Bacterial Translocation as Inflammatory Driver in Crohn's Disease.
Crohn's disease (CD) is a chronic inflammatory disorder of the gastrointestinal tract responsible for intestinal lesions. The multifactorial etiology attributed to CD includes a combination of environmental and host susceptibility factors, which result in an impaired host-microbe gut interactio...
| Autores: | , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2021 |
| País: | España |
| Institución: | Instituto de Investigación Biomédica y Sanitaria de Alicante (ISABIAL) |
| Repositorio: | r-ISABIAL. Repositorio Institucional de Producción Científica del Instituto de Investigación Biomédica y Sanitaria de Alicante |
| OAI Identifier: | oai:isabial.fundanetsuite.com:p7356 |
| Acceso en línea: | https://isabial.portalinvestigacion.com/publicaciones7356 |
| Access Level: | acceso abierto |
| Palabra clave: | Crohn’s disease NOD2 anti-TNF-a bacterial translocation dysbiosis inflammatory response intestinal permeability |
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Bacterial Translocation as Inflammatory Driver in Crohn's Disease.Linares RFrancés RGutiérrez AJuanola OCrohn’s diseaseNOD2anti-TNF-abacterial translocationdysbiosisinflammatory responseintestinal permeabilityCrohn's disease (CD) is a chronic inflammatory disorder of the gastrointestinal tract responsible for intestinal lesions. The multifactorial etiology attributed to CD includes a combination of environmental and host susceptibility factors, which result in an impaired host-microbe gut interaction. Bacterial overgrowth and dysbiosis, increased intestinal barrier permeability, and altered inflammatory responses in patients with CD have been described in the past. Those events explain the pathogenesis of luminal translocation of bacteria or its products into the blood, a frequent event in CD, which, in turn, favors a sustained inflammatory response in these patients. In this review, we navigate through the interaction between bacterial antigen translocation, permeability of the intestinal barrier, immunologic response of the host, and genetic predisposition as a combined effect on the inflammatory response observed in CD. Several lines of evidence support that translocation of bacterial products leads to uncontrolled inflammation in CD patients, and as a matter of fact, the presence of gut bacterial genomic fragments at a systemic level constitutes a marker for increased risk of relapse among CD patients. Also, the significant percentage of CD patients who lose response to biologic therapies may be influenced by the translocation of bacterial products, which are well-known drivers of proinflammatory cytokine production by host immune cells. Further mechanistic studies evaluating cellular and humoral immune responses, gut microbiota alterations, and genetic predisposition will help clinicians to better control and personalize the management of CD patients in the future.FRONTIERS MEDIA SA2021info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttps://isabial.portalinvestigacion.com/publicaciones7356Frontiers in Cell and Developmental BiologyISSN: 2296634Xreponame:r-ISABIAL. Repositorio Institucional de Producción Científica del Instituto de Investigación Biomédica y Sanitaria de Alicanteinstname:Instituto de Investigación Biomédica y Sanitaria de Alicante (ISABIAL)Inglésinfo:eu-repo/semantics/openAccessoai:isabial.fundanetsuite.com:p73562026-06-12T10:20:37Z |
| dc.title.none.fl_str_mv |
Bacterial Translocation as Inflammatory Driver in Crohn's Disease. |
| title |
Bacterial Translocation as Inflammatory Driver in Crohn's Disease. |
| spellingShingle |
Bacterial Translocation as Inflammatory Driver in Crohn's Disease. Linares R Crohn’s disease NOD2 anti-TNF-a bacterial translocation dysbiosis inflammatory response intestinal permeability |
| title_short |
Bacterial Translocation as Inflammatory Driver in Crohn's Disease. |
| title_full |
Bacterial Translocation as Inflammatory Driver in Crohn's Disease. |
| title_fullStr |
Bacterial Translocation as Inflammatory Driver in Crohn's Disease. |
| title_full_unstemmed |
Bacterial Translocation as Inflammatory Driver in Crohn's Disease. |
| title_sort |
Bacterial Translocation as Inflammatory Driver in Crohn's Disease. |
| dc.creator.none.fl_str_mv |
Linares R Francés R Gutiérrez A Juanola O |
| author |
Linares R |
| author_facet |
Linares R Francés R Gutiérrez A Juanola O |
| author_role |
author |
| author2 |
Francés R Gutiérrez A Juanola O |
| author2_role |
author author author |
| dc.subject.none.fl_str_mv |
Crohn’s disease NOD2 anti-TNF-a bacterial translocation dysbiosis inflammatory response intestinal permeability |
| topic |
Crohn’s disease NOD2 anti-TNF-a bacterial translocation dysbiosis inflammatory response intestinal permeability |
| description |
Crohn's disease (CD) is a chronic inflammatory disorder of the gastrointestinal tract responsible for intestinal lesions. The multifactorial etiology attributed to CD includes a combination of environmental and host susceptibility factors, which result in an impaired host-microbe gut interaction. Bacterial overgrowth and dysbiosis, increased intestinal barrier permeability, and altered inflammatory responses in patients with CD have been described in the past. Those events explain the pathogenesis of luminal translocation of bacteria or its products into the blood, a frequent event in CD, which, in turn, favors a sustained inflammatory response in these patients. In this review, we navigate through the interaction between bacterial antigen translocation, permeability of the intestinal barrier, immunologic response of the host, and genetic predisposition as a combined effect on the inflammatory response observed in CD. Several lines of evidence support that translocation of bacterial products leads to uncontrolled inflammation in CD patients, and as a matter of fact, the presence of gut bacterial genomic fragments at a systemic level constitutes a marker for increased risk of relapse among CD patients. Also, the significant percentage of CD patients who lose response to biologic therapies may be influenced by the translocation of bacterial products, which are well-known drivers of proinflammatory cytokine production by host immune cells. Further mechanistic studies evaluating cellular and humoral immune responses, gut microbiota alterations, and genetic predisposition will help clinicians to better control and personalize the management of CD patients in the future. |
| publishDate |
2021 |
| dc.date.none.fl_str_mv |
2021 |
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info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
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article |
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publishedVersion |
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https://isabial.portalinvestigacion.com/publicaciones7356 |
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https://isabial.portalinvestigacion.com/publicaciones7356 |
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Inglés |
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Inglés |
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info:eu-repo/semantics/openAccess |
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openAccess |
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FRONTIERS MEDIA SA |
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FRONTIERS MEDIA SA |
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Frontiers in Cell and Developmental Biology ISSN: 2296634X reponame:r-ISABIAL. Repositorio Institucional de Producción Científica del Instituto de Investigación Biomédica y Sanitaria de Alicante instname:Instituto de Investigación Biomédica y Sanitaria de Alicante (ISABIAL) |
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Instituto de Investigación Biomédica y Sanitaria de Alicante (ISABIAL) |
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r-ISABIAL. Repositorio Institucional de Producción Científica del Instituto de Investigación Biomédica y Sanitaria de Alicante |
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r-ISABIAL. Repositorio Institucional de Producción Científica del Instituto de Investigación Biomédica y Sanitaria de Alicante |
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