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Molecular composition of the alveolar lining fluid in the aging lung
Open accessAbstract
As we age, there is an increased risk for the development of pulmonary diseases, including infections, but few studies have considered changes in lung surfactant and components of the innate immune system as contributing factors to the increased susceptibility of the elderly to succumb to infections. We and others have demonstrated that human alveolar lining fluid (ALF) components, such as surfactant protein (SP)-A, SP-D, complement protein C3, and alveolar hydrolases, play a significant innate immune role in controlling microbial infections. However, there is a lack of information regarding the effect of increasing age on the level and function of ALF components in the lung. Here we addressed this gap in knowledge by determining the levels of ALF components in the aging lung that are important in controlling infection. Our findings demonstrate that pro-inflammatory cytokines, surfactant proteins and lipids, and complement components are significantly altered in the aged lung in both mice and humans. Further, we show that the aging lung is a relatively oxidized environment. Our study provides new information on how the pulmonary environment in old age can potentially modify mucosal immune responses, thereby impacting pulmonary infections and other pulmonary diseases in the elderly population.
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“Age-associated changes in the molecular composition of epithelial lining fluid, specifically a decrease in antioxidants, can also impact lung function (66).”
From Aging and Lung Disease (2020) · cites this paper as [66]
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“An age-associated impairment in AEC2 function, due to increased cellular senescence, contributes to the highly proinflammatory and oxidative environment within the lung (66).”
From Aging and Lung Disease (2020) · cites this paper as [66]
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“An age-associated reduction in BAL antioxidant levels and composition may underlie increased susceptibility of older persons to exposure with environmental toxins, such as ozone, cigarette smoke, and particulate matter (66).”
From Aging and Lung Disease (2020) · cites this paper as [66]
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Self-citation
Metadata
- Authors
- Moliva, J. I., Rajaram, M. V. S., Sidiki, S., Sasindran, S. J., Guirado, E., Pan, X. J., Wang, S.-H., Ross, P., Lafuse, W. P., Schlesinger, L. S., Turner, J., & Torrelles, J. B.
- Affiliations
- The Ohio State University (US)
- Corresponding author
- Turner, Joanne
- Torrelles, Jordi B.
- ORCID
- Venue
- AGE
- Published
- 2014-03-03
- Volume
- 36
- Issue
- 3
- Pages
- 9633-9633
- ISSN
- 0161-9152 (ISSN-L)
- 1574-4647
- PMC
- PMC4082594
- OpenAlex
- W2084628319
- Cited by
- 114
- References
- 79
- Citations by year
- 2026: 2 · 2025: 8 · 2024: 17 · 2023: 20 · 2022: 11 · 2021: 13 · 2020: 10 · 2019: 10 · 2018: 5 · 2017: 10 · 2016: 4 · 2015: 2 · 2014: 2
- FWCI
- 4.80
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- AGE (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ohio State University
- National Institutes of Health
- National Institute of General Medical Sciences (GM068412, T32GM068412)
- National Institute of Allergy and Infectious Diseases (R01AI093570)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Neonatal Respiratory Health Research
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Keywords
- alveolar lining fluid, lung aging, pulmonary innate immunity, surfactant proteins, surfactant protein A, surfactant protein D, complement C3, inflammatory cytokines, oxidative stress, pulmonary infection, mucosal immunity
- MeSH terms
- Adult, Aging, Animals, Female, Humans, Hydrolases, Lung, Male, Pulmonary Alveoli, Oxidative Stress, Pulmonary Surfactant-Associated Protein A, Mice
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