Pub Date : 2024-01-01Epub Date: 2024-01-04DOI: 10.1080/19490976.2023.2297864
Tariq Aziz, Nageen Hussain, Zunaira Hameed, Lin Lin
A healthy balanced diet is crucial in protecting the immune system against infections and diseases. Poor diets, such as the Western diet, contribute to the development of metabolic diseases, hypertension, and obesity. Microbiota, primarily composed of different microorganisms and residing in the gastrointestinal tract (GIT), also play a significant role in maintaining gut health. Polyphenols and probiotics found in fruits, vegetables, whole grains, legumes, nuts, and seeds promote gut health and support the growth of beneficial bacteria. Different types of diets, their categories, and their impact on health are also mentioned. The relationship between diet, gut health, and the risk of developing obesity, cardiovascular diseases, and inflammatory diseases is discussed in this review article. The rationale behind the review concludes future recommendations for maintaining gut health and reducing the occurrence of obesity, cardiometabolic diseases, and other inflammatory diseases. There is also the need for standardized research methods, long-term studies, and translating scientific knowledge into practical dietary recommendations.
{"title":"Elucidating the role of diet in maintaining gut health to reduce the risk of obesity, cardiovascular and other age-related inflammatory diseases: recent challenges and future recommendations.","authors":"Tariq Aziz, Nageen Hussain, Zunaira Hameed, Lin Lin","doi":"10.1080/19490976.2023.2297864","DOIUrl":"10.1080/19490976.2023.2297864","url":null,"abstract":"<p><p>A healthy balanced diet is crucial in protecting the immune system against infections and diseases. Poor diets, such as the Western diet, contribute to the development of metabolic diseases, hypertension, and obesity. Microbiota, primarily composed of different microorganisms and residing in the gastrointestinal tract (GIT), also play a significant role in maintaining gut health. Polyphenols and probiotics found in fruits, vegetables, whole grains, legumes, nuts, and seeds promote gut health and support the growth of beneficial bacteria. Different types of diets, their categories, and their impact on health are also mentioned. The relationship between diet, gut health, and the risk of developing obesity, cardiovascular diseases, and inflammatory diseases is discussed in this review article. The rationale behind the review concludes future recommendations for maintaining gut health and reducing the occurrence of obesity, cardiometabolic diseases, and other inflammatory diseases. There is also the need for standardized research methods, long-term studies, and translating scientific knowledge into practical dietary recommendations.</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/PMC10773664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139086662","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: 2024-01-02DOI: 10.1080/19490976.2023.2297860
Ashwin Chetty, Ran Blekhman
The gut microbiome interacts with the host through complex networks that affect physiology and health outcomes. It is becoming clear that these interactions can be measured across many different omics layers, including the genome, transcriptome, epigenome, metabolome, and proteome, among others. Multi-omic studies of the microbiome can provide insight into the mechanisms underlying host-microbe interactions. As more omics layers are considered, increasingly sophisticated statistical methods are required to integrate them. In this review, we provide an overview of approaches currently used to characterize multi-omic interactions between host and microbiome data. While a large number of studies have generated a deeper understanding of host-microbiome interactions, there is still a need for standardization across approaches. Furthermore, microbiome studies would also benefit from the collection and curation of large, publicly available multi-omics datasets.
{"title":"Multi-omic approaches for host-microbiome data integration.","authors":"Ashwin Chetty, Ran Blekhman","doi":"10.1080/19490976.2023.2297860","DOIUrl":"10.1080/19490976.2023.2297860","url":null,"abstract":"<p><p>The gut microbiome interacts with the host through complex networks that affect physiology and health outcomes. It is becoming clear that these interactions can be measured across many different omics layers, including the genome, transcriptome, epigenome, metabolome, and proteome, among others. Multi-omic studies of the microbiome can provide insight into the mechanisms underlying host-microbe interactions. As more omics layers are considered, increasingly sophisticated statistical methods are required to integrate them. In this review, we provide an overview of approaches currently used to characterize multi-omic interactions between host and microbiome data. While a large number of studies have generated a deeper understanding of host-microbiome interactions, there is still a need for standardization across approaches. Furthermore, microbiome studies would also benefit from the collection and curation of large, publicly available multi-omics datasets.</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/PMC10766395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139086663","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: 2024-02-01DOI: 10.1080/19490976.2024.2307586
Greta Viebahn, Phillipp Hartmann, Sonja Lang, Münevver Demir, Xinlian Zhang, Derrick E Fouts, Peter Stärkel, Bernd Schnabl
The fungal microbiota plays an important role in the pathogenesis of alcohol-associated liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD). In this study, we aimed to compare changes of the fecal fungal microbiota between patients with ALD and NAFLD and to elucidate patterns in different disease stages between the two conditions. We analyzed fungal internal transcribed spacer 2 (ITS2) sequencing using fecal samples from a cohort of 48 patients with ALD, 78 patients with NAFLD, and 34 controls. The fungal microbiota differed significantly between ALD and NAFLD. The genera Saccharomyces, Kluyveromyces, Scopulariopsis, and the species Candida albicans (C. albicans), Malassezia restricta (M. restricta), Scopulariopsis cordiae (S. cordiae) were significantly increased in patients with ALD, whereas the genera Kazachstania and Mucor were significantly increased in the NAFLD cohort. We identified the fungal signature consisting of Scopulariopsis, Kluyveromyces, M. restricta, and Mucor to have the highest discriminative ability to detect ALD vs NAFLD with an area under the curve (AUC) of 0.93. When stratifying the ALD and NAFLD cohorts by fibrosis severity, the fungal signature with the highest AUC of 0.92 to distinguish ALD F0-F1 vs NAFLD F0-F1 comprised Scopulariopsis, Kluyveromyces, Mucor, M. restricta, and Kazachstania. For more advanced fibrosis stages (F2-F4), the fungal signature composed of Scopulariopsis, Kluyveromyces, Mucor, and M. restricta achieved the highest AUC of 0.99 to differentiate ALD from NAFLD. This is the first study to identify a fungal signature to differentiate two metabolic fatty liver diseases from each other, specifically ALD from NAFLD. This might have clinical utility in unclear cases and might hence help shape treatment approaches. However, larger studies are required to validate this fungal signature in other populations of ALD and NAFLD.
{"title":"Fungal signature differentiates alcohol-associated liver disease from nonalcoholic fatty liver disease.","authors":"Greta Viebahn, Phillipp Hartmann, Sonja Lang, Münevver Demir, Xinlian Zhang, Derrick E Fouts, Peter Stärkel, Bernd Schnabl","doi":"10.1080/19490976.2024.2307586","DOIUrl":"10.1080/19490976.2024.2307586","url":null,"abstract":"<p><p>The fungal microbiota plays an important role in the pathogenesis of alcohol-associated liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD). In this study, we aimed to compare changes of the fecal fungal microbiota between patients with ALD and NAFLD and to elucidate patterns in different disease stages between the two conditions. We analyzed fungal internal transcribed spacer 2 (ITS2) sequencing using fecal samples from a cohort of 48 patients with ALD, 78 patients with NAFLD, and 34 controls. The fungal microbiota differed significantly between ALD and NAFLD. The genera <i>Saccharomyces</i>, <i>Kluyveromyces</i>, <i>Scopulariopsis</i>, and the species <i>Candida albicans</i> (<i>C. albicans</i>), <i>Malassezia restricta</i> (<i>M. restricta</i>), <i>Scopulariopsis cordiae</i> (<i>S. cordiae</i>) were significantly increased in patients with ALD, whereas the genera <i>Kazachstania</i> and <i>Mucor</i> were significantly increased in the NAFLD cohort. We identified the fungal signature consisting of <i>Scopulariopsis</i>, <i>Kluyveromyces</i>, <i>M. restricta</i>, and <i>Mucor</i> to have the highest discriminative ability to detect ALD vs NAFLD with an area under the curve (AUC) of 0.93. When stratifying the ALD and NAFLD cohorts by fibrosis severity, the fungal signature with the highest AUC of 0.92 to distinguish ALD F0-F1 vs NAFLD F0-F1 comprised <i>Scopulariopsis</i>, <i>Kluyveromyces</i>, <i>Mucor</i>, <i>M. restricta</i>, and <i>Kazachstania</i>. For more advanced fibrosis stages (F2-F4), the fungal signature composed of <i>Scopulariopsis</i>, <i>Kluyveromyces</i>, <i>Mucor</i>, and <i>M. restricta</i> achieved the highest AUC of 0.99 to differentiate ALD from NAFLD. This is the first study to identify a fungal signature to differentiate two metabolic fatty liver diseases from each other, specifically ALD from NAFLD. This might have clinical utility in unclear cases and might hence help shape treatment approaches. However, larger studies are required to validate this fungal signature in other populations of ALD and NAFLD.</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/PMC10841010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139650599","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: 2024-02-01DOI: 10.1080/19490976.2024.2307568
Byeong Hyun Min, Shivani Devi, Goo Hyun Kwon, Haripriya Gupta, Jin-Ju Jeong, Satya Priya Sharma, Sung-Min Won, Ki-Kwang Oh, Sang Jun Yoon, Hee Jin Park, Jung A Eom, Min Kyo Jeong, Ji Ye Hyun, Nattan Stalin, Tae-Sik Park, Jieun Choi, Do Yup Lee, Sang Hak Han, Dong Joon Kim, Ki Tae Suk
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease, and its prevalence has increased worldwide in recent years. Additionally, there is a close relationship between MASLD and gut microbiota-derived metabolites. However, the mechanisms of MASLD and its metabolites are still unclear. We demonstrated decreased indole-3-propionic acid (IPA) and indole-3-acetic acid (IAA) in the feces of patients with hepatic steatosis compared to healthy controls. Here, IPA and IAA administration ameliorated hepatic steatosis and inflammation in an animal model of WD-induced MASLD by suppressing the NF-κB signaling pathway through a reduction in endotoxin levels and inactivation of macrophages. Bifidobacterium bifidum metabolizes tryptophan to produce IAA, and B. bifidum effectively prevents hepatic steatosis and inflammation through the production of IAA. Our study demonstrates that IPA and IAA derived from the gut microbiota have novel preventive or therapeutic potential for MASLD treatment.
{"title":"Gut microbiota-derived indole compounds attenuate metabolic dysfunction-associated steatotic liver disease by improving fat metabolism and inflammation.","authors":"Byeong Hyun Min, Shivani Devi, Goo Hyun Kwon, Haripriya Gupta, Jin-Ju Jeong, Satya Priya Sharma, Sung-Min Won, Ki-Kwang Oh, Sang Jun Yoon, Hee Jin Park, Jung A Eom, Min Kyo Jeong, Ji Ye Hyun, Nattan Stalin, Tae-Sik Park, Jieun Choi, Do Yup Lee, Sang Hak Han, Dong Joon Kim, Ki Tae Suk","doi":"10.1080/19490976.2024.2307568","DOIUrl":"10.1080/19490976.2024.2307568","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease, and its prevalence has increased worldwide in recent years. Additionally, there is a close relationship between MASLD and gut microbiota-derived metabolites. However, the mechanisms of MASLD and its metabolites are still unclear. We demonstrated decreased indole-3-propionic acid (IPA) and indole-3-acetic acid (IAA) in the feces of patients with hepatic steatosis compared to healthy controls. Here, IPA and IAA administration ameliorated hepatic steatosis and inflammation in an animal model of WD-induced MASLD by suppressing the NF-κB signaling pathway through a reduction in endotoxin levels and inactivation of macrophages. <i>Bifidobacterium bifidum</i> metabolizes tryptophan to produce IAA, and <i>B. bifidum</i> effectively prevents hepatic steatosis and inflammation through the production of IAA. Our study demonstrates that IPA and IAA derived from the gut microbiota have novel preventive or therapeutic potential for MASLD treatment.</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/PMC10841017/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139650600","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}
Melatonin has various physiological effects, such as the maintenance of circadian rhythms, anti-inflammatory functions, and regulation of intestinal barriers. The regulatory functions of melatonin in gut microbiota remodeling have also been well clarified; however, the role of gut microbiota in regulating host melatonin production remains poorly understood. To address this, we studied the contribution of gut microbiota to host melatonin production using gut microbiota-perturbed models. We demonstrated that antibiotic-treated and germ-free mice possessed diminished melatonin levels in the serum and elevated melatonin levels in the colon. The influence of the intestinal microbiota on host melatonin production was further confirmed by fecal microbiota transplantation. Notably, Lactobacillus reuteri (L. R) and Escherichia coli (E. coli) recapitulated the effects of gut microbiota on host melatonin production. Mechanistically, L. R and E. coli activated the TLR2/4/MyD88/NF-κB signaling pathway to promote expression of arylalkylamine N-acetyltransferase (AANAT, a rate-limiting enzyme for melatonin production), and MyD88 deficiency in colonic epithelial cells abolished the influence of intestinal microbiota on colonic melatonin production. Collectively, we revealed a specific underlying mechanism of gut microbiota to modulate host melatonin production, which might provide novel therapeutic ideas for melatonin-related diseases.
{"title":"Gut microbiota regulates host melatonin production through epithelial cell MyD88.","authors":"Bingnan Liu, Lijuan Fan, Youxia Wang, Hao Wang, Yuqi Yan, Shuai Chen, Ifen Hung, Chunxue Liu, Hong Wei, Liangpeng Ge, Wenkai Ren","doi":"10.1080/19490976.2024.2313769","DOIUrl":"10.1080/19490976.2024.2313769","url":null,"abstract":"<p><p>Melatonin has various physiological effects, such as the maintenance of circadian rhythms, anti-inflammatory functions, and regulation of intestinal barriers. The regulatory functions of melatonin in gut microbiota remodeling have also been well clarified; however, the role of gut microbiota in regulating host melatonin production remains poorly understood. To address this, we studied the contribution of gut microbiota to host melatonin production using gut microbiota-perturbed models. We demonstrated that antibiotic-treated and germ-free mice possessed diminished melatonin levels in the serum and elevated melatonin levels in the colon. The influence of the intestinal microbiota on host melatonin production was further confirmed by fecal microbiota transplantation. Notably, <i>Lactobacillus reuteri</i> (<i>L. R</i>) and <i>Escherichia coli</i> (<i>E. coli</i>) recapitulated the effects of gut microbiota on host melatonin production. Mechanistically, <i>L. R</i> and <i>E. coli</i> activated the TLR2/4/MyD88/NF-κB signaling pathway to promote expression of arylalkylamine N-acetyltransferase (AANAT, a rate-limiting enzyme for melatonin production), and MyD88 deficiency in colonic epithelial cells abolished the influence of intestinal microbiota on colonic melatonin production. Collectively, we revealed a specific underlying mechanism of gut microbiota to modulate host melatonin production, which might provide novel therapeutic ideas for melatonin-related diseases.</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/PMC10868534/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139729500","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: 2024-02-28DOI: 10.1080/19490976.2024.2323236
Li Zhang, Zhiyi Zheng, Huanhuan Huang, Ya Fu, Tianbin Chen, Can Liu, Qiang Yi, Caorui Lin, Yongjun Zeng, Qishui Ou, Yongbin Zeng
Deoxycholic acid (DCA) serves essential functions in both physiological and pathological liver processes; nevertheless, the relationship among DCA, gut microbiota, and metabolism in chronic liver injury remain insufficiently understood. The primary objective of this study is to elucidate the potential of DCA in ameliorating chronic liver injury and evaluate its regulatory effect on gut microbiota and metabolism via a comprehensive multi-omics approach. Our study found that DCA supplementation caused significant changes in the composition of gut microbiota, which were essential for its antagonistic effect against CCl4-induced chronic liver injury. When gut microbiota was depleted with antibiotics, the observed protective efficacy of DCA against chronic liver injury became noticeably attenuated. Mechanistically, we discovered that DCA regulates the metabolism of bile acids (BAs), including 3-epi DCA, Apo-CA, and its isomers 12-KLCA and 7-KLCA, IHDCA, and DCA, by promoting the growth of A.muciniphila in gut microbiota. This might lead to the inhibition of the IL-17 and TNF inflammatory signaling pathway, thereby effectively countering CCl4-induced chronic liver injury. This study illustrates that the enrichment of A. muciniphila in the gut microbiota, mediated by DCA, enhances the production of secondary bile acids, thereby mitigating chronic liver injury induced by CCl4. The underlying mechanism may involve the inhibition of hepatic IL-17 and TNF signaling pathways. These findings propose a promising approach to alleviate chronic liver injury by modulating both the gut microbiota and bile acids metabolism.
{"title":"Multi-omics reveals deoxycholic acid modulates bile acid metabolism via the gut microbiota to antagonize carbon tetrachloride-induced chronic liver injury.","authors":"Li Zhang, Zhiyi Zheng, Huanhuan Huang, Ya Fu, Tianbin Chen, Can Liu, Qiang Yi, Caorui Lin, Yongjun Zeng, Qishui Ou, Yongbin Zeng","doi":"10.1080/19490976.2024.2323236","DOIUrl":"10.1080/19490976.2024.2323236","url":null,"abstract":"<p><p>Deoxycholic acid (DCA) serves essential functions in both physiological and pathological liver processes; nevertheless, the relationship among DCA, gut microbiota, and metabolism in chronic liver injury remain insufficiently understood. The primary objective of this study is to elucidate the potential of DCA in ameliorating chronic liver injury and evaluate its regulatory effect on gut microbiota and metabolism via a comprehensive multi-omics approach. Our study found that DCA supplementation caused significant changes in the composition of gut microbiota, which were essential for its antagonistic effect against CCl<sub>4</sub>-induced chronic liver injury. When gut microbiota was depleted with antibiotics, the observed protective efficacy of DCA against chronic liver injury became noticeably attenuated. Mechanistically, we discovered that DCA regulates the metabolism of bile acids (BAs), including 3-epi DCA, Apo-CA, and its isomers 12-KLCA and 7-KLCA, IHDCA, and DCA, by promoting the growth of <i>A.muciniphila</i> in gut microbiota. This might lead to the inhibition of the IL-17 and TNF inflammatory signaling pathway, thereby effectively countering CCl<sub>4</sub>-induced chronic liver injury. This study illustrates that the enrichment of <i>A. muciniphila</i> in the gut microbiota, mediated by DCA, enhances the production of secondary bile acids, thereby mitigating chronic liver injury induced by CCl<sub>4</sub>. The underlying mechanism may involve the inhibition of hepatic IL-17 and TNF signaling pathways. These findings propose a promising approach to alleviate chronic liver injury by modulating both the gut microbiota and bile acids metabolism.</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/PMC10903553/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139982815","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}
Chronic obstructive pulmonary disease (COPD), a condition primarily linked to oxidative stress, poses significant health burdens worldwide. Recent evidence has shed light on the association between the dysbiosis of gut microbiota and COPD, and their metabolites have emerged as potential modulators of disease progression through the intricate gut-lung axis. Here, we demonstrate the efficacy of oral administration of the probiotic Pediococcus pentosaceus SMM914 (SMM914) in delaying the progression of COPD by attenuating pulmonary oxidative stress. Specially, SMM914 induces a notable shift in the gut microbiota toward a community structure characterized by an augmented abundance of probiotics producing short-chain fatty acids and antioxidant metabolisms. Concurrently, SMM914 synthesizes L-tryptophanamide, 5-hydroxy-L-tryptophan, and 3-sulfino-L-alanine, thereby enhancing the tryptophan-melatonin pathway and elevating 6-hydroxymelatonin and hypotaurine in the lung environment. This modulation amplifies the secretion of endogenous anti-inflammatory factors, diminishes macrophage polarization toward the M1 phenotype, and ultimately mitigates the oxidative stress in mice with COPD. The demonstrated efficacy of the probiotic intervention, specifically with SMM914, not only highlights the modulation of intestine microbiota but also emphasizes the consequential impact on the intricate interplay between the gastrointestinal system and respiratory health.
{"title":"Modulation of chronic obstructive pulmonary disease progression by antioxidant metabolites from <i>Pediococcus pentosaceus</i>: enhancing gut probiotics abundance and the tryptophan-melatonin pathway.","authors":"Yiting Liu, Longjie Li, Jing Feng, Bing Wan, Qiang Tu, Wei Cai, Fa Jin, Guiying Tang, Lígia R Rodrigues, Xiuwei Zhang, Jia Yin, Yunlei Zhang","doi":"10.1080/19490976.2024.2320283","DOIUrl":"10.1080/19490976.2024.2320283","url":null,"abstract":"<p><p>Chronic obstructive pulmonary disease (COPD), a condition primarily linked to oxidative stress, poses significant health burdens worldwide. Recent evidence has shed light on the association between the dysbiosis of gut microbiota and COPD, and their metabolites have emerged as potential modulators of disease progression through the intricate gut-lung axis. Here, we demonstrate the efficacy of oral administration of the probiotic <i>Pediococcus pentosaceus</i> SMM914 (SMM914) in delaying the progression of COPD by attenuating pulmonary oxidative stress. Specially, SMM914 induces a notable shift in the gut microbiota toward a community structure characterized by an augmented abundance of probiotics producing short-chain fatty acids and antioxidant metabolisms. Concurrently, SMM914 synthesizes L-tryptophanamide, 5-hydroxy-L-tryptophan, and 3-sulfino-L-alanine, thereby enhancing the tryptophan-melatonin pathway and elevating 6-hydroxymelatonin and hypotaurine in the lung environment. This modulation amplifies the secretion of endogenous anti-inflammatory factors, diminishes macrophage polarization toward the M1 phenotype, and ultimately mitigates the oxidative stress in mice with COPD. The demonstrated efficacy of the probiotic intervention, specifically with SMM914, not only highlights the modulation of intestine microbiota but also emphasizes the consequential impact on the intricate interplay between the gastrointestinal system and respiratory health.</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/PMC10936690/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140039184","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}
Vancomycin (VAN) treatment in Clostridioides difficile infection (CDI) suffers from a relatively high rate of recurrence, with a variety of reasons behind this, including biofilm-induced recurrent infections. C. difficile can form monophyletic or symbiotic biofilms with other microbes in the gut, and these biofilms protect C. difficile from being killed by antibiotics. In this study, we analyzed the ecological relationship between Bacteroides thetaiotaomicron and C. difficile and their formation of symbiotic biofilm in the VAN environment. The production of symbiotic biofilm formed by C. difficile and B. thetaiotaomicron was higher than that of C. difficile and B. thetaiotaomicron alone in the VAN environment. In symbiotic biofilms, C. difficile was characterized by increased production of the toxin protein TcdA and TcdB, up-regulation of the expression levels of the virulence genes tcdA and tcdB, enhanced bacterial cell swimming motility and c-di-GMP content, and increased adhesion to Caco-2 cells. The scanning electron microscope (SEM) combined with confocal laser scanning microscopy (CLSM) results indicated that the symbiotic biofilm was elevated in thickness, dense, and had an increased amount of mixed bacteria, while the fluorescence in situ hybridization (FISH) probe and plate colony counting results further indicated that the symbiotic biofilm had a significant increase in the amount of C. difficile cells, and was able to better tolerate the killing of the simulated intestinal fluid. Taken together, C. difficile and B. thetaiotaomicron become collaborative in the VAN environment, and targeted deletion or attenuation of host gut B. thetaiotaomicron content may improve the actual efficacy of VAN in CDI treatment.
万古霉素(VAN)治疗艰难梭菌感染(CDI)的复发率相对较高,这背后有多种原因,包括生物膜诱导的反复感染。艰难梭菌可与肠道中的其他微生物形成单生或共生生物膜,这些生物膜可保护艰难梭菌不被抗生素杀死。在本研究中,我们分析了艰难梭菌和泰氏乳杆菌之间的生态关系,以及它们在 VAN 环境中形成共生生物膜的情况。在 VAN 环境中,艰难梭菌和 B. thetaiotaomicron 形成的共生生物膜的产量高于艰难梭菌和 B. thetaiotaomicron 单独形成的生物膜。在共生生物膜中,艰难梭菌的特点是毒素蛋白 TcdA 和 TcdB 的产量增加,毒力基因 tcdA 和 tcdB 的表达水平上调,细菌细胞游动性和 c-di-GMP 含量增强,对 Caco-2 细胞的粘附性增强。扫描电子显微镜(SEM)结合共焦激光扫描显微镜(CLSM)的结果表明,共生生物膜厚度增加、致密、混合细菌数量增加,而荧光原位杂交(FISH)探针和平板菌落计数结果进一步表明,共生生物膜中艰难梭菌细胞数量显著增加,并能更好地耐受模拟肠液的杀灭。综上所述,艰难梭菌和B. thetaiotaomicron在VAN环境中会相互协作,有针对性地删除或减少宿主肠道中B. thetaiotaomicron的含量可能会提高VAN治疗CDI的实际疗效。
{"title":"Symbiotic biofilms formed by <i>Clostridioides difficile</i> and <i>bacteroides thetaiotaomicron</i> in the presence of vancomycin.","authors":"Jingpeng Yang, Wen Rui, Saiwei Zhong, Xiaoqian Li, Wenzheng Liu, Lingtong Meng, Yanan Li, He Huang","doi":"10.1080/19490976.2024.2390133","DOIUrl":"10.1080/19490976.2024.2390133","url":null,"abstract":"<p><p>Vancomycin (VAN) treatment in <i>Clostridioides difficile</i> infection (CDI) suffers from a relatively high rate of recurrence, with a variety of reasons behind this, including biofilm-induced recurrent infections. <i>C. difficile</i> can form monophyletic or symbiotic biofilms with other microbes in the gut, and these biofilms protect <i>C. difficile</i> from being killed by antibiotics. In this study, we analyzed the ecological relationship between <i>Bacteroides thetaiotaomicron</i> and <i>C. difficile</i> and their formation of symbiotic biofilm in the VAN environment. The production of symbiotic biofilm formed by <i>C. difficile</i> and <i>B. thetaiotaomicron</i> was higher than that of <i>C. difficile</i> and <i>B. thetaiotaomicron</i> alone in the VAN environment. In symbiotic biofilms, <i>C. difficile</i> was characterized by increased production of the toxin protein TcdA and TcdB, up-regulation of the expression levels of the virulence genes <i>tcdA</i> and <i>tcdB</i>, enhanced bacterial cell swimming motility and c-di-GMP content, and increased adhesion to Caco-2 cells. The scanning electron microscope (SEM) combined with confocal laser scanning microscopy (CLSM) results indicated that the symbiotic biofilm was elevated in thickness, dense, and had an increased amount of mixed bacteria, while the fluorescence in situ hybridization (FISH) probe and plate colony counting results further indicated that the symbiotic biofilm had a significant increase in the amount of <i>C. difficile</i> cells, and was able to better tolerate the killing of the simulated intestinal fluid. Taken together, <i>C. difficile</i> and <i>B. thetaiotaomicron</i> become collaborative in the VAN environment, and targeted deletion or attenuation of host gut <i>B. thetaiotaomicron</i> content may improve the actual efficacy of VAN in CDI treatment.</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/PMC11321409/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141916587","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}
Background: Chronic infection with the neurotropic parasite Toxoplasma gondii (T. gondii) can cause anxiety and gut microbiota dysbiosis in hosts. However, the potential role of gut microbiota in anxiety induced by the parasite remains unclear.
Methods: C57BL/6J mice were infected with 10 cysts of T. gondii. Antibiotic depletion of gut microbiota and fecal microbiota transplantation experiments were utilized to investigate the causal relationship between gut microbiota and anxiety. Anxiety-like behaviors were examined by the elevated plus maze test and the open field test; blood, feces, colon and amygdala were collected to evaluate the profiles of serum endotoxin (Lipopolysaccharide, LPS) and serotonin (5-hydroxytryptamine, 5-HT), gut microbiota composition, metabolomics, global transcriptome and neuroinflammation in the amygdala. Furthermore, the effects of Diethyl butylmalonate (DBM, an inhibitor of mitochondrial succinate transporter, which causes the accumulation of endogenous succinate) on the disorders of the gut-brain axis were evaluated.
Results: Here, we found that T. gondii chronic infection induced anxiety-like behaviors and disturbed the composition of the gut microbiota in mice. In the amygdala, T. gondii infection triggered the microglial activation and neuroinflammation. In the colon, T. gondii infection caused the intestinal dyshomeostasis including elevated colonic inflammation, enhanced bacterial endotoxin translocation to blood and compromised intestinal barrier. In the serum, T. gondii infection increased the LPS levels and decreased the 5-HT levels. Interestingly, antibiotics ablation of gut microbiota alleviated the anxiety-like behaviors induced by T.gondii infection. More importantly, transplantation of the fecal microbiota from T. gondii-infected mice resulted in anxiety and the transcriptomic alteration in the amygdala of the antibiotic-pretreated mice. Notably, the decreased abundance of succinate-producing bacteria and the decreased production of succinate were observed in the feces of the T. gondii-infected mice. Moreover, DBM administration ameliorated the anxiety and gut barrier impairment induced by T.gondii infection.
Conclusions: The present study uncovers a novel role of gut microbiota in mediating the anxiety-like behaviors induced by chronic T. gondii infection. Moreover, we show that DBM supplementation has a beneficial effect on anxiety. Overall, these findings provide new insights into the treatment of T. gondii-related mental disorders.
{"title":"Gut microbiota mediates anxiety-like behaviors induced by chronic infection of <i>Toxoplasma gondii</i> in mice.","authors":"Xiaotong Luo, Xiaoying Yang, Shimin Tan, Yongsheng Zhang, Yunqiu Liu, Xiaokang Tian, Yingting Huang, Yuying Zhou, Cheng He, Kun Yin, Daxiang Xu, Xiangyang Li, Fenfen Sun, Renxian Tang, Jianping Cao, Kuiyang Zheng, Yinghua Yu, Wei Pan","doi":"10.1080/19490976.2024.2391535","DOIUrl":"10.1080/19490976.2024.2391535","url":null,"abstract":"<p><strong>Background: </strong>Chronic infection with the neurotropic parasite <i>Toxoplasma gondii (T. gondii)</i> can cause anxiety and gut microbiota dysbiosis in hosts. However, the potential role of gut microbiota in anxiety induced by the parasite remains unclear.</p><p><strong>Methods: </strong>C57BL/6J mice were infected with 10 cysts of <i>T. gondii.</i> Antibiotic depletion of gut microbiota and fecal microbiota transplantation experiments were utilized to investigate the causal relationship between gut microbiota and anxiety. Anxiety-like behaviors were examined by the elevated plus maze test and the open field test; blood, feces, colon and amygdala were collected to evaluate the profiles of serum endotoxin (Lipopolysaccharide, LPS) and serotonin (5-hydroxytryptamine, 5-HT), gut microbiota composition, metabolomics, global transcriptome and neuroinflammation in the amygdala. Furthermore, the effects of Diethyl butylmalonate (DBM, an inhibitor of mitochondrial succinate transporter, which causes the accumulation of endogenous succinate) on the disorders of the gut-brain axis were evaluated.</p><p><strong>Results: </strong>Here, we found that <i>T. gondii</i> chronic infection induced anxiety-like behaviors and disturbed the composition of the gut microbiota in mice. In the amygdala, <i>T. gondii</i> infection triggered the microglial activation and neuroinflammation. In the colon, <i>T. gondii</i> infection caused the intestinal dyshomeostasis including elevated colonic inflammation, enhanced bacterial endotoxin translocation to blood and compromised intestinal barrier. In the serum, <i>T. gondii</i> infection increased the LPS levels and decreased the 5-HT levels. Interestingly, antibiotics ablation of gut microbiota alleviated the anxiety-like behaviors induced by <i>T.</i> <i>gondii</i> infection. More importantly, transplantation of the fecal microbiota from <i>T. gondii</i>-infected mice resulted in anxiety and the transcriptomic alteration in the amygdala of the antibiotic-pretreated mice. Notably, the decreased abundance of succinate-producing bacteria and the decreased production of succinate were observed in the feces of the <i>T. gondii</i>-infected mice. Moreover, DBM administration ameliorated the anxiety and gut barrier impairment induced by <i>T.</i> <i>gondii</i> infection.</p><p><strong>Conclusions: </strong>The present study uncovers a novel role of gut microbiota in mediating the anxiety-like behaviors induced by chronic <i>T. gondii</i> infection. Moreover, we show that DBM supplementation has a beneficial effect on anxiety. Overall, these findings provide new insights into the treatment of <i>T. gondii</i>-related mental disorders.</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/PMC11346544/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055373","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: 2024-08-25DOI: 10.1080/19490976.2024.2387800
Miaomiao Zhuang, Xun Zhang, Jun Cai
The human gastrointestinal tract, boasting the most diverse microbial community, harbors approximately 100 trillion microorganisms comprising viruses, bacteria, fungi, and archaea. The profound genetic and metabolic capabilities of the gut microbiome underlie its involvement in nearly every facet of human biology, from health maintenance and development to aging and disease. Recent recognition of microbiota - gut - brain axis, referring to the bidirectional communication network between gut microbes and their host, has led to a surge in interdisciplinary research. This review begins with an overview of the current understandings regarding the influence of gut microbes on intestinal and blood-brain barrier integrity. Subsequently, we discuss the mechanisms of the microbiota - gut - brain axis, examining the role of gut microbiota-related neural transmission, metabolites, gut hormones and immunity. We propose the concept of microbiota-mediated multi-barrier modulation in the potential treatment in gastrointestinal and neurological disorders. Furthermore, the role of lymphatic network in the development and maintenance of barrier function is discussed, providing insights into lesser-known conduits of communication between the microbial ecosystem within the gut and the brain. In the final section, we conclude by describing the ongoing frontiers in understanding of the microbiota - gut - brain axis's impact on human health and disease.
{"title":"Microbiota-gut-brain axis: interplay between microbiota, barrier function and lymphatic system.","authors":"Miaomiao Zhuang, Xun Zhang, Jun Cai","doi":"10.1080/19490976.2024.2387800","DOIUrl":"10.1080/19490976.2024.2387800","url":null,"abstract":"<p><p>The human gastrointestinal tract, boasting the most diverse microbial community, harbors approximately 100 trillion microorganisms comprising viruses, bacteria, fungi, and archaea. The profound genetic and metabolic capabilities of the gut microbiome underlie its involvement in nearly every facet of human biology, from health maintenance and development to aging and disease. Recent recognition of microbiota - gut - brain axis, referring to the bidirectional communication network between gut microbes and their host, has led to a surge in interdisciplinary research. This review begins with an overview of the current understandings regarding the influence of gut microbes on intestinal and blood-brain barrier integrity. Subsequently, we discuss the mechanisms of the microbiota - gut - brain axis, examining the role of gut microbiota-related neural transmission, metabolites, gut hormones and immunity. We propose the concept of microbiota-mediated multi-barrier modulation in the potential treatment in gastrointestinal and neurological disorders. Furthermore, the role of lymphatic network in the development and maintenance of barrier function is discussed, providing insights into lesser-known conduits of communication between the microbial ecosystem within the gut and the brain. In the final section, we conclude by describing the ongoing frontiers in understanding of the microbiota - gut - brain axis's impact on human health and 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/PMC11346530/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055402","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}