肠道微生物群与宿主健康的微妙相互作用,因此本综述旨在讨论益生菌联合补充对管理中肠道微生物群改变的预测:酰基辅酶 A-酰基辅酶 A;抗菌肽 AMP-;AMP 激活蛋白激酶 AMPK-;激活蛋白 1-AP-1;胆酸 BA-;胆酸受体 BAR-;支链氨基酸 BCAA-;醋酸盐 C2-;丙酸盐 C3-;丁酸盐 C4-;戊酸盐 C5-;细胞毒素相关基因 A CagA-;环磷酸腺苷 cAMP-;克罗恩病 CD-;艰难梭菌感染 CDI-;环加氧酶-2 COX-2-;树突细胞 DC-;上皮-间充质转化 EMT-;黄素单加氧酶 FMO-;法尼醇 X 受体 FXR-;G 蛋白偶联胆汁酸受体 1 GPBAR1-;G 蛋白偶联受体 4 GPR4-;过氧化氢 H2O2-;肝细胞癌 HCC-;肝星状细胞 HSC-;炎症性肠病 IBD-;肠易激综合征 IBS-;干扰素-γ IFN-γ;免疫球蛋白 A IgA-;白细胞介素 IL-;诱导型一氧化氮合酶 iNOS-;Janus 激酶 1 JAK1-;连接黏附分子 A JAM-A-;乳酸菌 LAB-;脂多糖 LPS-;黏膜相关淋巴组织 MALT-;微生物相关分子模式 MAMP-;单核细胞趋化蛋白-1 MCP-1-;多药耐药 MDR-;雷帕霉素哺乳动物靶标 mTOR-;粘蛋白 MUC-;非酒精性脂肪性肝病 NAFLD-;核因子 kappa B NF-κB-;自然杀伤细胞 NK-;NLR 家族包含吡啶结构域 3 NLRP3-;亚硝胺 NOC-;核苷酸结合寡聚化结构域 NOD-;未观察到状态重建的群落系统发育研究 PICRUSt-;模式识别受体 PRR-;视黄酸 RA-;活性氮物种 RNS-;活性氧物种 ROS-;核糖体 RNA rRNA-;短链脂肪酸 SCFA-;单一药物耐药 SDR-;分泌型免疫球蛋白 A SIgA-;信号转导和转录激活因子 3 STAT3-;1 型糖尿病 T1D-;2 型糖尿病 T2D-;辅助性 T 细胞 17 Th17-;Toll 样受体 TLR-;氧化三甲胺 TMAO-;三甲基赖氨酸 TML-;肿瘤坏死因子-α TNF-α;1 型调节性 T 细胞 Tr1-;调节性 T 细胞 Treg-;溃疡性结肠炎 UC-;空泡毒素 A VacA-。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/51c6/9373750/1ddc1e7b167b/KGMI_A_2108655_F0001_OC.jpg

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