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      Comparative analysis of gut microbiota in elderly people of urbanized towns and longevity villages.

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          Abstract

          To understand differences in the gut microbiota between elderly people of urbanized town communities (UTC) and longevity village communities (LVC), we analyzed fecal microbiota collected from individuals living in 2 UTC (Seoul and Chuncheon) and 3 LVC (Gurye, Damyang, and Soonchang) selected on the basis of indices for superlongevity (the ratio of centenarians to the total population) and longevity (the ratio of those aged 85 years or greater to those aged 65 years or greater) in South Korea by 454 pyrosequencing.

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          Introducing EzTaxon-e: a prokaryotic 16S rRNA gene sequence database with phylotypes that represent uncultured species.

          Ok-Sun Kim, Yong-Joon Cho, Kihyun Lee … (2012)
          Despite recent advances in commercially optimized identification systems, bacterial identification remains a challenging task in many routine microbiological laboratories, especially in situations where taxonomically novel isolates are involved. The 16S rRNA gene has been used extensively for this task when coupled with a well-curated database, such as EzTaxon, containing sequences of type strains of prokaryotic species with validly published names. Although the EzTaxon database has been widely used for routine identification of prokaryotic isolates, sequences from uncultured prokaryotes have not been considered. Here, the next generation database, named EzTaxon-e, is formally introduced. This new database covers not only species within the formal nomenclatural system but also phylotypes that may represent species in nature. In addition to an identification function based on Basic Local Alignment Search Tool (blast) searches and pairwise global sequence alignments, a new objective method of assessing the degree of completeness in sequencing is proposed. All sequences that are held in the EzTaxon-e database have been subjected to phylogenetic analysis and this has resulted in a complete hierarchical classification system. It is concluded that the EzTaxon-e database provides a useful taxonomic backbone for the identification of cultured and uncultured prokaryotes and offers a valuable means of communication among microbiologists who routinely encounter taxonomically novel isolates. The database and its analytical functions can be found at http://eztaxon-e.ezbiocloud.net/.
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            Through Ageing, and Beyond: Gut Microbiota and Inflammatory Status in Seniors and Centenarians

            Elena Biagi, Lotta Nylund, Marco Candela … (2010)
            Background Age-related physiological changes in the gastrointestinal tract, as well as modifications in lifestyle, nutritional behaviour, and functionality of the host immune system, inevitably affect the gut microbiota, resulting in a greater susceptibility to infections. Methodology/Principal Findings By using the Human Intestinal Tract Chip (HITChip) and quantitative PCR of 16S rRNA genes of Bacteria and Archaea, we explored the age-related differences in the gut microbiota composition among young adults, elderly, and centenarians, i.e subjects who reached the extreme limits of the human lifespan, living for over 100 years. We observed that the microbial composition and diversity of the gut ecosystem of young adults and seventy-years old people is highly similar but differs significantly from that of the centenarians. After 100 years of symbiotic association with the human host, the microbiota is characterized by a rearrangement in the Firmicutes population and an enrichment in facultative anaerobes, notably pathobionts. The presence of such a compromised microbiota in the centenarians is associated with an increased inflammatory status, also known as inflammageing, as determined by a range of peripheral blood inflammatory markers. This may be explained by a remodelling of the centenarians' microbiota, with a marked decrease in Faecalibacterium prauznitzii and relatives, symbiotic species with reported anti-inflammatory properties. As signature bacteria of the long life we identified specifically Eubacterium limosum and relatives that were more than ten-fold increased in the centenarians. Conclusions/Significance We provide evidence for the fact that the ageing process deeply affects the structure of the human gut microbiota, as well as its homeostasis with the host's immune system. Because of its crucial role in the host physiology and health status, age-related differences in the gut microbiota composition may be related to the progression of diseases and frailty in the elderly population.
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              High Fat Diet-Induced Gut Microbiota Exacerbates Inflammation and Obesity in Mice via the TLR4 Signaling Pathway

              Kyung-Ah Kim, Wan-Qing Gu, In‐Ah Lee … (2012)
              Background & Aims While it is widely accepted that obesity is associated with low-grade systemic inflammation, the molecular origin of the inflammation remains unknown. Here, we investigated the effect of endotoxin-induced inflammation via TLR4 signaling pathway at both systemic and intestinal levels in response to a high-fat diet. Methods C57BL/6J and TLR4-deficient C57BL/10ScNJ mice were maintained on a low-fat (10 kcal % fat) diet (LFD) or a high–fat (60 kcal % fat) diet (HFD) for 8 weeks. Results HFD induced macrophage infiltration and inflammation in the adipose tissue, as well as an increase in the circulating proinflammatory cytokines. HFD increased both plasma and fecal endotoxin levels and resulted in dysregulation of the gut microbiota by increasing the Firmicutes to Bacteriodetes ratio. HFD induced the growth of Enterobecteriaceae and the production of endotoxin in vitro. Furthermore, HFD induced colonic inflammation, including the increased expression of proinflammatory cytokines, the induction of Toll-like receptor 4 (TLR4), iNOS, COX-2, and the activation of NF-κB in the colon. HFD reduced the expression of tight junction-associated proteins claudin-1 and occludin in the colon. HFD mice demonstrated higher levels of Akt and FOXO3 phosphorylation in the colon compared to the LFD mice. While the body weight of HFD-fed mice was significantly increased in both TLR4-deficient and wild type mice, the epididymal fat weight and plasma endotoxin level of HFD-fed TLR4-deficient mice were 69% and 18% of HFD-fed wild type mice, respectively. Furthermore, HFD did not increase the proinflammatory cytokine levels in TLR4-deficient mice. Conclusions HFD induces inflammation by increasing endotoxin levels in the intestinal lumen as well as in the plasma by altering the gut microbiota composition and increasing its intestinal permeability through the induction of TLR4, thereby accelerating obesity.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): BMC Microbiol.
                Title: BMC microbiology
                Publisher: Springer Science and Business Media LLC
                ISSN (Electronic): 1471-2180
                ISSN (Print): 1471-2180
                Publication date (Electronic): Feb 26 2015
                Volume: 15
                Affiliations
                [1 ] R &B D Center, Korea Yakult Co., Ltd., Yongin-si, Kyunggi-do, 446-901, Korea. p000729@re.yakult.co.kr.
                [2 ] Department of Life and Nanopharmaceutical Sciences, College of Pharmacy, 1, Hoegi, Dongdaemun-ku, Seoul, 130-701, Korea. imkimkyungah@gmail.com.
                [3 ] R &B D Center, Korea Yakult Co., Ltd., Yongin-si, Kyunggi-do, 446-901, Korea. ytahn@re.yakult.co.kr.
                [4 ] Department of Life and Nanopharmaceutical Sciences, College of Pharmacy, 1, Hoegi, Dongdaemun-ku, Seoul, 130-701, Korea. bongoori7@naver.com.
                [5 ] Agricultural Biotechnology, College of Agriculture and Life Sciences, Seoul National University, Seoul, 151-742, Korea. cshuh@snu.ac.kr.
                [6 ] Department of Life and Nanopharmaceutical Sciences, College of Pharmacy, 1, Hoegi, Dongdaemun-ku, Seoul, 130-701, Korea. dhkim@khu.ac.kr.
                Article
                Publisher Item ID: 10.1186/s12866-015-0386-8
                DOI: 10.1186/s12866-015-0386-8
                PMC ID: 4345030
                PubMed ID: 25887483
                SO-VID: 099bae4a-1d3e-4424-b989-d6ac05f9875d
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