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      Microbiota in health and diseases

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          Abstract

          The role of microbiota in health and diseases is being highlighted by numerous studies since its discovery. Depending on the localized regions, microbiota can be classified into gut, oral, respiratory, and skin microbiota. The microbial communities are in symbiosis with the host, contributing to homeostasis and regulating immune function. However, microbiota dysbiosis can lead to dysregulation of bodily functions and diseases including cardiovascular diseases (CVDs), cancers, respiratory diseases, etc. In this review, we discuss the current knowledge of how microbiota links to host health or pathogenesis. We first summarize the research of microbiota in healthy conditions, including the gut-brain axis, colonization resistance and immune modulation. Then, we highlight the pathogenesis of microbiota dysbiosis in disease development and progression, primarily associated with dysregulation of community composition, modulation of host immune response, and induction of chronic inflammation. Finally, we introduce the clinical approaches that utilize microbiota for disease treatment, such as microbiota modulation and fecal microbial transplantation.

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          An obesity-associated gut microbiome with increased capacity for energy harvest.

          The worldwide obesity epidemic is stimulating efforts to identify host and environmental factors that affect energy balance. Comparisons of the distal gut microbiota of genetically obese mice and their lean littermates, as well as those of obese and lean human volunteers have revealed that obesity is associated with changes in the relative abundance of the two dominant bacterial divisions, the Bacteroidetes and the Firmicutes. Here we demonstrate through metagenomic and biochemical analyses that these changes affect the metabolic potential of the mouse gut microbiota. Our results indicate that the obese microbiome has an increased capacity to harvest energy from the diet. Furthermore, this trait is transmissible: colonization of germ-free mice with an 'obese microbiota' results in a significantly greater increase in total body fat than colonization with a 'lean microbiota'. These results identify the gut microbiota as an additional contributing factor to the pathophysiology of obesity.
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            NF-κB signaling in inflammation

            The transcription factor NF-κB regulates multiple aspects of innate and adaptive immune functions and serves as a pivotal mediator of inflammatory responses. NF-κB induces the expression of various pro-inflammatory genes, including those encoding cytokines and chemokines, and also participates in inflammasome regulation. In addition, NF-κB plays a critical role in regulating the survival, activation and differentiation of innate immune cells and inflammatory T cells. Consequently, deregulated NF-κB activation contributes to the pathogenic processes of various inflammatory diseases. In this review, we will discuss the activation and function of NF-κB in association with inflammatory diseases and highlight the development of therapeutic strategies based on NF-κB inhibition.
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              Gut microbiome influences efficacy of PD-1–based immunotherapy against epithelial tumors

              Immune checkpoint inhibitors (ICI) targeting the PD-1/PD-L1 axis induce sustained clinical responses in a sizeable minority of cancer patients. Here, we show that primary resistance to ICI can be due to abnormal gut microbiome composition. Antibiotics (ATB) inhibited the clinical benefit of ICI in patients with advanced cancer. Fecal microbiota transplantation (FMT) from cancer patients who responded to ICI (but not from non-responding patients) into germ-free or ATB-treated mice ameliorated the antitumor effects of PD-1 blockade. Metagenomics of patient stools at diagnosis revealed correlations between clinical responses to ICI and the relative abundance of Akkermansia muciniphila. Oral supplementation with A. muciniphila post-FMT with non-responder feces restored the efficacy of PD-1 blockade in an IL-12-dependent manner, by increasing the recruitment of CCR9+CXCR3+CD4+ T lymphocytes into tumor beds.
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                Author and article information

                Contributors
                lijilin@126.com
                chenz@stjohns.edu
                Journal
                Signal Transduct Target Ther
                Signal Transduct Target Ther
                Signal Transduction and Targeted Therapy
                Nature Publishing Group UK (London )
                2095-9907
                2059-3635
                23 April 2022
                23 April 2022
                2022
                : 7
                : 135
                Affiliations
                [1 ]GRID grid.411679.c, ISNI 0000 0004 0605 3373, Department of Endocrine and Metabolic Diseases, Longhu Hospital, , The First Affiliated Hospital of Medical College of Shantou University, ; Shantou, Guangdong 515000 China
                [2 ]GRID grid.264091.8, ISNI 0000 0001 1954 7928, Department of Pharmaceutical Sciences, Institute for Biotechnology, College of Pharmacy and Health Sciences, , St. John’s University, ; Queens, NY 11439 USA
                [3 ]Microbiome Research Center, Moon (Guangzhou) Biotech Ltd, Guangzhou, 510535 China
                [4 ]GRID grid.268079.2, ISNI 0000 0004 1790 6079, School of Pharmacy, , Weifang Medical University, ; Weifang, Shandong 261053 China
                [5 ]GRID grid.411679.c, ISNI 0000 0004 0605 3373, Department of Cardiovascular, , The Second Affiliated Hospital of Medical College of Shantou University, ; Shantou, Guangdong 515000 China
                Author information
                http://orcid.org/0000-0003-1733-0068
                http://orcid.org/0000-0002-8289-097X
                Article
                974
                10.1038/s41392-022-00974-4
                9034083
                35461318
                b21fd11d-f92f-42f8-8df1-cb96bec50f29
                © The Author(s) 2022

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 31 October 2021
                : 11 March 2022
                : 15 March 2022
                Categories
                Review Article
                Custom metadata
                © The Author(s) 2022

                microbiology,endocrine system and metabolic diseases

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