ABSTRACT

As Helicobacter pylori 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 H. pylori 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 H. pylori management to predict the comprehensive effectiveness of probiotic oral administration.

Abbreviations: 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

随着幽门螺杆菌管理在过去十年中变得更具挑战性和效率降低，对创新干预措施的兴趣与日俱增。几项研究报告了抗生素疗法的益生菌联合补充剂，显示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参与益生菌共同补充能力的重要性，这表明在益生菌和药物吸收后宿主胃肠道微生物群发生了变化。由于缺乏长期随访研究来确定益生菌干预幽门螺杆菌的效率根除，以及肠道微生物群与宿主健康的微妙相互作用，本综述旨在讨论在幽门螺杆菌管理中通过益生菌共同补充来改变肠道微生物群，以预测益生菌口服给药的综合有效性。

缩写：酰基辅酶A-酰基辅酶A；AMP-抗菌肽；AMPK-AMP-活化蛋白激酶；AP-1-激活蛋白1；BA-胆汁酸；BAR-胆汁酸受体；BCAA-支链氨基酸；C2-醋酸盐；C3-丙酸盐；C4-丁酸盐；C5-戊酸；CagA-细胞毒素相关基因A；cAMP-环磷酸腺苷；CD-克罗恩病；CDI-艰难梭菌感染；COX-2-环氧合酶-2；DC-树突状细胞；EMT-上皮-间质转化；FMO-黄素单加氧酶；FXR- 法尼醇 X 受体；GPBAR1-G蛋白偶联胆汁酸受体1；GPR4-G蛋白偶联受体4；H2O2-过氧化氢；HCC-肝细胞癌；HSC-肝星状细胞；IBD-炎症性肠病；IBS-肠易激综合征；IFN-γ-干扰素-γ；IgA 免疫球蛋白 A；IL-白细胞介素；iNOS-诱导的一氧化氮合酶；JAK1-janus激酶1；JAM-A-连接粘附分子A；LAB-乳酸菌；LPS-脂多糖；MALT-黏膜相关淋巴组织；MAMP-微生物相关分子模式；MCP-1-单核细胞趋化蛋白-1；MDR-多重耐药性；mTOR-雷帕霉素的哺乳动物靶标；MUC-粘蛋白；NAFLD-非酒精性脂肪肝；NF-κB-核因子κB；NK-自然杀手；NLRP3-含有3个NLR家族pyrin结构域；NOC-N-亚硝基化合物；NOD-核苷酸结合寡聚化结构域；PICRUSt- 通过重建未观察到的状态对社区进行系统发育调查；PRR-模式识别受体；RA-视黄酸；RNS-活性氮物种；ROS——活性氧；rRNA-核糖体 RNA；SCFA-短链脂肪酸；SDR——单一耐药；SIgA-分泌型免疫球蛋白 A；STAT3-信号转导和转录激活因子 3；T1D-1 型糖尿病；T2D-2型糖尿病；Th17-T 助手 17；TLR-toll 样受体；TMAO-三甲胺 N-氧化物；TML-三甲基赖氨酸；TNF-α-肿瘤坏死因子-α；Tr1- 1型调节性T细胞；Treg-调节性T细胞；UC-溃疡性结肠炎；VacA-空泡毒素A。