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A Decline in p38 MAPK Signaling Underlies Immunosenescence in Caenorhabditis elegans

Author(s)
Youngman, Matthew J.; Rogers, Zoe N.; Kim, Dennis H.
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Abstract
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.
Date issued
2011-05
URI
http://hdl.handle.net/1721.1/66261
Department
Massachusetts Institute of Technology. Department of Biology
Journal
PLoS Genetics
Publisher
Public Library of Science
Citation
Youngman, Matthew J., Zoë N. Rogers, and Dennis H. Kim. “A Decline in p38 MAPK Signaling Underlies Immunosenescence in Caenorhabditis elegans.” Ed. Stuart K. Kim. PLoS Genetics 7 (2011): e1002082.
Version: Final published version
ISSN
1553-7404
1553-7390

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