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January 19, 2023
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Prostaglandin E2 potentially increases susceptibility to influenza A infection in the elderly
A new study tested whether age-related elevation in Prostaglandin E2 is a driver that impairs host defense against influenza.
Influenza (Flu) infection by influenza A virus leads to mild-to-moderate symptoms for most young individuals. However, older adults aged ≥65 years infected with this virus suffer from higher morbidity and mortality rates compared to young adults. Studies also indicate that 86% of deaths during the 2017-2018 Flu season in the US were linked to older adults. In addition to increased susceptibility, anti-influenza A medications show limited efficacy in this age group, further complicating the issue.
Prostaglandin E2 (PGE2) is an immune-modulating molecule associated with several inflammatory conditions, like rheumatoid arthritis, infections, and different cancer types. Preclinical research on murine models has shown that PGE2 levels increase in the lungs of aging mice. However, it is yet to be discovered whether this is also the case in humans. Additionally, it remains unclear whether cellular senescence (a hallmark of aging) contributes to PGE2 accumulation or if a cell type drives this process in response to aging or infection.
To better understand the abovementioned gaps, Chen et al. tested their hypothesis of whether age-related elevation in PGE2 is a driver that impairs host defense against influenza A infections on human and murine models. The group used patient-derived samples of lung tissue as an experimental model.
Results showed that:
- Age-related elevation of PGE2 in murine models is linked to senescent type II alveolar epithelial cells (these cells have regenerative and secretory roles, maintaining lung homeostasis).
- PGE2 levels increase in human lungs as a consequence of aging.
- With aging, PGE2, through the PGE2 receptor 2, limits alveolar macrophage proliferation and mitochondrial fitness, affecting lung homeostasis and the ability to respond to pathogens.
- Blocking the EP2 receptor improves the survival of old mice exposed to a lethal viral load of influenza A but not young ones.
The authors concluded that study results show a potential pathway that could contribute to increased mortality associated with influenza A and other possible respiratory infections. These findings could pave the way for new therapeutic or preventive approaches protecting the elderly against viral respiratory infections. Further research in this area is warranted.
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Influenza (Flu) infection by influenza A virus leads to mild-to-moderate symptoms for most young individuals. However, older adults aged ≥65 years infected with this virus suffer from higher morbidity and mortality rates compared to young adults. Studies also indicate that 86% of deaths during the 2017-2018 Flu season in the US were linked to older adults. In addition to increased susceptibility, anti-influenza A medications show limited efficacy in this age group, further complicating the issue.
Prostaglandin E2 (PGE2) is an immune-modulating molecule associated with several inflammatory conditions, like rheumatoid arthritis, infections, and different cancer types. Preclinical research on murine models has shown that PGE2 levels increase in the lungs of aging mice. However, it is yet to be discovered whether this is also the case in humans. Additionally, it remains unclear whether cellular senescence (a hallmark of aging) contributes to PGE2 accumulation or if a cell type drives this process in response to aging or infection.
To better understand the abovementioned gaps, Chen et al. tested their hypothesis of whether age-related elevation in PGE2 is a driver that impairs host defense against influenza A infections on human and murine models. The group used patient-derived samples of lung tissue as an experimental model.
Results showed that:
- Age-related elevation of PGE2 in murine models is linked to senescent type II alveolar epithelial cells (these cells have regenerative and secretory roles, maintaining lung homeostasis).
- PGE2 levels increase in human lungs as a consequence of aging.
- With aging, PGE2, through the PGE2 receptor 2, limits alveolar macrophage proliferation and mitochondrial fitness, affecting lung homeostasis and the ability to respond to pathogens.
- Blocking the EP2 receptor improves the survival of old mice exposed to a lethal viral load of influenza A but not young ones.
The authors concluded that study results show a potential pathway that could contribute to increased mortality associated with influenza A and other possible respiratory infections. These findings could pave the way for new therapeutic or preventive approaches protecting the elderly against viral respiratory infections. Further research in this area is warranted.
Article reviewed by
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Dr. Ana Baroni MD. Ph.D.
Scientific & Medical Advisor
Quality Garant
Ana has over 20 years of consultancy experience in longevity, regenerative and precision medicine. She has a multifaceted understanding of genomics, molecular biology, clinical biochemistry, nutrition, aging markers, hormones and physical training. This background allows her to bridge the gap between longevity basic sciences and evidence-based real interventions, putting them into the clinic, to enhance the healthy aging of people. She is co-founder of Origen.life, and Longevityzone. Board member at Breath of Health, BioOx and American Board of Clinical Nutrition. She is Director of International Medical Education of the American College of Integrative Medicine, Professor in IL3 Master of Longevity at Barcelona University and Professor of Nutrigenomics in Nutrition Grade in UNIR University.
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