A decline in p38 MAPK signaling underlies immunosenescence in Caenorhabditis elegans.

The decline in immune function with aging, known as immunosenescence, has been implicated in evolutionarily diverse species, but the underlying molecular mechanisms are not understood. During aging in Caenorhabditis elegans, intestinal tissue deterioration and the increased intestinal proliferation...

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Main Authors: Matthew J Youngman, Zoë N Rogers, Dennis H Kim
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2011-05-01
Series:PLoS Genetics
Online Access:http://europepmc.org/articles/PMC3098197?pdf=render
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author Matthew J Youngman
Zoë N Rogers
Dennis H Kim
author_facet Matthew J Youngman
Zoë N Rogers
Dennis H Kim
author_sort Matthew J Youngman
collection DOAJ
description The decline in immune function with aging, known as immunosenescence, has been implicated in evolutionarily diverse species, but the underlying molecular mechanisms are not understood. During aging in Caenorhabditis elegans, intestinal tissue deterioration and the increased intestinal proliferation of bacteria are observed, but how innate immunity changes during C. elegans aging has not been defined. Here we show that C. elegans exhibits increased susceptibility to bacterial infection with age, and we establish that aging is associated with a decline in the activity of the conserved PMK-1 p38 mitogen-activated protein kinase pathway, which regulates innate immunity in C. elegans. Our data define the phenomenon of innate immunosenescence in C. elegans in terms of the age-dependent dynamics of the PMK-1 innate immune signaling pathway, and they suggest that a cycle of intestinal tissue aging, immunosenescence, and bacterial proliferation leads to death in aging C. elegans.
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spelling doaj.art-46a92d05f2db43cd8490e2c64def3af82022-12-21T22:32:33ZengPublic Library of Science (PLoS)PLoS Genetics1553-73901553-74042011-05-0175e100208210.1371/journal.pgen.1002082A decline in p38 MAPK signaling underlies immunosenescence in Caenorhabditis elegans.Matthew J YoungmanZoë N RogersDennis H KimThe decline in immune function with aging, known as immunosenescence, has been implicated in evolutionarily diverse species, but the underlying molecular mechanisms are not understood. During aging in Caenorhabditis elegans, intestinal tissue deterioration and the increased intestinal proliferation of bacteria are observed, but how innate immunity changes during C. elegans aging has not been defined. Here we show that C. elegans exhibits increased susceptibility to bacterial infection with age, and we establish that aging is associated with a decline in the activity of the conserved PMK-1 p38 mitogen-activated protein kinase pathway, which regulates innate immunity in C. elegans. Our data define the phenomenon of innate immunosenescence in C. elegans in terms of the age-dependent dynamics of the PMK-1 innate immune signaling pathway, and they suggest that a cycle of intestinal tissue aging, immunosenescence, and bacterial proliferation leads to death in aging C. elegans.http://europepmc.org/articles/PMC3098197?pdf=render
spellingShingle Matthew J Youngman
Zoë N Rogers
Dennis H Kim
A decline in p38 MAPK signaling underlies immunosenescence in Caenorhabditis elegans.
PLoS Genetics
title A decline in p38 MAPK signaling underlies immunosenescence in Caenorhabditis elegans.
title_full A decline in p38 MAPK signaling underlies immunosenescence in Caenorhabditis elegans.
title_fullStr A decline in p38 MAPK signaling underlies immunosenescence in Caenorhabditis elegans.
title_full_unstemmed A decline in p38 MAPK signaling underlies immunosenescence in Caenorhabditis elegans.
title_short A decline in p38 MAPK signaling underlies immunosenescence in Caenorhabditis elegans.
title_sort decline in p38 mapk signaling underlies immunosenescence in caenorhabditis elegans
url http://europepmc.org/articles/PMC3098197?pdf=render
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