dc.contributor.authorYin, Lu
dc.contributor.authorZheng, Dahai
dc.contributor.authorLimmon, Gino V
dc.contributor.authorLeung, Nicola HN
dc.contributor.authorXu, Shuoyu
dc.contributor.authorRajapakse, Jagath C
dc.contributor.authorHanry, Yu
dc.contributor.authorChow, Vincent T. K.
dc.contributor.authorChen, Jianzhu
dc.date.accessioned2014-10-21T02:02:07Z
dc.date.available2014-10-21T02:02:07Z
dc.date.copyright2014en_US
dc.date.issued2014
dc.identifier.citationYin, L., Zheng, D., Limmon, G., Leung, N. HN., Xu, S., Rajapakse, J. C., et al. (2014). Aging exacerbates damage and delays repair of alveolar epithelia following influenza viral pneumonia. Respiratory research, 15(1).en_US
dc.identifier.issn1465-9921en_US
dc.identifier.urihttp://hdl.handle.net/10220/24081
dc.description.abstractBackground: Influenza virus infection causes significantly higher levels of morbidity and mortality in the elderly. Studies have shown that impaired immunity in the elderly contributes to the increased susceptibility to influenza virus infection, however, how aging affects the lung tissue damage and repair has not been completely elucidated. Methods: Aged (16–18 months old) and young (2–3 months old) mice were infected with influenza virus intratracheally. Body weight and mortality were monitored. Different days after infection, lung sections were stained to estimate the overall lung tissue damage and for club cells, pro-SPC+ bronchiolar epithelial cells, alveolar type I and II cells to quantify their frequencies using automated image analysis algorithms. Results: Following influenza infection, aged mice lose more weight and die from otherwise sub-lethal influenza infection in young mice. Although there is no difference in damage and regeneration of club cells between the young and the aged mice, damage to alveolar type I and II cells (AT1s and AT2s) is exacerbated, and regeneration of AT2s and their precursors (pro-SPC-positive bronchiolar epithelial cells) is significantly delayed in the aged mice. We further show that oseltamivir treatment reduces virus load and lung damage, and promotes pulmonary recovery from infection in the aged mice. Conclusions: These findings show that aging increases susceptibility of the distal lung epithelium to influenza infection and delays the emergence of pro-SPC positive progenitor cells during the repair process. Our findings also shed light on possible approaches to enhance the clinical management of severe influenza pneumonia in the elderly.en_US
dc.format.extent13 p.en_US
dc.language.isoenen_US
dc.relation.ispartofseriesRespiratory researchen_US
dc.rights© 2014 Yin et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.en_US
dc.subjectDRNTU::Science::Biological sciences::Microbiology::Immunology
dc.titleAging exacerbates damage and delays repair of alveolar epithelia following influenza viral pneumoniaen_US
dc.typeJournal Article
dc.contributor.schoolSchool of Computer Engineeringen_US
dc.identifier.doihttp://dx.doi.org/10.1186/s12931-014-0116-z
dc.description.versionPublished versionen_US


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record