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Microbe-Induced Inflammatory Signals Triggering Acquired Bone Marrow Failure Syndromes

Acquired bone marrow failure syndromes encompass a unique set of disorders characterized by a reduction in the effective production of mature cells by the bone marrow (BM). In the majority of cases, these syndromes are the result of the immune-mediated destruction of hematopoietic stem cells or thei...

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Autores principales: Espinoza, J. Luis, Kotecha, Ritesh, Nakao, Shinji
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5323400/
https://www.ncbi.nlm.nih.gov/pubmed/28286502
http://dx.doi.org/10.3389/fimmu.2017.00186
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author Espinoza, J. Luis
Kotecha, Ritesh
Nakao, Shinji
author_facet Espinoza, J. Luis
Kotecha, Ritesh
Nakao, Shinji
author_sort Espinoza, J. Luis
collection PubMed
description Acquired bone marrow failure syndromes encompass a unique set of disorders characterized by a reduction in the effective production of mature cells by the bone marrow (BM). In the majority of cases, these syndromes are the result of the immune-mediated destruction of hematopoietic stem cells or their progenitors at various stages of differentiation. Microbial infection has also been associated with hematopoietic stem cell injury and may lead to associated transient or persistent BM failure, and recent evidence has highlighted the potential impact of commensal microbes and their metabolites on hematopoiesis. We summarize the interactions between microorganisms and the host immune system and emphasize how they may impact the development of acquired BM failure.
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spelling pubmed-53234002017-03-10 Microbe-Induced Inflammatory Signals Triggering Acquired Bone Marrow Failure Syndromes Espinoza, J. Luis Kotecha, Ritesh Nakao, Shinji Front Immunol Immunology Acquired bone marrow failure syndromes encompass a unique set of disorders characterized by a reduction in the effective production of mature cells by the bone marrow (BM). In the majority of cases, these syndromes are the result of the immune-mediated destruction of hematopoietic stem cells or their progenitors at various stages of differentiation. Microbial infection has also been associated with hematopoietic stem cell injury and may lead to associated transient or persistent BM failure, and recent evidence has highlighted the potential impact of commensal microbes and their metabolites on hematopoiesis. We summarize the interactions between microorganisms and the host immune system and emphasize how they may impact the development of acquired BM failure. Frontiers Media S.A. 2017-02-24 /pmc/articles/PMC5323400/ /pubmed/28286502 http://dx.doi.org/10.3389/fimmu.2017.00186 Text en Copyright © 2017 Espinoza, Kotecha and Nakao. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Espinoza, J. Luis
Kotecha, Ritesh
Nakao, Shinji
Microbe-Induced Inflammatory Signals Triggering Acquired Bone Marrow Failure Syndromes
title Microbe-Induced Inflammatory Signals Triggering Acquired Bone Marrow Failure Syndromes
title_full Microbe-Induced Inflammatory Signals Triggering Acquired Bone Marrow Failure Syndromes
title_fullStr Microbe-Induced Inflammatory Signals Triggering Acquired Bone Marrow Failure Syndromes
title_full_unstemmed Microbe-Induced Inflammatory Signals Triggering Acquired Bone Marrow Failure Syndromes
title_short Microbe-Induced Inflammatory Signals Triggering Acquired Bone Marrow Failure Syndromes
title_sort microbe-induced inflammatory signals triggering acquired bone marrow failure syndromes
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5323400/
https://www.ncbi.nlm.nih.gov/pubmed/28286502
http://dx.doi.org/10.3389/fimmu.2017.00186
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