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Cited by 114Neonatal Respiratory Health ResearchImmune Response and InflammationInterstitial Lung Diseases and Idiopathic Pulmonary Fibrosis

The DOI matches its Crossref record; 78 of the 79 references it cites were found in a registry or an index.

Molecular composition of the alveolar lining fluid in the aging lung

Open access
Moliva, Juan I., Rajaram, Murugesan V. S., Sidiki, Sabeen, Sasindran, Smitha J., Guirado, Evelyn, Pan, Xueliang Jeff, Wang, Shu-Hua, Ross, Patrick, Lafuse, William P., Schlesinger, Larry S., Turner, Joanne, Torrelles, Jordi B.·2014·AGE
DOI 10.1007/s11357-014-9633-4PMC PMC4082594
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Abstract

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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Research works printed but not linked: 1

  1. Carlson TK, Brooks M, Meyer D, Henning L, Murugesan V et al (2010) Pulmonary innnate immunity: soluble and cellular host defenses of the lung. In: Marsh C, Tridandapani S, Piper M (eds) Regulation of innate immune function. Transworld Research Network, Kerala, pp 165–211

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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
Publisher
Springer Science and Business Media LLC
Published
2014-03-03
Volume
36
Issue
3
Pages
9633-9633
ISSN
  • 0161-9152 (ISSN-L)
  • 1574-4647
DOI
10.1007/s11357-014-9633-4
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
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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