Pub Date : 2024-12-26DOI: 10.1080/19490976.2024.2446374
Wei-Kai Wu,Yi-Ling Lo,Jian-Ying Chiu,Chia-Lang Hsu,I-Hsuan Lo,Suraphan Panyod,Yu-Chieh Liao,Tina H T Chiu,Yu-Tang Yang,Han-Chun Kuo,Hsin-Bai Zou,Yi-Hsun Chen,Hsiao-Li Chuang,Jeffrey J Y Yen,Jin-Town Wang,Han-Mo Chiu,Cheng-Chih Hsu,Ching-Hua Kuo,Lee-Yan Sheen,Hsien-Li Kao,Ming-Shiang Wu
Gut microbial metabolism of L-carnitine, which leads to the production of detrimental trimethylamine N-oxide (TMAO), offers a plausible link between red meat consumption and cardiovascular risks. Several microbial genes, including cntA/B, the cai operon, and the recently identified gbu gene cluster, have been implicated in the conversion of dietary L-carnitine into TMA(O). However, the key microbial genes and associated gut microbes involved in this pathway have not been fully explored. Utilizing the oral carnitine challenge test (OCCT), which specifically measures TMAO production from L-carnitine intake and identifies TMAO producer phenotypes, we compared the abundance of microbial genes between low- and high-TMAO producers across three independent cohorts. Our findings consistently revealed that the gbu gene cluster, rather than cntA/B or the cai operon, was significantly enriched in high-TMAO producers. We further analyzed 292 paired multi-omic datasets from OCCT and shotgun metagenomic sequencing, which demonstrated a significant positive correlation between the abundance of fecal gbu genes and L-carnitine-induced TMAO production, with gbuB showing the strongest correlation. Interestingly, these fecal gbu genes were found to increase with L-carnitine supplementation and decrease with a plant-based diet. Notably, we verified a previously uncultured gbu-containing bacterium, JAGTTR01 sp018223385, as the major contributor to TMA formation in the human gut. We isolated these gbu-containing gut microbes and confirmed their role in TMA/TMAO production using anaerobic incubation and a gnotobiotic mouse model. Using an in-house collection of gbu-containing isolates, we developed a qPCR-based method to quantify fecal gbuB and validated its correlation with L-carnitine-mediated TMAO production as measured by OCCT. Overall, these findings suggest that gbu-containing gut microbes are crucial for TMAO increases following L-carnitine intake and may serve as biomarkers or targets for personalized nutrition.
{"title":"Gut microbes with the gbu genes determine TMAO production from L-carnitine intake and serve as a biomarker for precision nutrition.","authors":"Wei-Kai Wu,Yi-Ling Lo,Jian-Ying Chiu,Chia-Lang Hsu,I-Hsuan Lo,Suraphan Panyod,Yu-Chieh Liao,Tina H T Chiu,Yu-Tang Yang,Han-Chun Kuo,Hsin-Bai Zou,Yi-Hsun Chen,Hsiao-Li Chuang,Jeffrey J Y Yen,Jin-Town Wang,Han-Mo Chiu,Cheng-Chih Hsu,Ching-Hua Kuo,Lee-Yan Sheen,Hsien-Li Kao,Ming-Shiang Wu","doi":"10.1080/19490976.2024.2446374","DOIUrl":"https://doi.org/10.1080/19490976.2024.2446374","url":null,"abstract":"Gut microbial metabolism of L-carnitine, which leads to the production of detrimental trimethylamine N-oxide (TMAO), offers a plausible link between red meat consumption and cardiovascular risks. Several microbial genes, including cntA/B, the cai operon, and the recently identified gbu gene cluster, have been implicated in the conversion of dietary L-carnitine into TMA(O). However, the key microbial genes and associated gut microbes involved in this pathway have not been fully explored. Utilizing the oral carnitine challenge test (OCCT), which specifically measures TMAO production from L-carnitine intake and identifies TMAO producer phenotypes, we compared the abundance of microbial genes between low- and high-TMAO producers across three independent cohorts. Our findings consistently revealed that the gbu gene cluster, rather than cntA/B or the cai operon, was significantly enriched in high-TMAO producers. We further analyzed 292 paired multi-omic datasets from OCCT and shotgun metagenomic sequencing, which demonstrated a significant positive correlation between the abundance of fecal gbu genes and L-carnitine-induced TMAO production, with gbuB showing the strongest correlation. Interestingly, these fecal gbu genes were found to increase with L-carnitine supplementation and decrease with a plant-based diet. Notably, we verified a previously uncultured gbu-containing bacterium, JAGTTR01 sp018223385, as the major contributor to TMA formation in the human gut. We isolated these gbu-containing gut microbes and confirmed their role in TMA/TMAO production using anaerobic incubation and a gnotobiotic mouse model. Using an in-house collection of gbu-containing isolates, we developed a qPCR-based method to quantify fecal gbuB and validated its correlation with L-carnitine-mediated TMAO production as measured by OCCT. Overall, these findings suggest that gbu-containing gut microbes are crucial for TMAO increases following L-carnitine intake and may serve as biomarkers or targets for personalized nutrition.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"25 1","pages":"2446374"},"PeriodicalIF":12.2,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142887675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-26DOI: 10.1080/19490976.2024.2446391
Pan Wang,Ruiqi Wang,Wenting Zhao,Yuanyuan Zhao,Dan Wang,Shuang Zhao,Zhiwen Ge,Yue Ma,Xiaoyan Zhao
Resveratrol (RSV), a natural polyphenol, has been suggested to influence glucose and lipid metabolism. However, the underlying molecular mechanism of its action remains largely unknown due to its multiple biological targets and low bioavailability. In this study, we demonstrate that RSV supplementation ameliorates high-fat-diet (HFD)-induced gut microbiota dysbiosis, enhancing the abundance of anti-obesity bacterial strains such as Akkermansia, Bacteroides and Blautia. The critical role of gut microbiota in RSV-mediated anti-obesity effects was confirmed through antibiotic-induced microbiome depletion and fecal microbiota transplantation (FMT), which showed that RSV treatment effectively mitigates body weight, histopathological damage, glucose dysregulation and systematic inflammation associated with HFD. Metabolomics analysis revealed that RSV supplementation significantly increases the levels of the gut microbial flavonoid catabolite 4-hydroxyphenylacetic acid (4-HPA). Notably, 4-HPA was sufficient to reverse obesity and glucose intolerance in HFD-fed mice. Mechanistically,4-HPA treatment markedly regulates SIRT1 signaling pathways and induces the expression of beige fat and thermogenesis-specific markers in white adipose tissue (WAT). These beneficial effects of 4-HPA are partially abolished by EX527, a known SIRT1 inhibitor. Collectively, our findings indicate that RSV improve obesity through a gut microbiota-derived 4-HPA-SIRT1 axis, highlighting gut microbiota metabolites as a promising target for obesity prevention.
{"title":"Gut microbiota-derived 4-hydroxyphenylacetic acid from resveratrol supplementation prevents obesity through SIRT1 signaling activation.","authors":"Pan Wang,Ruiqi Wang,Wenting Zhao,Yuanyuan Zhao,Dan Wang,Shuang Zhao,Zhiwen Ge,Yue Ma,Xiaoyan Zhao","doi":"10.1080/19490976.2024.2446391","DOIUrl":"https://doi.org/10.1080/19490976.2024.2446391","url":null,"abstract":"Resveratrol (RSV), a natural polyphenol, has been suggested to influence glucose and lipid metabolism. However, the underlying molecular mechanism of its action remains largely unknown due to its multiple biological targets and low bioavailability. In this study, we demonstrate that RSV supplementation ameliorates high-fat-diet (HFD)-induced gut microbiota dysbiosis, enhancing the abundance of anti-obesity bacterial strains such as Akkermansia, Bacteroides and Blautia. The critical role of gut microbiota in RSV-mediated anti-obesity effects was confirmed through antibiotic-induced microbiome depletion and fecal microbiota transplantation (FMT), which showed that RSV treatment effectively mitigates body weight, histopathological damage, glucose dysregulation and systematic inflammation associated with HFD. Metabolomics analysis revealed that RSV supplementation significantly increases the levels of the gut microbial flavonoid catabolite 4-hydroxyphenylacetic acid (4-HPA). Notably, 4-HPA was sufficient to reverse obesity and glucose intolerance in HFD-fed mice. Mechanistically,4-HPA treatment markedly regulates SIRT1 signaling pathways and induces the expression of beige fat and thermogenesis-specific markers in white adipose tissue (WAT). These beneficial effects of 4-HPA are partially abolished by EX527, a known SIRT1 inhibitor. Collectively, our findings indicate that RSV improve obesity through a gut microbiota-derived 4-HPA-SIRT1 axis, highlighting gut microbiota metabolites as a promising target for obesity prevention.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"124 1","pages":"2446391"},"PeriodicalIF":12.2,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142887677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-27DOI: 10.1080/19490976.2024.2416922
Ha T Doan, Li-Chieh Cheng, Yi-Ling Chiu, Yuan-Kai Cheng, Cheng-Chih Hsu, Yee-Chun Chen, Hsiu-Jung Lo, Hao-Sen Chiang
Candida tropicalis-a prevalent gut commensal fungus in healthy individuals – contributes to intestinal health and disease. However, how commensal C. tropicalis influences intestinal homeostasis and...
The current studies have shown that the occurrence and development of chronic obstructive pulmonary disease (COPD) are closely related to the changes in gut health and its microenvironment, and even some gut diseases have significant clinical correlation with COPD. The dysbiosis of gut microbiota observed in COPD patients also suggests a potential bidirectional interaction between the gut and lung. Communication between the gut and lung may occur through circulating inflammatory cells, gut microbial metabolites, and circulating inflammatory mediators, but the mechanism of bidirectional communication between the gut and lung in COPD is still under study. Therefore, more research is still needed in this area. In this review, we summarize recent clinical studies and animal models on the role of the gut-lung axis in the occurrence and development of COPD and its mechanisms, so as to provide ideas for further research in this field. In addition, we also summarized the negative effects of COPD medication on gut microbiota and the gut microbiota risk factors for COPD and proposed the potential prevention and treatment strategies.
{"title":"The role and mechanism of gut-lung axis mediated bidirectional communication in the occurrence and development of chronic obstructive pulmonary disease.","authors":"Xiaofan Song,Xina Dou,Jiajing Chang,Xiaonan Zeng,Qinhong Xu,Chunlan Xu","doi":"10.1080/19490976.2024.2414805","DOIUrl":"https://doi.org/10.1080/19490976.2024.2414805","url":null,"abstract":"The current studies have shown that the occurrence and development of chronic obstructive pulmonary disease (COPD) are closely related to the changes in gut health and its microenvironment, and even some gut diseases have significant clinical correlation with COPD. The dysbiosis of gut microbiota observed in COPD patients also suggests a potential bidirectional interaction between the gut and lung. Communication between the gut and lung may occur through circulating inflammatory cells, gut microbial metabolites, and circulating inflammatory mediators, but the mechanism of bidirectional communication between the gut and lung in COPD is still under study. Therefore, more research is still needed in this area. In this review, we summarize recent clinical studies and animal models on the role of the gut-lung axis in the occurrence and development of COPD and its mechanisms, so as to provide ideas for further research in this field. In addition, we also summarized the negative effects of COPD medication on gut microbiota and the gut microbiota risk factors for COPD and proposed the potential prevention and treatment strategies.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"97 1","pages":"2414805"},"PeriodicalIF":12.2,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142489731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-23DOI: 10.1080/19490976.2024.2417729
Nicolas Vitari,Salma Singh,Junyi Tao,Bridget Truitt,Udhghatri Kolli,Richa Jalodia,Kathryn M LaPorte,Yaa Abu,Danielle Antoine,Umakant Sharma,Sabita Roy
IgA binding dictates the composition of the intestinal microbiome and reflects dysbiotic states during chronic disease. Both pathogenic and commensal bacteria differentially bind to IgA with varying outcomes. Little is known regarding IgA dynamics immediately following microbial dysbiosis. Recent work shows that morphine treatment rapidly induces microbial dysbiosis within hours of administration. This microbial shift is characterized by the expansion of pathogenic bacteria with a concurrent decrease in commensal bacteria. Because of this rapid microbial shift, a murine model of chronic morphine treatment was used to gain insight on the host IgA response during early microbial disruption. Within 24 h, morphine treatment induces microbial dysbiosis which disrupts IgA-bacterial homeostasis, resulting in an increased concentration of unbound IgA with a corresponding decrease in the frequency of IgA-bound bacteria. Additionally, the increased concentration of unbound IgA is dependent on the microbiome, as microbial depletion abolishes the increase. At 48 h of morphine treatment, the frequency of IgA-bound bacteria increases and IgA-seq reveals increased IgA targeting of gram-positive bacteria. Both a whole-body TLR2 KO and treatment with the TLR inhibitor OxPAPC resulted in abrogation of IgA binding to bacteria, implicating modulation of IgA binding through TLR signaling. Finally, we identify that a sub-population of IgA+ B cells in the intestinal lamina propria has increased CD11b and TLR2 expression at 24 h of morphine treatment which could be a potential source of the observed IgA that targets gram-positive bacteria. Together, we demonstrate for the first time the role of TLR2 in IgA targeting of intestinal bacteria, and this study sheds light on the IgA dynamics during the initial hours of microbial dysbiosis.
IgA 结合决定了肠道微生物群的组成，并反映了慢性疾病期间的菌群失调状态。致病菌和共生菌与 IgA 的结合方式不同，结果也各异。人们对微生物菌群失调后的 IgA 动态知之甚少。最近的研究表明，吗啡治疗可在用药后数小时内迅速诱导微生物菌群失调。这种微生物转变的特点是致病菌增多，同时共生菌减少。由于这种快速的微生物转变，我们使用了一种慢性吗啡治疗的小鼠模型，以深入了解在早期微生物紊乱过程中宿主的 IgA 反应。吗啡治疗会在 24 小时内诱发微生物菌群失调，从而破坏 IgA-细菌平衡，导致非结合 IgA 浓度增加，而 IgA 结合细菌的频率相应减少。此外，非结合 IgA 浓度的增加取决于微生物群，因为微生物的减少会导致非结合 IgA 浓度的增加。吗啡治疗 48 小时后，IgA 结合细菌的频率增加，IgA-seq 发现革兰氏阳性细菌的 IgA 靶向性增加。全身 TLR2 KO 和用 TLR 抑制剂 OxPAPC 处理都会导致 IgA 与细菌的结合减弱，这表明 IgA 的结合是通过 TLR 信号调节的。最后，我们发现在吗啡治疗 24 小时后，肠固有层中的 IgA+ B 细胞亚群的 CD11b 和 TLR2 表达增加，这可能是观察到的针对革兰氏阳性细菌的 IgA 的潜在来源。综上所述，我们首次证明了 TLR2 在以肠道细菌为靶标的 IgA 中的作用，这项研究还揭示了微生物菌群失调初期 IgA 的动态变化。
{"title":"Morphine-induced intestinal microbial dysbiosis drives TLR-dependent IgA targeting of gram-positive bacteria and upregulation of CD11b and TLR2 on a sub-population of IgA+ B cells.","authors":"Nicolas Vitari,Salma Singh,Junyi Tao,Bridget Truitt,Udhghatri Kolli,Richa Jalodia,Kathryn M LaPorte,Yaa Abu,Danielle Antoine,Umakant Sharma,Sabita Roy","doi":"10.1080/19490976.2024.2417729","DOIUrl":"https://doi.org/10.1080/19490976.2024.2417729","url":null,"abstract":"IgA binding dictates the composition of the intestinal microbiome and reflects dysbiotic states during chronic disease. Both pathogenic and commensal bacteria differentially bind to IgA with varying outcomes. Little is known regarding IgA dynamics immediately following microbial dysbiosis. Recent work shows that morphine treatment rapidly induces microbial dysbiosis within hours of administration. This microbial shift is characterized by the expansion of pathogenic bacteria with a concurrent decrease in commensal bacteria. Because of this rapid microbial shift, a murine model of chronic morphine treatment was used to gain insight on the host IgA response during early microbial disruption. Within 24 h, morphine treatment induces microbial dysbiosis which disrupts IgA-bacterial homeostasis, resulting in an increased concentration of unbound IgA with a corresponding decrease in the frequency of IgA-bound bacteria. Additionally, the increased concentration of unbound IgA is dependent on the microbiome, as microbial depletion abolishes the increase. At 48 h of morphine treatment, the frequency of IgA-bound bacteria increases and IgA-seq reveals increased IgA targeting of gram-positive bacteria. Both a whole-body TLR2 KO and treatment with the TLR inhibitor OxPAPC resulted in abrogation of IgA binding to bacteria, implicating modulation of IgA binding through TLR signaling. Finally, we identify that a sub-population of IgA+ B cells in the intestinal lamina propria has increased CD11b and TLR2 expression at 24 h of morphine treatment which could be a potential source of the observed IgA that targets gram-positive bacteria. Together, we demonstrate for the first time the role of TLR2 in IgA targeting of intestinal bacteria, and this study sheds light on the IgA dynamics during the initial hours of microbial dysbiosis.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"235 1","pages":"2417729"},"PeriodicalIF":12.2,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142488288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-22DOI: 10.1080/19490976.2024.2416912
Julia Rode,Linnea Brengesjö Johnson,Julia König,Ignacio Rangel,Lars Engstrand,Dirk Repsilber,Robert J Brummer
The appropriateness of the fecal microbiota to adequately reflect the gut microbiota composition from more difficult to access luminal content at different colonic locations has been debated. Here, in a healthy population, luminal samples were collected from terminal ileum to rectum using an unique sampling technique without the need of prior bowel cleansing/preparation. Rectal swabs were collected immediately prior colonoscopy by an experienced physician, and fecal samples were collected at home by the participants themselves. Microbiota composition was evaluated as relative abundance, α-diversity and Bray-Curtis dissimilarities. Our data suggest that fecal samples and rectal swabs present noninvasive, easily accessible, low-cost sampling tools that are accurate proxies to characterize luminal large intestinal microbiota composition.
{"title":"Fecal samples and rectal swabs adequately reflect the human colonic luminal microbiota.","authors":"Julia Rode,Linnea Brengesjö Johnson,Julia König,Ignacio Rangel,Lars Engstrand,Dirk Repsilber,Robert J Brummer","doi":"10.1080/19490976.2024.2416912","DOIUrl":"https://doi.org/10.1080/19490976.2024.2416912","url":null,"abstract":"The appropriateness of the fecal microbiota to adequately reflect the gut microbiota composition from more difficult to access luminal content at different colonic locations has been debated. Here, in a healthy population, luminal samples were collected from terminal ileum to rectum using an unique sampling technique without the need of prior bowel cleansing/preparation. Rectal swabs were collected immediately prior colonoscopy by an experienced physician, and fecal samples were collected at home by the participants themselves. Microbiota composition was evaluated as relative abundance, α-diversity and Bray-Curtis dissimilarities. Our data suggest that fecal samples and rectal swabs present noninvasive, easily accessible, low-cost sampling tools that are accurate proxies to characterize luminal large intestinal microbiota composition.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"48 1","pages":"2416912"},"PeriodicalIF":12.2,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142488289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-22DOI: 10.1080/19490976.2024.2418412
Maria Lucia Orsini Delgado,Joao Gamelas Magalhaes,Rachel Morra,Antonietta Cultrone
In bacteria, the cell envelope is the key element surrounding and protecting the bacterial content from mechanical or osmotic damages. It allows the selective interchanges of solutes, ions, cellular debris, and drugs between the cellular compartments and the external environment, thanks to the presence of transmembrane proteins called transporters. The major component of the cell envelope is the peptidoglycan, consisting of long linear glycan strands cross-linked by short peptide stems. During cell growth or under stress conditions, peptidoglycan fragments, the muropeptides, are released by bacteria and recognized by the host Pattern Recognition Receptor, promoting the activation of their innate defense mechanisms. The review sums up the salient aspects of microbiota-host interaction with a focus on the NOD-dependent immune response to bacterial peptidoglycan and on the accountability of muropeptide transporters in the crosstalk with the host and in antibiotic resistance. Furthermore, it retraces the discoveries and applications of microorganisms-derived components such as vaccines or vaccine adjuvants.
{"title":"Muropeptides and muropeptide transporters impact on host immune response.","authors":"Maria Lucia Orsini Delgado,Joao Gamelas Magalhaes,Rachel Morra,Antonietta Cultrone","doi":"10.1080/19490976.2024.2418412","DOIUrl":"https://doi.org/10.1080/19490976.2024.2418412","url":null,"abstract":"In bacteria, the cell envelope is the key element surrounding and protecting the bacterial content from mechanical or osmotic damages. It allows the selective interchanges of solutes, ions, cellular debris, and drugs between the cellular compartments and the external environment, thanks to the presence of transmembrane proteins called transporters. The major component of the cell envelope is the peptidoglycan, consisting of long linear glycan strands cross-linked by short peptide stems. During cell growth or under stress conditions, peptidoglycan fragments, the muropeptides, are released by bacteria and recognized by the host Pattern Recognition Receptor, promoting the activation of their innate defense mechanisms. The review sums up the salient aspects of microbiota-host interaction with a focus on the NOD-dependent immune response to bacterial peptidoglycan and on the accountability of muropeptide transporters in the crosstalk with the host and in antibiotic resistance. Furthermore, it retraces the discoveries and applications of microorganisms-derived components such as vaccines or vaccine adjuvants.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"5 1","pages":"2418412"},"PeriodicalIF":12.2,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142488283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-20DOI: 10.1080/19490976.2024.2413372
Xiao Han, Joannie M. Allaire, Shauna M. Crowley, Jocelyn J. Chan, Kelly Lau, Conghao Zhang, Simon A. Hirota, Kirk Bergstrom, Leigh A. Knodler, Bruce A. Vallance
The host restricts Salmonella enterica serovar Typhimurium infection of the gut via inflammasome-dependent sloughing of infected epithelial cells. Here we determined that concurrent caspase 1/11-de...
{"title":"Inflammasome activation links enteric Salmonella Typhimurium infection to a rapid, cytokine-dependent increase in intestinal mucin release","authors":"Xiao Han, Joannie M. Allaire, Shauna M. Crowley, Jocelyn J. Chan, Kelly Lau, Conghao Zhang, Simon A. Hirota, Kirk Bergstrom, Leigh A. Knodler, Bruce A. Vallance","doi":"10.1080/19490976.2024.2413372","DOIUrl":"https://doi.org/10.1080/19490976.2024.2413372","url":null,"abstract":"The host restricts Salmonella enterica serovar Typhimurium infection of the gut via inflammasome-dependent sloughing of infected epithelial cells. Here we determined that concurrent caspase 1/11-de...","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"11 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142451908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-18DOI: 10.1080/19490976.2024.2401654
Enriqueta Garcia-Gutierrez,A Kate O'Mahony,Reinaldo Sousa Dos Santos,Laura Marroquí,Paul D Cotter
Diabetes mellitus can be subdivided into several categories based on origin and clinical characteristics. The most common forms of diabetes are type 1 (T1D), type 2 diabetes (T2D) and gestational diabetes mellitus (GDM). T1D and T2D are chronic diseases affecting around 537 million adults worldwide and it is projected that these numbers will increase by 12% over the next two decades, while GDM affects up to 30% of women during pregnancy, depending on diagnosis methods. These forms of diabetes have varied origins: T1D is an autoimmune disease, while T2D is commonly associated with, but not limited to, certain lifestyle patterns and GDM can result of a combination of genetic predisposition and pregnancy factors. Despite some pathogenic differences among these forms of diabetes, there are some common markers associated with their development. For instance, gut barrier impairment and inflammation associated with an unbalanced gut microbiota and their metabolites may be common factors in diabetes development and progression. Here, we summarize the microbial signatures that have been linked to diabetes, how they are connected to diet and, ultimately, the impact on metabolite profiles resulting from host-gut microbiota-diet interactions. Additionally, we summarize recent advances relating to promising preventive and therapeutic interventions focusing on the targeted modulation of the gut microbiota to alleviate T1D, T2D and GDM.
{"title":"Gut microbial metabolic signatures in diabetes mellitus and potential preventive and therapeutic applications.","authors":"Enriqueta Garcia-Gutierrez,A Kate O'Mahony,Reinaldo Sousa Dos Santos,Laura Marroquí,Paul D Cotter","doi":"10.1080/19490976.2024.2401654","DOIUrl":"https://doi.org/10.1080/19490976.2024.2401654","url":null,"abstract":"Diabetes mellitus can be subdivided into several categories based on origin and clinical characteristics. The most common forms of diabetes are type 1 (T1D), type 2 diabetes (T2D) and gestational diabetes mellitus (GDM). T1D and T2D are chronic diseases affecting around 537 million adults worldwide and it is projected that these numbers will increase by 12% over the next two decades, while GDM affects up to 30% of women during pregnancy, depending on diagnosis methods. These forms of diabetes have varied origins: T1D is an autoimmune disease, while T2D is commonly associated with, but not limited to, certain lifestyle patterns and GDM can result of a combination of genetic predisposition and pregnancy factors. Despite some pathogenic differences among these forms of diabetes, there are some common markers associated with their development. For instance, gut barrier impairment and inflammation associated with an unbalanced gut microbiota and their metabolites may be common factors in diabetes development and progression. Here, we summarize the microbial signatures that have been linked to diabetes, how they are connected to diet and, ultimately, the impact on metabolite profiles resulting from host-gut microbiota-diet interactions. Additionally, we summarize recent advances relating to promising preventive and therapeutic interventions focusing on the targeted modulation of the gut microbiota to alleviate T1D, T2D and GDM.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"77 1","pages":"2401654"},"PeriodicalIF":12.2,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142449296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-17DOI: 10.1080/19490976.2024.2416915
Wenjing Wang,Zhexin Fan,Qingqing Yan,Tong Pan,Jing Luo,Yijiang Wei,Baokun Li,Zhifeng Fang,Wenwei Lu
Epidemiological investigation confirmed that the intake of dietary fiber (DF) is closely related to human health, and the most important factor affecting the physiological function of DF, besides its physicochemical properties, is the gut microbiota. This paper mainly summarizes the interaction between DF and gut microbiota, including the influence of DF on the colonization of gut microbiota based on its different physicochemical properties, and the physiological role of gut microbiota in destroying the complex molecular structure of DF by encoding carbohydrate-active enzymes, thus producing small molecular products that affect the metabolism of the host. Taking cardiovascular disease (Atherosclerosis and hypertension), liver disease, and immune diseases as examples, it is confirmed that some DF, such as fructo-oligosaccharide, galactooligosaccharide, xylo-oligosaccharide, and inulin, have prebiotic-like physiological effects. These effects are dependent on the metabolites produced by the gut microbiota. Therefore, this paper further explores how DF affects the gut microbiota's production of substances such as short-chain fatty acids, bile acids, and tryptophan metabolites, and provides a preliminary explanation of the mechanisms associated with their impact on host health. Finally, based on the structural properties of DF and the large heterogeneity in the composition of the population gut microbiota, it may be a future trend to utilize DF and the gut microbiota to correlate host health for precision nutrition by combining the information from population disease databases.
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