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Age-elevated prostaglandin E2 enhances mortality to influenza infection

View ORCID ProfileJudy Chen, View ORCID ProfileJane C. Deng, Rachel Zemans, Min Zhang, View ORCID ProfileMarc Peters-Golden, View ORCID ProfileDaniel R. Goldstein
doi: https://doi.org/10.1101/2021.12.02.470775
Judy Chen
1Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109
2Program in Immunology, University of Michigan, Ann Arbor, Michigan 48109
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  • ORCID record for Judy Chen
Jane C. Deng
1Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109
2Program in Immunology, University of Michigan, Ann Arbor, Michigan 48109
4Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, Michigan, 48109
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Rachel Zemans
1Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109
4Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, Michigan, 48109
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Min Zhang
3Department of Biostatistics, University of Michigan, Ann Arbor, Michigan 48109
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Marc Peters-Golden
2Program in Immunology, University of Michigan, Ann Arbor, Michigan 48109
4Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, Michigan, 48109
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Daniel R. Goldstein
1Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109
2Program in Immunology, University of Michigan, Ann Arbor, Michigan 48109
5Department of Microbiology and Immunology, University of Michigan, Ann Arbor, Michigan 48109
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  • For correspondence: drgoldst@umich.edu
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Summary

Aging impairs the immune responses to influenza A virus (IAV), resulting in increased mortality to IAV infections in older adults. With aging, there is reduced number and impaired function of alveolar macrophages (AMs), cells critical for defense against IAV. However, factors within the aged lung that impair AMs are not fully known. Using a murine model of IAV infection, we observed that aging increased the level of prostaglandin E2 (PGE2) in the bronchoalveolar lavage fluid (BALF) of aged mice compared to young mice. Blockade of the PGE2 receptor EP2 in aged mice increased AM numbers and subsequently enhanced survival to IAV. Additionally, PGE2 impaired the mitochondrial health of AMs. We also identified senescent type II alveolar epithelial cells (AECs) as a source of the aged-associated PGE2 in the lung. Our results reveal a crosstalk between AECs and AMs, via PGE2, that compromises host defense to IAV infection with aging.

Competing Interest Statement

The authors have declared no competing interest.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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Posted December 03, 2021.
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Age-elevated prostaglandin E2 enhances mortality to influenza infection
Judy Chen, Jane C. Deng, Rachel Zemans, Min Zhang, Marc Peters-Golden, Daniel R. Goldstein
bioRxiv 2021.12.02.470775; doi: https://doi.org/10.1101/2021.12.02.470775
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Age-elevated prostaglandin E2 enhances mortality to influenza infection
Judy Chen, Jane C. Deng, Rachel Zemans, Min Zhang, Marc Peters-Golden, Daniel R. Goldstein
bioRxiv 2021.12.02.470775; doi: https://doi.org/10.1101/2021.12.02.470775

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