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近日，江南大学食品科学与资源挖掘全国重点实验室陈卫院士团队在国际期刊《Microbiological Research》（IF：6.1）发表了题为“The gut core microbial species Bifidobacterium longum: Colonization, mechanisms, and health benefits”的综述论文。肖越副研究员为第一作者兼通讯作者，Lijuan Huang为共同第一作者。
长双歧杆菌（B. longum）是一种人类肠道核心微生物，其数量与宿主的年龄和健康状况密切相关。已有研究表明，长双歧杆菌能够调节宿主肠道微生态，并有缓解多种疾病的潜力。全面了解长双歧杆菌的定殖机制以及宿主与长双歧杆菌相互作用的机制，能够为我们通过以长双歧杆菌为导向的策略来预防和治疗人类疾病提供可能。在这篇综述中，我们总结了长双歧杆菌在肠道定殖的特点，探讨了能够使固有的和 / 或摄入的长双歧杆菌菌株增殖的饮食因素，并回顾了长双歧杆菌对多种疾病的干预机制。关键发现如下：首先，长双歧杆菌具有特殊的定殖机制，例如其碳水化合物利用谱较广，这使其能够适应宿主的饮食；其具有编码胆盐水解酶（BSHs）的物种水平的保守基因，以及适宜的细菌表面结构。其次，饮食干预（如摄入花青素）能够有效改善长双歧杆菌在肠道的定殖情况，这证明了通过饮食调节菌株定殖的可行性。最后，我们分析了长双歧杆菌在不同类型疾病中的数量变化情况，并总结了长双歧杆菌缓解消化系统疾病（通过刺激潘氏细胞活性来修复肠黏膜屏障）、免疫系统疾病（上调调节性 T 细胞（Treg）数量并维持 Th1/Th2 平衡）以及神经系统疾病（通过肠 - 脑轴调节大脑中的犬尿氨酸途径和喹啉酸水平）的主要机制。
目前关于机制见解的研究通常存在高度质量异质性，其中大多数研究较为肤浅，并且缺乏临床证据。尽管我们已经了解了长双歧杆菌在定殖以及缓解疾病方面的机制，但在我们能够选择或定制一种合适的方式来改变长双歧杆菌的数量以实现治疗效果之前，仍有大量工作要做。例如，目前大多数研究仅聚焦于长双歧杆菌的种 / 亚种数量的变化。我们需要开展更深入的研究，以确定与宿主生理状况相关的关键菌株或其代谢产物，期望能利用这些已确定的菌株 / 代谢产物来治疗相关疾病。此外，口服补充长双歧杆菌目前是弥补肠道内长双歧杆菌水平不足的最可行方法之一；然而，要确保长双歧杆菌在已形成的肠道基线微生物群落中定殖是很困难的。为了解决这一问题，多项研究已经证实了长双歧杆菌的外部保护技术，尤其是微胶囊技术的有效性；然而，由于资金限制和生产技术的局限，该技术并不适合工业化规模生产。因此，受饮食对长双歧杆菌肠道定殖的调节作用的启发，我们可以尝试改变日常饮食成分或定制合生元 / 益生菌来达到预期效果。然而，还需要付出更多努力来探索这些益生菌或合生元的最佳配方以及它们缓解各类疾病所涉及的机制，以最终推动它们在改善人类健康方面的转化应用。
Fig. 1. Alteration of intestinal B. longum and Bifidobacterium in diseases according to the combined information from the databases "Disbiome" and "Peryton". We sorted out the results retrieved from the “Disbiome” and “Peryton” databases into supplementary Table S1, and the consistent results of two databases have been prioritizedly cited in this figure, and further supplemented with data retrieved from the database “Disbiome” focusing on diseases of general concerns. It should be mentioned that we could only draw conclusion on association direction based on summarizing the current available data, and the conclusions on the positive, and negative associations might be changed if new contrast evidences are reported. PD, Parkinson’s disease; CD, celiac disease; OB, obesity; LC, lung cancer; ASD, autism spectrum disorders; RS, Rett syndrome; IBS, irritable bowel syndrome; UC, ulcerative colitis; AD, Alzheimer’s disease.
Fig. 2. The proposed mechanisms of B. longum colonization in the human gut. B. longum colonization of the human gut is affected by various factors such as intestinal epithelial adhesion, bile acid resistance, acid tolerance, selection of available carbon resources, microbial interactions, and host immune recognition. EPS, exopolysaccharides; EV, extracellular vesicle; BSH, bile salt hydrolase; HMOs, human milk oligosaccharides; SCFAs, short chain fatty acids; AXOS, arabinoxylan oligosaccharides; ABC Transporter, ATP-binding cassette transporter; EPS, extracellular polysaccharides; CPS, capsule polysaccharides.
Fig. 3. The proposed mechanisms of B. longum alleviates digestive diseases. (a) B. longum could stimulate the intestinal epithelial cells to reduce water reabsorption. (b) B. longum has an active effect on treating constipation; it could promote intestinal motility through the 5-hydroxytryptamine pathway and/or increase the production of gastrointestinal peptides. (c) B. longum increased the levels of CLA and produced EPS to upregulate the expression of tight junction proteins, and the pili proteins of B. longum could inhibit pathogen adhesion. (d) B. longum could stimulate Paneth cells to maintain epithelial homeostasis in IBS or IBD by releasing intestinal stem cell proliferation signals, such as Wnt3A and PLA II. (e) B. longum plays a significant role in regulating inflammatory factors and reactions. VIP, vasoactive intestinal peptide; MTL, motilin; GAS, gastrin; cAMP, cyclic adenosine monophosphate; 5-HT4R, 5 hydroxytryptamine 4 receptor; TLR, Toll-like receptors; PKA, protein kinase A; SCFAs, short chain fatty acids; AQP, aquaporin; WNT3a and PLAⅡ, intestinal stem cells proliferation signals; Fim M, a type of pili protein; LA, linoleic acid; CLA, conjugated linoleic acid; ROS, reactive oxygen species; IKK, inhibitor of kappa B kinase.
Fig. 4. The proposed mechanisms of B. longum alleviating allergic diseases. (a) B. longum could reduce the number of Th2 cells and inhibits IgE activity. (b) B. longum could induce IgE to bind with IgETRAP to reduce the negative effects of IgE on the host immune system. (c) B. longum could regulate the Th1/Th2 balance and upregulate the function of Tregs to alleviate allergic rhinitis. (d) ESBP, a protein derived from B. longum EV, could stimulate mast cell death and inhibits food allergies. (e) B. longum significantly increased the expression of antimicrobial peptide genes (e.g., CAMP, hBD-2, hBD-3) to enhance the skin immune barrier function significantly. ESBP, extracellular solute-binding protein; IgE, immunoglobulin E; IgETRAP, the binding form of IgE; CAMP, cathelicidin protein; hBD-2, human β-defensin 2; hBD-3, human β-defensin 3.
Fig. 5. The proposed mechanisms of B. longum alleviating cognitive disorders. The SCFAs produced by B. longum could induce cytokine changes to reduce neuronal damage. Additionally, SCFAs could induce the 5-HT pathway to enhance epithelial barrier function. B. longum could eliminate the negative effect of LPS, which could reduce the expression of BDNF through the NF-κB pathway. B. longum could regulate tryptophan metabolism, and its secondary metabolites KYN and IAA could subsequently affect nerve cells. QUIN, quinolinic acid; KYN, kynurenine; KYNA, kynurenic acid; SERT, serotonin transporter; ECC, enterochromaffin cells; 5-HT, 5-hydroxytryptophan; IAA, 3-indoleacetic acid; TLR4, toll-like receptor 4; IAM, iodoacetamide; 5-HTP, 5-hydroxytryptophan; CLDN-8, claudin-8; CLDN-10, claudin-10; IDO1, indoleamine 2,3-dioxygenase 1; TMO, toluenemonooxygenase; AMPK, adenosine 5’-monophosphate (AMP)-activated protein kinase; SIRT1, silent mating type information regulation 2 homolog 1; PGC-1α, peroxisome proliferator-activated receptor-γ coactivator 1α; AhR, aryl Hydrocarbon Receptor; 5-HT1A, 5-hydroxytryptamine/serotonin receptor 1A; cAMP, cyclic adenosine monophosphate; PKA, cAMP dependent protein kinase A; CERB, cyclic-AMP response binding protein; AFMID, kynurenine formamidase; TPH1, tryptophan hydroxylase 1; AAAD, aromatic amino acid decarboxylase; IaaH, indoleacetamide hydrolase; IaaM, tryptophan-2-monooxygenase.
https://doi.org/10.1016/j.micres.2024.127966
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肉与肉制品 蛋与蛋制品 水产品 奶及奶制品
豆及豆制品 果蔬及果蔬制品 大米及米制品 食用菌
炎症性肠病 糖尿病 肝病 神经疾病
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