Journal article
Cellular bioenergetics, caspase activity and glutathione in murine lungs infected with influenza A virus
Virology (New York, N.Y.), Vol.446(1-2), pp.180-188
11/2013
DOI: 10.1016/j.virol.2013.07.034
PMID: 24074580
Abstract
Inhibition of cellular respiration, oxidation of glutathione and induction of apoptosis have been reported in epithelial cells infected in vitro with influenza A virus (IAV). Here, the same biomarkers were investigated in vivo by assessing the lungs of BALB/c mice infected with IAV. Cellular respiration declined on day 3 and recovered on day 7 post-infection. For days 3–5, the rate (mean±SD) of respiration (µMO2min−1mg−1) in uninfected lungs was 0.103±0.021 (n=4) and in infected lungs was 0.076±0.025 (n=4, p=0.026). Relative cellular ATP (infected/uninfected) was 4.7 on day 2 and 1.07 on day 7. Intracellular caspase activity peaked on day 7. Cellular glutathione decreased by ≥10% on days 3–7. Lung pathology was prominent on day 3 and caspase-3 labeling was prominent on day 5. IAV infection was associated with suppression of cellular respiration, diminished glutathione, and induction of apoptosis. These functional biomarkers were associated with structural changes noted in infected mice.
•In BALB/c mice, lung cellular respiration is suppressed in influenza A virus infection.•Lung cellular ATP is transiently increased in influenza A virus infection.•Lung cellular glutathione is partially depleted in influenza A virus infection.•Lung cellular caspase activity is increased in influenza A virus infection.
Details
- Title: Subtitle
- Cellular bioenergetics, caspase activity and glutathione in murine lungs infected with influenza A virus
- Creators
- Ahmed R Alsuwaidi - Departments of Pediatrics, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666, Al Ain, United Arab EmiratesSaeeda Almarzooqi - Departments of Pathology, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666, Al Ain, United Arab EmiratesAlia Albawardi - Departments of Pathology, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666, Al Ain, United Arab EmiratesSheela Benedict - Departments of Pediatrics, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666, Al Ain, United Arab EmiratesJose Kochiyil - Departments of Pediatrics, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666, Al Ain, United Arab EmiratesFarah Mustafa - Departments of Biochemistry, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666, Al Ain, United Arab EmiratesStacey M Hartwig - Department of Microbiology, University of Iowa, Iowa City, IA 52242, USASteven M Varga - Department of Microbiology, University of Iowa, Iowa City, IA 52242, USAAbdul-Kader Souid - Departments of Pediatrics, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666, Al Ain, United Arab Emirates
- Resource Type
- Journal article
- Publication Details
- Virology (New York, N.Y.), Vol.446(1-2), pp.180-188
- DOI
- 10.1016/j.virol.2013.07.034
- PMID
- 24074580
- NLM abbreviation
- Virology
- ISSN
- 0042-6822
- eISSN
- 1096-0341
- Publisher
- Elsevier Inc
- Grant note
- DOI: 10.13039/501100006013, name: United Arab Emirates University
- Language
- English
- Date published
- 11/2013
- Academic Unit
- Graduate College Admin and Gen; Microbiology and Immunology; Pathology
- Record Identifier
- 9984083278002771
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