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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s00281-014-0454-4.

Title:
The gut microbiota and inflammatory bowel disease | Seminars in Immunopathology
Description:
Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory disorder of the gut. Although the precise cause of IBD remains unknown, the most accepted hypothesis of IBD pathogenesis to date is that an aberrant immune response against the gut microbiota is triggered by environmental factors in a genetically susceptible host. The advancement of next-generation sequencing technology has enabled identification of various alterations of the gut microbiota composition in IBD. While some results related to dysbiosis in IBD are different between studies owing to variations of sample type, method of investigation, patient profiles, and medication, the most consistent observation in IBD is reduced bacterial diversity, a decrease of Firmicutes, and an increase of Proteobacteria. It has not yet been established how dysbiosis contributes to intestinal inflammation. Many of the known IBD susceptibility genes are associated with recognition and processing of bacteria, which is consistent with a role of the gut microbiota in the pathogenesis of IBD. A number of trials have shown that therapies correcting dysbiosis, including fecal microbiota transplantation and probiotics, are promising in IBD.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Health & Fitness
  • Science
  • Education

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,642,828 visitors per month in the current month.

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How Does Link.springer.com Make Money? {πŸ’Έ}

We're unsure how the site profits.

Not all websites focus on profit; some are designed to educate, connect people, or share useful tools. People create websites for numerous reasons. And this could be one such example. Link.springer.com might be earning cash quietly, but we haven't detected the monetization method.

Keywords {πŸ”}

pubmed, gut, microbiota, article, google, scholar, patients, ibd, disease, cas, colitis, intestinal, bacteria, bowel, ulcerative, central, inflammatory, cells, dysbiosis, inflammation, crohns, remission, reported, mice, genes, mucosal, gastroenterol, observed, bacterial, composition, susceptibility, clinical, fmt, vsl, immune, studies, fecal, nod, essential, treatment, active, trial, cell, paneth, analysis, host, genetic, human, study, epithelial,

Topics {βœ’οΈ}

double-blinded placebo-controlled trials article download pdf germ-free il-10-deficient mice nuclear ribonucleoprotein hnrnp-a1 anti-inflammatory cytokine il-10 adherent-invasive escherichia coli takanori kanai received activity-specific core microbiome serum anti-map antibody mucosal alkaline sphingomyelinase inflammatory bowel disease article matsuoka enabled culture-independent analysis bacterial-derived products tbx21/t-bet t-bet deficiency inflammatory bowel diseases newly diagnosed patients privacy choices/manage cookies genome-wide association study bifidobacterium longum/synergy 1 microbial community imbalances fecal microbiota transplantation microbiota-dependent intestinal inflammation germ-free animals takanori kanai periodically repeated transplantation controlled pilot trial keio university school placebo-controlled trial relapsing inflammatory disorder intestinal microbial ecology randomized controlled trial full access anti-inflammatory effect faecal microbiota transplantation microbial constituents specific distal digestive tract ileo-cecal valves dominant fecal microbiota experimental ulcerative colitis develop spontaneous colitis il-10-deficient mice mucosal barrier function fecal microbiota profiles disease susceptibility genes placebo-controlled study culture-independent analyses cd susceptibility gene developed similar colitis

Questions {❓}

  • How does dysbiosis lead to intestinal inflammation?

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:The gut microbiota and inflammatory bowel disease
         description:Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory disorder of the gut. Although the precise cause of IBD remains unknown, the most accepted hypothesis of IBD pathogenesis to date is that an aberrant immune response against the gut microbiota is triggered by environmental factors in a genetically susceptible host. The advancement of next-generation sequencing technology has enabled identification of various alterations of the gut microbiota composition in IBD. While some results related to dysbiosis in IBD are different between studies owing to variations of sample type, method of investigation, patient profiles, and medication, the most consistent observation in IBD is reduced bacterial diversity, a decrease of Firmicutes, and an increase of Proteobacteria. It has not yet been established how dysbiosis contributes to intestinal inflammation. Many of the known IBD susceptibility genes are associated with recognition and processing of bacteria, which is consistent with a role of the gut microbiota in the pathogenesis of IBD. A number of trials have shown that therapies correcting dysbiosis, including fecal microbiota transplantation and probiotics, are promising in IBD.
         datePublished:2014-11-25T00:00:00Z
         dateModified:2014-11-25T00:00:00Z
         pageStart:47
         pageEnd:55
         sameAs:https://doi.org/10.1007/s00281-014-0454-4
         keywords:
            Inflammatory bowel disease
            Ulcerative colitis
            Crohn’s disease
            Dysbiosis
            Immunology
            Internal Medicine
            Pathology
         image:
         isPartOf:
            name:Seminars in Immunopathology
            issn:
               1863-2300
               1863-2297
            volumeNumber:37
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer Berlin Heidelberg
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Katsuyoshi Matsuoka
               affiliation:
                     name:Keio University School of Medicine
                     address:
                        name:Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku, Japan
                        type:PostalAddress
                     type:Organization
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               name:Takanori Kanai
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                     name:Keio University School of Medicine
                     address:
                        name:Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku, Japan
                        type:PostalAddress
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         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:The gut microbiota and inflammatory bowel disease
      description:Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory disorder of the gut. Although the precise cause of IBD remains unknown, the most accepted hypothesis of IBD pathogenesis to date is that an aberrant immune response against the gut microbiota is triggered by environmental factors in a genetically susceptible host. The advancement of next-generation sequencing technology has enabled identification of various alterations of the gut microbiota composition in IBD. While some results related to dysbiosis in IBD are different between studies owing to variations of sample type, method of investigation, patient profiles, and medication, the most consistent observation in IBD is reduced bacterial diversity, a decrease of Firmicutes, and an increase of Proteobacteria. It has not yet been established how dysbiosis contributes to intestinal inflammation. Many of the known IBD susceptibility genes are associated with recognition and processing of bacteria, which is consistent with a role of the gut microbiota in the pathogenesis of IBD. A number of trials have shown that therapies correcting dysbiosis, including fecal microbiota transplantation and probiotics, are promising in IBD.
      datePublished:2014-11-25T00:00:00Z
      dateModified:2014-11-25T00:00:00Z
      pageStart:47
      pageEnd:55
      sameAs:https://doi.org/10.1007/s00281-014-0454-4
      keywords:
         Inflammatory bowel disease
         Ulcerative colitis
         Crohn’s disease
         Dysbiosis
         Immunology
         Internal Medicine
         Pathology
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            type:ImageObject
         type:Organization
      author:
            name:Katsuyoshi Matsuoka
            affiliation:
                  name:Keio University School of Medicine
                  address:
                     name:Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku, Japan
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Takanori Kanai
            affiliation:
                  name:Keio University School of Medicine
                  address:
                     name:Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku, Japan
                     type:PostalAddress
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      name:Seminars in Immunopathology
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         1863-2300
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      volumeNumber:37
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      name:Springer Berlin Heidelberg
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         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
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      name:Keio University School of Medicine
      address:
         name:Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku, Japan
         type:PostalAddress
      name:Keio University School of Medicine
      address:
         name:Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku, Japan
         type:PostalAddress
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      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Katsuyoshi Matsuoka
      affiliation:
            name:Keio University School of Medicine
            address:
               name:Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku, Japan
               type:PostalAddress
            type:Organization
      name:Takanori Kanai
      affiliation:
            name:Keio University School of Medicine
            address:
               name:Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku, Japan
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku, Japan
      name:Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku, Japan

External Links {πŸ”—}(338)

Analytics and Tracking {πŸ“Š}

  • Google Tag Manager

Libraries {πŸ“š}

  • Clipboard.js
  • Prism.js

CDN Services {πŸ“¦}

  • Crossref

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