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Purinergic signaling during Porphyromonas gingivalis infection

Despite recent advances unraveling mechanisms of host–pathogen interactions in innate immunity, the participation of purinergic signaling in infection-driven inflammation remains an emerging research field with many unanswered questions. As one of the most-studied oral pathogens, Porphyromonas gingi...

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Autores principales: Almeida-da-Silva, Cássio Luiz Coutinho, Morandini, Ana Carolina, Ulrich, Henning, Ojcius, David M., Coutinho-Silva, Robson
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Chang Gung University 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6140136/
https://www.ncbi.nlm.nih.gov/pubmed/27793267
http://dx.doi.org/10.1016/j.bj.2016.08.003
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author Almeida-da-Silva, Cássio Luiz Coutinho
Morandini, Ana Carolina
Ulrich, Henning
Ojcius, David M.
Coutinho-Silva, Robson
author_facet Almeida-da-Silva, Cássio Luiz Coutinho
Morandini, Ana Carolina
Ulrich, Henning
Ojcius, David M.
Coutinho-Silva, Robson
author_sort Almeida-da-Silva, Cássio Luiz Coutinho
collection PubMed
description Despite recent advances unraveling mechanisms of host–pathogen interactions in innate immunity, the participation of purinergic signaling in infection-driven inflammation remains an emerging research field with many unanswered questions. As one of the most-studied oral pathogens, Porphyromonas gingivalis is considered as a keystone pathogen with a central role in development of periodontal disease. This pathogen needs to evade immune-mediated defense mechanisms and tolerate inflammation in order to survive in the host. In this review, we summarize evidence showing that purinergic signaling modulates P. gingivalis survival and cellular immune responses, and discuss the role played by inflammasome activation and cell death during P. gingivalis infection.
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spelling pubmed-61401362018-09-27 Purinergic signaling during Porphyromonas gingivalis infection Almeida-da-Silva, Cássio Luiz Coutinho Morandini, Ana Carolina Ulrich, Henning Ojcius, David M. Coutinho-Silva, Robson Biomed J Review Articles: Special Edition Despite recent advances unraveling mechanisms of host–pathogen interactions in innate immunity, the participation of purinergic signaling in infection-driven inflammation remains an emerging research field with many unanswered questions. As one of the most-studied oral pathogens, Porphyromonas gingivalis is considered as a keystone pathogen with a central role in development of periodontal disease. This pathogen needs to evade immune-mediated defense mechanisms and tolerate inflammation in order to survive in the host. In this review, we summarize evidence showing that purinergic signaling modulates P. gingivalis survival and cellular immune responses, and discuss the role played by inflammasome activation and cell death during P. gingivalis infection. Chang Gung University 2016-08 2016-09-24 /pmc/articles/PMC6140136/ /pubmed/27793267 http://dx.doi.org/10.1016/j.bj.2016.08.003 Text en © 2016 Chang Gung University. Publishing services by Elsevier B.V. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Review Articles: Special Edition
Almeida-da-Silva, Cássio Luiz Coutinho
Morandini, Ana Carolina
Ulrich, Henning
Ojcius, David M.
Coutinho-Silva, Robson
Purinergic signaling during Porphyromonas gingivalis infection
title Purinergic signaling during Porphyromonas gingivalis infection
title_full Purinergic signaling during Porphyromonas gingivalis infection
title_fullStr Purinergic signaling during Porphyromonas gingivalis infection
title_full_unstemmed Purinergic signaling during Porphyromonas gingivalis infection
title_short Purinergic signaling during Porphyromonas gingivalis infection
title_sort purinergic signaling during porphyromonas gingivalis infection
topic Review Articles: Special Edition
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6140136/
https://www.ncbi.nlm.nih.gov/pubmed/27793267
http://dx.doi.org/10.1016/j.bj.2016.08.003
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