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Senescence and Host–Pathogen Interactions
Damage to our genomes triggers cellular senescence characterised by stable cell cycle arrest and a pro-inflammatory secretome that prevents the unrestricted growth of cells with pathological potential. In this way, senescence can be considered a powerful innate defence against cancer and viral infec...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7409240/ https://www.ncbi.nlm.nih.gov/pubmed/32708331 http://dx.doi.org/10.3390/cells9071747 |
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author | Humphreys, Daniel ElGhazaly, Mohamed Frisan, Teresa |
author_facet | Humphreys, Daniel ElGhazaly, Mohamed Frisan, Teresa |
author_sort | Humphreys, Daniel |
collection | PubMed |
description | Damage to our genomes triggers cellular senescence characterised by stable cell cycle arrest and a pro-inflammatory secretome that prevents the unrestricted growth of cells with pathological potential. In this way, senescence can be considered a powerful innate defence against cancer and viral infection. However, damage accumulated during ageing increases the number of senescent cells and this contributes to the chronic inflammation and deregulation of the immune function, which increases susceptibility to infectious disease in ageing organisms. Bacterial and viral pathogens are masters of exploiting weak points to establish infection and cause devastating diseases. This review considers the emerging importance of senescence in the host–pathogen interaction: we discuss the pathogen exploitation of ageing cells and senescence as a novel hijack target of bacterial pathogens that deploys senescence-inducing toxins to promote infection. The persistent induction of senescence by pathogens, mediated directly through virulence determinants or indirectly through inflammation and chronic infection, also contributes to age-related pathologies such as cancer. This review highlights the dichotomous role of senescence in infection: an innate defence that is exploited by pathogens to cause disease. |
format | Online Article Text |
id | pubmed-7409240 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-74092402020-08-26 Senescence and Host–Pathogen Interactions Humphreys, Daniel ElGhazaly, Mohamed Frisan, Teresa Cells Review Damage to our genomes triggers cellular senescence characterised by stable cell cycle arrest and a pro-inflammatory secretome that prevents the unrestricted growth of cells with pathological potential. In this way, senescence can be considered a powerful innate defence against cancer and viral infection. However, damage accumulated during ageing increases the number of senescent cells and this contributes to the chronic inflammation and deregulation of the immune function, which increases susceptibility to infectious disease in ageing organisms. Bacterial and viral pathogens are masters of exploiting weak points to establish infection and cause devastating diseases. This review considers the emerging importance of senescence in the host–pathogen interaction: we discuss the pathogen exploitation of ageing cells and senescence as a novel hijack target of bacterial pathogens that deploys senescence-inducing toxins to promote infection. The persistent induction of senescence by pathogens, mediated directly through virulence determinants or indirectly through inflammation and chronic infection, also contributes to age-related pathologies such as cancer. This review highlights the dichotomous role of senescence in infection: an innate defence that is exploited by pathogens to cause disease. MDPI 2020-07-21 /pmc/articles/PMC7409240/ /pubmed/32708331 http://dx.doi.org/10.3390/cells9071747 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Humphreys, Daniel ElGhazaly, Mohamed Frisan, Teresa Senescence and Host–Pathogen Interactions |
title | Senescence and Host–Pathogen Interactions |
title_full | Senescence and Host–Pathogen Interactions |
title_fullStr | Senescence and Host–Pathogen Interactions |
title_full_unstemmed | Senescence and Host–Pathogen Interactions |
title_short | Senescence and Host–Pathogen Interactions |
title_sort | senescence and host–pathogen interactions |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7409240/ https://www.ncbi.nlm.nih.gov/pubmed/32708331 http://dx.doi.org/10.3390/cells9071747 |
work_keys_str_mv | AT humphreysdaniel senescenceandhostpathogeninteractions AT elghazalymohamed senescenceandhostpathogeninteractions AT frisanteresa senescenceandhostpathogeninteractions |