Pub Date : 2024-01-01Epub Date: 2024-01-04DOI: 10.1080/19490976.2023.2298246
Giorgio Gargari, Giacomo Mantegazza, Cesare Cremon, Valentina Taverniti, Alice Valenza, Maria Raffaella Barbaro, Giovanni Marasco, Robin Duncan, Walter Fiore, Roberto Ferrari, Valerio De Vitis, Giovanni Barbara, Simone Guglielmetti
Probiotics are exploited for adjuvant treatment in IBS, but reliable guidance for selecting the appropriate probiotic to adopt for different forms of IBS is lacking. We aimed to identify markers for recognizing non-constipated (NC) IBS patients that may show significant clinical improvements upon treatment with the probiotic strain Lacticaseibacillus paracasei DG (LDG). To this purpose, we performed a post-hoc analysis of samples collected during a multicenter, double-blind, parallel-group, placebo-controlled trial in which NC-IBS patients were randomized to receive at least 24 billion CFU LDG or placebo capsules b.i.d. for 12 weeks. The primary clinical endpoint was the composite response based on improved abdominal pain and fecal type. The fecal microbiome and serum markers of intestinal (PV1 and zonulin), liver, and kidney functions were investigated. We found that responders (R) in the probiotic arm (25%) differed from non-responders (NR) based on the abundance of 18 bacterial taxa, including the families Coriobacteriaceae, Dorea spp. and Collinsella aerofaciens, which were overrepresented in R patients. These taxa also distinguished R (but not NR) patients from healthy controls. Probiotic intervention significantly reduced the abundance of these bacteria in R, but not in NR. Analogous results emerged for C. aerofaciens from the analysis of data from a previous trial on IBS with the same probiotic. Finally, C. aerofaciens was positively correlated with the plasmalemmal vesicle associated protein-1 (PV-1) and the markers of liver function. In conclusion, LDG is effective on NC-IBS patients with NC-IBS with a greater abundance of potential pathobionts. Among these, C. aerofaciens has emerged as a potential predictor of probiotic efficacy.
益生菌可用于肠易激综合征的辅助治疗,但目前还缺乏针对不同形式肠易激综合征选择合适益生菌的可靠指导。我们的目的是找出识别非便秘(NC)肠易激综合征患者的标志物,这些患者在接受益生菌菌株副乳酸杆菌 DG(LDG)治疗后,临床症状可能会明显改善。为此,我们对一项多中心、双盲、平行组、安慰剂对照试验中收集的样本进行了事后分析,在该试验中,NC 肠易激综合征患者被随机分配到至少 240 亿 CFU LDG 或安慰剂胶囊中,每日服用 12 周。主要临床终点是基于腹痛和粪便类型改善的综合反应。我们对粪便微生物群以及肠道(PV1 和 zonulin)、肝脏和肾脏功能的血清标志物进行了调查。我们发现,益生菌组中的应答者(R)(25%)与非应答者(NR)在 18 个细菌类群的丰度上存在差异,其中包括 Coriobacteriaceae、Dorea spp.和 Collinsella aerofaciens 科,这些类群在 R 患者中的比例较高。这些分类群还将 R 型(而非 NR 型)患者与健康对照组区分开来。益生菌干预大大降低了这些细菌在 R 患者中的含量,但在 NR 患者中却没有。通过对之前使用同一种益生菌进行的肠易激综合征试验数据进行分析,也得出了类似的结果。最后,铜绿假单胞菌与质膜囊泡相关蛋白-1(PV-1)和肝功能指标呈正相关。总之,LDG 对潜在致病菌较多的 NC-IBS 患者有效。其中,C. aerofaciens已成为益生菌疗效的潜在预测因子。
{"title":"<i>Collinsella aerofaciens</i> as a predictive marker of response to probiotic treatment in non-constipated irritable bowel syndrome.","authors":"Giorgio Gargari, Giacomo Mantegazza, Cesare Cremon, Valentina Taverniti, Alice Valenza, Maria Raffaella Barbaro, Giovanni Marasco, Robin Duncan, Walter Fiore, Roberto Ferrari, Valerio De Vitis, Giovanni Barbara, Simone Guglielmetti","doi":"10.1080/19490976.2023.2298246","DOIUrl":"10.1080/19490976.2023.2298246","url":null,"abstract":"<p><p>Probiotics are exploited for adjuvant treatment in IBS, but reliable guidance for selecting the appropriate probiotic to adopt for different forms of IBS is lacking. We aimed to identify markers for recognizing non-constipated (NC) IBS patients that may show significant clinical improvements upon treatment with the probiotic strain <i>Lacticaseibacillus paracasei</i> DG (LDG). To this purpose, we performed a post-hoc analysis of samples collected during a multicenter, double-blind, parallel-group, placebo-controlled trial in which NC-IBS patients were randomized to receive at least 24 billion CFU LDG or placebo capsules <i>b.i.d</i>. for 12 weeks. The primary clinical endpoint was the composite response based on improved abdominal pain and fecal type. The fecal microbiome and serum markers of intestinal (PV1 and zonulin), liver, and kidney functions were investigated. We found that responders (R) in the probiotic arm (25%) differed from non-responders (NR) based on the abundance of 18 bacterial taxa, including the families <i>Coriobacteriaceae</i>, <i>Dorea</i> spp. and <i>Collinsella aerofaciens</i>, which were overrepresented in R patients. These taxa also distinguished R (but not NR) patients from healthy controls. Probiotic intervention significantly reduced the abundance of these bacteria in R, but not in NR. Analogous results emerged for <i>C. aerofaciens</i> from the analysis of data from a previous trial on IBS with the same probiotic. Finally, <i>C. aerofaciens</i> was positively correlated with the plasmalemmal vesicle associated protein-1 (PV-1) and the markers of liver function. In conclusion, LDG is effective on NC-IBS patients with NC-IBS with a greater abundance of potential pathobionts. Among these, <i>C. aerofaciens</i> has emerged as a potential predictor of probiotic efficacy.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":null,"pages":null},"PeriodicalIF":12.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10773624/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139097653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hepatocellular carcinoma (HCC) is a leading cause of cancer-related deaths worldwide, and emerging evidence suggests that the gut microbiota may play a role in its development and progression. In this study, the association between B. thetaiotaomicron, a gut microbiota species, and HCC recurrence, as well as patient clinical outcomes, was investigated. It was observed that B. thetaiotaomicron-derived acetic acid has the potential to modulate the polarization of pro-pro-inflammatory macrophagess, which promotes the function of cytotoxic CD8+ T cells. The increased biosynthesis of fatty acids was implicated in the modulation of pro-inflammatory macrophages polarization by B. thetaiotaomicron-derived acetic acid. Furthermore, B. thetaiotaomicron-derived acetic acid was found to facilitate the transcription of ACC1, a key enzyme involved in fatty acid biosynthesis, through histone acetylation modification in the ACC1 promoter region. Curcumin, an acetylation modification inhibitor, significantly blocked the inhibitory effects of B. thetaiotaomicron and acetic acid on HCC tumor growth. These findings highlight the potential role of gut microbiota-derived acetic acid in HCC recurrence and patient clinical outcomes, and suggest a complex interplay between gut microbiota, immune modulation, fatty acid metabolism, and epigenetic regulation in the context of HCC development. Further research in this area may provide insights into novel strategies for HCC prevention and treatment by targeting the gut microbiota and its metabolites.
肝细胞癌(HCC)是全球癌症相关死亡的主要原因之一,而新出现的证据表明,肠道微生物群可能在其发展和恶化过程中起着一定的作用。本研究调查了肠道微生物群物种 B. thetaiotaomicron 与 HCC 复发以及患者临床预后之间的关系。研究发现,B. thetaiotaomicron 衍生的乙酸有可能调节促炎症巨噬细胞的极化,从而促进细胞毒性 CD8+ T 细胞的功能。脂肪酸生物合成的增加与泰妙菌素衍生乙酸对促炎巨噬细胞极化的调节有关。此外,研究还发现源于B. Thetaiotaomicron的乙酸可通过ACC1启动子区域的组蛋白乙酰化修饰促进参与脂肪酸生物合成的关键酶ACC1的转录。姜黄素是一种乙酰化修饰抑制剂,它能明显阻断B. thetaiotaomicron和乙酸对HCC肿瘤生长的抑制作用。这些发现凸显了肠道微生物群衍生的乙酸在 HCC 复发和患者临床预后中的潜在作用,并表明在 HCC 的发展过程中,肠道微生物群、免疫调节、脂肪酸代谢和表观遗传调控之间存在着复杂的相互作用。该领域的进一步研究可能会为针对肠道微生物群及其代谢产物的新型 HCC 预防和治疗策略提供新的见解。
{"title":"<i>B. thetaiotaomicron</i>-derived acetic acid modulate immune microenvironment and tumor growth in hepatocellular carcinoma.","authors":"Hongbin Ma, Liang Yang, Yingchao Liang, Fenghua Liu, Jinxiang Hu, Rui Zhang, Yong Li, Lei Yuan, Feiling Feng","doi":"10.1080/19490976.2023.2297846","DOIUrl":"10.1080/19490976.2023.2297846","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a leading cause of cancer-related deaths worldwide, and emerging evidence suggests that the gut microbiota may play a role in its development and progression. In this study, the association between <i>B. thetaiotaomicron</i>, a gut microbiota species, and HCC recurrence, as well as patient clinical outcomes, was investigated. It was observed that <i>B. thetaiotaomicron</i>-derived acetic acid has the potential to modulate the polarization of <b>pro-pro-inflammatory macrophagess</b>, which promotes the function of cytotoxic CD8+ T cells. The increased biosynthesis of fatty acids was implicated in the modulation of <b>pro-inflammatory macrophages</b> polarization by <i>B. thetaiotaomicron</i>-derived acetic acid. Furthermore, <i>B. thetaiotaomicron</i>-derived acetic acid was found to facilitate the transcription of ACC1, a key enzyme involved in fatty acid biosynthesis, through histone acetylation modification in the ACC1 promoter region. Curcumin, an acetylation modification inhibitor, significantly blocked the inhibitory effects of <i>B. thetaiotaomicron</i> and acetic acid on HCC tumor growth. These findings highlight the potential role of gut microbiota-derived acetic acid in HCC recurrence and patient clinical outcomes, and suggest a complex interplay between gut microbiota, immune modulation, fatty acid metabolism, and epigenetic regulation in the context of HCC development. Further research in this area may provide insights into novel strategies for HCC prevention and treatment by targeting the gut microbiota and its metabolites.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":null,"pages":null},"PeriodicalIF":12.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10813637/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139546120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Probiotics are live microorganisms that offer potential benefits to their hosts and can occasionally influence behavioral responses. However, the detailed mechanisms by which probiotics affect the behavior of their hosts and the underlying biogenic effects remain unclear. Lactic acid bacteria, specifically Lactobacillus spp. are known probiotics. Drosophila melanogaster, commonly known as the fruit fly, is a well-established model organism for investigating the interaction between the host and gut microbiota in translational research. Herein, we showed that 5-day administration of Lactobacillus acidophilus (termed GMNL-185) or Lacticaseibacillus rhamnosus (termed GMNL-680) enhances olfactory-associative memory in Drosophila. Moreover, a combined diet of GMNL-185 and GMNL-680 demonstrated synergistic effects on memory functions. Live brain imaging revealed a significant increase in calcium responses to the training odor in the mushroom body β and γ lobes of flies that underwent mixed feeding with GMNL-185 and GMNL-680. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and whole-mount brain immunohistochemistry revealed significant upregulation of lactate dehydrogenase (LDH) expression in the fly brain following the mixed feeding. Notably, the genetic knockdown of Ldh in neurons, specifically in mushroom body, ameliorated the beneficial effects of mixed feeding with GMNL-185 and GMNL-680 on memory improvement. Altogether, our results demonstrate that supplementation with L. acidophilus and L. rhamnosus enhances memory functions in flies by increasing brain LDH levels.
{"title":"Probiotic <i>Lactobacillus</i> spp. improves <i>Drosophila</i> memory by increasing lactate dehydrogenase levels in the brain mushroom body neurons.","authors":"Shuk-Man Ho, Wan-Hua Tsai, Chih-Ho Lai, Meng-Hsuan Chiang, Wang-Po Lee, Hui-Yu Wu, Pei-Yi Bai, Tony Wu, Chia-Lin Wu","doi":"10.1080/19490976.2024.2316533","DOIUrl":"10.1080/19490976.2024.2316533","url":null,"abstract":"<p><p>Probiotics are live microorganisms that offer potential benefits to their hosts and can occasionally influence behavioral responses. However, the detailed mechanisms by which probiotics affect the behavior of their hosts and the underlying biogenic effects remain unclear. Lactic acid bacteria, specifically <i>Lactobacillus</i> spp. are known probiotics. <i>Drosophila melanogaster</i>, commonly known as the fruit fly, is a well-established model organism for investigating the interaction between the host and gut microbiota in translational research. Herein, we showed that 5-day administration of <i>Lactobacillus acidophilus</i> (termed GMNL-185) or <i>Lacticaseibacillus rhamnosus</i> (termed GMNL-680) enhances olfactory-associative memory in <i>Drosophila</i>. Moreover, a combined diet of GMNL-185 and GMNL-680 demonstrated synergistic effects on memory functions. Live brain imaging revealed a significant increase in calcium responses to the training odor in the mushroom body β and γ lobes of flies that underwent mixed feeding with GMNL-185 and GMNL-680. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and whole-mount brain immunohistochemistry revealed significant upregulation of lactate dehydrogenase (LDH) expression in the fly brain following the mixed feeding. Notably, the genetic knockdown of <i>Ldh</i> in neurons, specifically in mushroom body, ameliorated the beneficial effects of mixed feeding with GMNL-185 and GMNL-680 on memory improvement. Altogether, our results demonstrate that supplementation with <i>L. acidophilus</i> and <i>L. rhamnosus</i> enhances memory functions in flies by increasing brain LDH levels.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":null,"pages":null},"PeriodicalIF":12.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10877976/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139899703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01Epub Date: 2024-02-23DOI: 10.1080/19490976.2024.2319889
Won Jun Kim, Bum Ju Kil, Chaewon Lee, Tae Young Kim, Goeun Han, Yukyung Choi, Kyunghwan Kim, Chang Hun Shin, Seung-Young Park, Heebal Kim, Myunghoo Kim, Chul Sung Huh
The gut microbiota plays a pivotal role in metabolic disorders, notably type 2 diabetes mellitus (T2DM). In this study, we investigated the synergistic potential of combining the effects of Bifidobacterium longum NBM7-1 (CKD1) with anti-diabetic medicines, LobeglitazoneⓇ (LO), SitagliptinⓇ (SI), and MetforminⓇ (Met), to alleviate hyperglycemia in a diabetic mouse model. CKD1 effectively mitigated insulin resistance, hepatic steatosis, and enhanced pancreatic β-cell function, as well as fortifying gut-tight junction integrity. In the same way, SI-CKD1 and Met- CKD1 synergistically improved insulin sensitivity and prevented hepatic steatosis, as evidenced by the modulation of key genes associated with insulin signaling, β-oxidation, gluconeogenesis, adipogenesis, and inflammation by qRT-PCR. The comprehensive impact on modulating gut microbiota composition was observed, particularly when combined with MetforminⓇ. This combination induced an increase in the abundance of Rikenellaceae and Alistipes related negatively to the T2DM incidence while reducing the causative species of Cryptosporangium, Staphylococcaceae, and Muribaculaceae. These alterations intervene in gut microbiota metabolites to modulate the level of butyrate, indole-3-acetic acid, propionate, and inflammatory cytokines and to activate the IL-22 pathway. However, it is meaningful that the combination of B. longum NBM7-1(CKD1) reduced the medicines' dose to the level of the maximal inhibitory concentrations (IC50). This study advances our understanding of the intricate relationship between gut microbiota and metabolic disorders. We expect this study to contribute to developing a prospective therapeutic strategy modulating the gut microbiota.
{"title":"<i>B. longum</i> CKD1 enhances the efficacy of anti-diabetic medicines through upregulation of IL- 22 response in type 2 diabetic mice.","authors":"Won Jun Kim, Bum Ju Kil, Chaewon Lee, Tae Young Kim, Goeun Han, Yukyung Choi, Kyunghwan Kim, Chang Hun Shin, Seung-Young Park, Heebal Kim, Myunghoo Kim, Chul Sung Huh","doi":"10.1080/19490976.2024.2319889","DOIUrl":"10.1080/19490976.2024.2319889","url":null,"abstract":"<p><p>The gut microbiota plays a pivotal role in metabolic disorders, notably type 2 diabetes mellitus (T2DM). In this study, we investigated the synergistic potential of combining the effects of <i>Bifidobacterium longum</i> NBM7-1 (CKD1) with anti-diabetic medicines, Lobeglitazone<sup>Ⓡ</sup> (LO), Sitagliptin<sup>Ⓡ</sup> (SI), and Metformin<sup>Ⓡ</sup> (Met), to alleviate hyperglycemia in a diabetic mouse model. CKD1 effectively mitigated insulin resistance, hepatic steatosis, and enhanced pancreatic β-cell function, as well as fortifying gut-tight junction integrity. In the same way, SI-CKD1 and Met- CKD1 synergistically improved insulin sensitivity and prevented hepatic steatosis, as evidenced by the modulation of key genes associated with insulin signaling, β-oxidation, gluconeogenesis, adipogenesis, and inflammation by qRT-PCR. The comprehensive impact on modulating gut microbiota composition was observed, particularly when combined with Metformin<sup>Ⓡ</sup>. This combination induced an increase in the abundance of <i>Rikenellaceae</i> and <i>Alistipes</i> related negatively to the T2DM incidence while reducing the causative species of <i>Cryptosporangium, Staphylococcaceae</i>, and <i>Muribaculaceae</i>. These alterations intervene in gut microbiota metabolites to modulate the level of butyrate, indole-3-acetic acid, propionate, and inflammatory cytokines and to activate the IL-22 pathway. However, it is meaningful that the combination of <i>B. longum</i> NBM7-1(CKD1) reduced the medicines' dose to the level of the maximal inhibitory concentrations (IC50). This study advances our understanding of the intricate relationship between gut microbiota and metabolic disorders. We expect this study to contribute to developing a prospective therapeutic strategy modulating the gut microbiota.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":null,"pages":null},"PeriodicalIF":12.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10896159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139930916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01Epub Date: 2024-02-23DOI: 10.1080/19490976.2024.2314201
Sirena C Tran, Kaeli N Bryant, Timothy L Cover
Helicobacter pylori strains can be broadly classified into two groups based on whether they contain or lack a chromosomal region known as the cag pathogenicity island (cag PAI). Colonization of the human stomach with cag PAI-positive strains is associated with an increased risk of gastric cancer and peptic ulcer disease, compared to colonization with cag PAI-negative strains. The cag PAI encodes a secreted effector protein (CagA) and components of a type IV secretion system (Cag T4SS) that delivers CagA and non-protein substrates into host cells. Animal model experiments indicate that CagA and the Cag T4SS stimulate a gastric mucosal inflammatory response and contribute to the development of gastric cancer. In this review, we discuss recent studies defining structural and functional features of CagA and the Cag T4SS and mechanisms by which H. pylori strains containing the cag PAI promote the development of gastric cancer and peptic ulcer disease.
幽门螺杆菌菌株大致可分为两类,依据是它们是否含有被称为 cag 致病性岛(cag PAI)的染色体区域。与 cag PAI 阴性菌株相比,cag PAI 阳性菌株在人胃中的定植与胃癌和消化性溃疡病风险的增加有关。cag PAI 编码一种分泌型效应蛋白(CagA)和一种 IV 型分泌系统(Cag T4SS)的组成部分,该系统可将 CagA 和非蛋白底物送入宿主细胞。动物模型实验表明,CagA 和 Cag T4SS 会刺激胃粘膜炎症反应,并导致胃癌的发生。在这篇综述中,我们讨论了最近的一些研究,这些研究确定了 CagA 和 Cag T4SS 的结构和功能特征,以及含有 cag PAI 的幽门螺杆菌菌株促进胃癌和消化性溃疡病发展的机制。
{"title":"The <i>Helicobacter pylori cag</i> pathogenicity island as a determinant of gastric cancer risk.","authors":"Sirena C Tran, Kaeli N Bryant, Timothy L Cover","doi":"10.1080/19490976.2024.2314201","DOIUrl":"10.1080/19490976.2024.2314201","url":null,"abstract":"<p><p><i>Helicobacter pylori</i> strains can be broadly classified into two groups based on whether they contain or lack a chromosomal region known as the <i>cag</i> pathogenicity island (<i>cag</i> PAI). Colonization of the human stomach with <i>cag</i> PAI-positive strains is associated with an increased risk of gastric cancer and peptic ulcer disease, compared to colonization with <i>cag</i> PAI-negative strains. The <i>cag</i> PAI encodes a secreted effector protein (CagA) and components of a type IV secretion system (Cag T4SS) that delivers CagA and non-protein substrates into host cells. Animal model experiments indicate that CagA and the Cag T4SS stimulate a gastric mucosal inflammatory response and contribute to the development of gastric cancer. In this review, we discuss recent studies defining structural and functional features of CagA and the Cag T4SS and mechanisms by which <i>H. pylori</i> strains containing the <i>cag</i> PAI promote the development of gastric cancer and peptic ulcer disease.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":null,"pages":null},"PeriodicalIF":12.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10896142/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139930917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01Epub Date: 2024-03-04DOI: 10.1080/19490976.2024.2323234
Ye Peng, Hein M Tun, Siew C Ng, Hogan Kok-Fung Wai, Xi Zhang, Jaclyn Parks, Catherine J Field, Piush Mandhane, Theo J Moraes, Elinor Simons, Stuart E Turvey, Padmaja Subbarao, Jeffrey R Brook, Tim K Takaro, James A Scott, Francis Kl Chan, Anita L Kozyrskyj
Childhood obesity is linked to maternal smoking during pregnancy. Gut microbiota may partially mediate this association and could be potential targets for intervention; however, its role is understudied. We included 1,592 infants from the Canadian Healthy Infants Longitudinal Development Cohort. Data on environmental exposure and lifestyle factors were collected prenatally and throughout the first three years. Weight outcomes were measured at one and three years of age. Stool samples collected at 3 and 12 months were analyzed by sequencing the V4 region of 16S rRNA to profile microbial compositions and magnetic resonance spectroscopy to quantify the metabolites. We showed that quitting smoking during pregnancy did not lower the risk of offspring being overweight. However, exclusive breastfeeding until the third month of age may alleviate these risks. We also reported that maternal smoking during pregnancy significantly increased Firmicutes abundance and diversity. We further revealed that Firmicutes diversity mediates the elevated risk of childhood overweight and obesity linked to maternal prenatal smoking. This effect possibly occurs through excessive microbial butyrate production. These findings add to the evidence that women should quit smoking before their pregnancies to prevent microbiome-mediated childhood overweight and obesity risk, and indicate the potential obesogenic role of excessive butyrate production in early life.
{"title":"Maternal smoking during pregnancy increases the risk of gut microbiome-associated childhood overweight and obesity.","authors":"Ye Peng, Hein M Tun, Siew C Ng, Hogan Kok-Fung Wai, Xi Zhang, Jaclyn Parks, Catherine J Field, Piush Mandhane, Theo J Moraes, Elinor Simons, Stuart E Turvey, Padmaja Subbarao, Jeffrey R Brook, Tim K Takaro, James A Scott, Francis Kl Chan, Anita L Kozyrskyj","doi":"10.1080/19490976.2024.2323234","DOIUrl":"10.1080/19490976.2024.2323234","url":null,"abstract":"<p><p>Childhood obesity is linked to maternal smoking during pregnancy. Gut microbiota may partially mediate this association and could be potential targets for intervention; however, its role is understudied. We included 1,592 infants from the Canadian Healthy Infants Longitudinal Development Cohort. Data on environmental exposure and lifestyle factors were collected prenatally and throughout the first three years. Weight outcomes were measured at one and three years of age. Stool samples collected at 3 and 12 months were analyzed by sequencing the V4 region of 16S rRNA to profile microbial compositions and magnetic resonance spectroscopy to quantify the metabolites. We showed that quitting smoking during pregnancy did not lower the risk of offspring being overweight. However, exclusive breastfeeding until the third month of age may alleviate these risks. We also reported that maternal smoking during pregnancy significantly increased Firmicutes abundance and diversity. We further revealed that Firmicutes diversity mediates the elevated risk of childhood overweight and obesity linked to maternal prenatal smoking. This effect possibly occurs through excessive microbial butyrate production. These findings add to the evidence that women should quit smoking before their pregnancies to prevent microbiome-mediated childhood overweight and obesity risk, and indicate the potential obesogenic role of excessive butyrate production in early life.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":null,"pages":null},"PeriodicalIF":12.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10913716/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140021581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01Epub Date: 2024-03-04DOI: 10.1080/19490976.2024.2323220
Wenjie Tang, Yusen Wei, Zhixiang Ni, Kangwei Hou, Xin M Luo, Haifeng Wang
The mechanisms of how host-microbe mutualistic relationships are established at weaning contingently upon B-cell surveillance remain inadequately elucidated. We found that CD138+ plasmacyte (PC)-mediated promotion of IgA response regulates the symbiosis between Bacteroides uniformis (B. uniformis) and the host during the weaning period. The IgA-skewed response of CD138+ PCs is essential for B. uniformis to occupy a defined gut luminal niche, thereby fostering stable colonization. Furthermore, B. uniformis within the natural gut niche was perturbed in the absence of IgA, resulting in exacerbated gut inflammation in IgA-deficient mice and weaned piglets. Thus, we propose that the priming and maintenance of intestinal IgA response from CD138+ PCs are required for host-microbial symbiosis, whereas the perturbation of which would enhance inflammation in weaning process.
在断奶时,宿主与微生物之间的共生关系是如何在B细胞监控下建立起来的,其机制仍未得到充分阐明。我们发现,CD138+质粒(PC)介导的 IgA 反应促进调节了断奶期均匀乳杆菌(B. uniformis)与宿主之间的共生关系。CD138+ PC 的 IgA 偏斜反应对于制服乳杆菌占据确定的肠腔生态位从而促进稳定定殖至关重要。此外,在缺乏 IgA 的情况下,B. uniformis 在自然肠道壁龛内的活动受到干扰,导致 IgA 缺乏的小鼠和断奶仔猪的肠道炎症加剧。因此,我们认为 CD138+ PCs 启动和维持肠道 IgA 反应是宿主-微生物共生所必需的,而干扰这种共生会加剧断奶过程中的炎症。
{"title":"IgA-mediated control of host-microbial interaction during weaning reaction influences gut inflammation.","authors":"Wenjie Tang, Yusen Wei, Zhixiang Ni, Kangwei Hou, Xin M Luo, Haifeng Wang","doi":"10.1080/19490976.2024.2323220","DOIUrl":"10.1080/19490976.2024.2323220","url":null,"abstract":"<p><p>The mechanisms of how host-microbe mutualistic relationships are established at weaning contingently upon B-cell surveillance remain inadequately elucidated. We found that <i>CD138</i><sup>+</sup> plasmacyte (PC)-mediated promotion of IgA response regulates the symbiosis between <i>Bacteroides uniformis</i> (<i>B. uniformis</i>) and the host during the weaning period. The IgA-skewed response of <i>CD138</i><sup>+</sup> PCs is essential for <i>B. uniformis</i> to occupy a defined gut luminal niche, thereby fostering stable colonization. Furthermore, <i>B. uniformis</i> within the natural gut niche was perturbed in the absence of IgA, resulting in exacerbated gut inflammation in IgA-deficient mice and weaned piglets. Thus, we propose that the priming and maintenance of intestinal IgA response from <i>CD138</i><sup>+</sup> PCs are required for host-microbial symbiosis, whereas the perturbation of which would enhance inflammation in weaning process.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":null,"pages":null},"PeriodicalIF":12.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10936605/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140027963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01Epub Date: 2024-03-14DOI: 10.1080/19490976.2024.2328868
Lingxi Li, Xiaowen Huang, Haoyan Chen
The role of gut fungal species in tumor-related processes remains largely unexplored, with most studies still focusing on fungal infections. This review examines the accumulating evidence suggesting the involvement of commensal and pathogenic fungi in cancer biological process, including oncogenesis, progression, and treatment response. Mechanisms explored include fungal influence on host immunity, secretion of bioactive toxins/metabolites, interaction with bacterial commensals, and migration to other tissues in certain types of cancers. Attempts to utilize fungal molecular signatures for cancer diagnosis and fungal-derived products for treatment are discussed. A few studies highlight fungi's impact on the responsiveness and sensitivity to chemotherapy, radiotherapy, immunotherapy, and fecal microbiota transplant. Given the limited understanding and techniques in fungal research, the studies on gut fungi are still facing great challenges, despite having great potentials.
{"title":"Unveiling the hidden players: exploring the role of gut mycobiome in cancer development and treatment dynamics.","authors":"Lingxi Li, Xiaowen Huang, Haoyan Chen","doi":"10.1080/19490976.2024.2328868","DOIUrl":"10.1080/19490976.2024.2328868","url":null,"abstract":"<p><p>The role of gut fungal species in tumor-related processes remains largely unexplored, with most studies still focusing on fungal infections. This review examines the accumulating evidence suggesting the involvement of commensal and pathogenic fungi in cancer biological process, including oncogenesis, progression, and treatment response. Mechanisms explored include fungal influence on host immunity, secretion of bioactive toxins/metabolites, interaction with bacterial commensals, and migration to other tissues in certain types of cancers. Attempts to utilize fungal molecular signatures for cancer diagnosis and fungal-derived products for treatment are discussed. A few studies highlight fungi's impact on the responsiveness and sensitivity to chemotherapy, radiotherapy, immunotherapy, and fecal microbiota transplant. Given the limited understanding and techniques in fungal research, the studies on gut fungi are still facing great challenges, despite having great potentials.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":null,"pages":null},"PeriodicalIF":12.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10950292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140131329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01Epub Date: 2024-05-05DOI: 10.1080/19490976.2024.2347722
Li-Wei Xie, Shang Cai, Hai-Yan Lu, Feng-Ling Tang, Rui-Qiu Zhu, Ye Tian, Ming Li
The intestine is prone to radiation damage in patients undergoing radiotherapy for pelvic tumors. However, there are currently no effective drugs available for the prevention or treatment of radiation-induced enteropathy (RIE). In this study, we aimed at investigating the impact of indole-3-carboxaldehyde (I3A) derived from the intestinal microbiota on RIE. Intestinal organoids were isolated and cultivated for screening radioprotective tryptophan metabolites. A RIE model was established using 13 Gy whole-abdominal irradiation in male C57BL/6J mice. After oral administration of I3A, its radioprotective ability was assessed through the observation of survival rates, clinical scores, and pathological analysis. Intestinal stem cell survival and changes in the intestinal barrier were observed through immunofluorescence and immunohistochemistry. Subsequently, the radioprotective mechanisms of I3A was investigated through 16S rRNA and transcriptome sequencing, respectively. Finally, human colon cancer cells and organoids were cultured to assess the influence of I3A on tumor radiotherapy. I3A exhibited the most potent radioprotective effect on intestinal organoids. Oral administration of I3A treatment significantly increased the survival rate in irradiated mice, improved clinical and histological scores, mitigated mucosal damage, enhanced the proliferation and differentiation of Lgr5+ intestinal stem cells, and maintained intestinal barrier integrity. Furthermore, I3A enhanced the abundance of probiotics, and activated the AhR/IL-10/Wnt signaling pathway to promote intestinal epithelial proliferation. As a crucial tryptophan metabolite, I3A promotes intestinal epithelial cell proliferation through the AhR/IL-10/Wnt signaling pathway and upregulates the abundance of probiotics to treat RIE. Microbiota-derived I3A demonstrates potential clinical application value for the treatment of RIE.
{"title":"Microbiota-derived I3A protects the intestine against radiation injury by activating AhR/IL-10/Wnt signaling and enhancing the abundance of probiotics.","authors":"Li-Wei Xie, Shang Cai, Hai-Yan Lu, Feng-Ling Tang, Rui-Qiu Zhu, Ye Tian, Ming Li","doi":"10.1080/19490976.2024.2347722","DOIUrl":"10.1080/19490976.2024.2347722","url":null,"abstract":"<p><p>The intestine is prone to radiation damage in patients undergoing radiotherapy for pelvic tumors. However, there are currently no effective drugs available for the prevention or treatment of radiation-induced enteropathy (RIE). In this study, we aimed at investigating the impact of indole-3-carboxaldehyde (I3A) derived from the intestinal microbiota on RIE. Intestinal organoids were isolated and cultivated for screening radioprotective tryptophan metabolites. A RIE model was established using 13 Gy whole-abdominal irradiation in male C57BL/6J mice. After oral administration of I3A, its radioprotective ability was assessed through the observation of survival rates, clinical scores, and pathological analysis. Intestinal stem cell survival and changes in the intestinal barrier were observed through immunofluorescence and immunohistochemistry. Subsequently, the radioprotective mechanisms of I3A was investigated through 16S rRNA and transcriptome sequencing, respectively. Finally, human colon cancer cells and organoids were cultured to assess the influence of I3A on tumor radiotherapy. I3A exhibited the most potent radioprotective effect on intestinal organoids. Oral administration of I3A treatment significantly increased the survival rate in irradiated mice, improved clinical and histological scores, mitigated mucosal damage, enhanced the proliferation and differentiation of Lgr5<sup>+</sup> intestinal stem cells, and maintained intestinal barrier integrity. Furthermore, I3A enhanced the abundance of probiotics, and activated the AhR/IL-10/Wnt signaling pathway to promote intestinal epithelial proliferation. As a crucial tryptophan metabolite, I3A promotes intestinal epithelial cell proliferation through the AhR/IL-10/Wnt signaling pathway and upregulates the abundance of probiotics to treat RIE. Microbiota-derived I3A demonstrates potential clinical application value for the treatment of RIE.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":null,"pages":null},"PeriodicalIF":12.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11086037/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140854883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}