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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Am+J+Physiol+Lung+Cell+Mol+Physiol
2017 ; 313
(5
): L940-L949
Nephropedia Template TP
gab.com Text
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English Wikipedia
Oxygen-dependent changes in lung development do not affect epithelial infection
with influenza A virus
#MMPMID28798254
Domm W
; Yee M
; Misra RS
; Gelein R
; Nogales A
; Martinez-Sobrido L
; O'Reilly MA
Am J Physiol Lung Cell Mol Physiol
2017[Nov]; 313
(5
): L940-L949
PMID28798254
show ga
Infants born prematurely often require supplemental oxygen, which contributes to
aberrant lung development and increased pulmonary morbidity following a
respiratory viral infection. We have been using a mouse model to understand how
early-life hyperoxia affects the adult lung response to influenza A virus (IAV)
infection. Prior studies showed how neonatal hyperoxia (100% oxygen) increased
sensitivity of adult mice to infection with IAV [IAV (A/Hong Kong/X31) H3N2] as
defined by persistent inflammation, pulmonary fibrosis, and mortality. Since
neonatal hyperoxia alters lung structure, we used a novel fluorescence-expressing
reporter strain of H1N1 IAV [A/Puerto Rico/8/34 mCherry (PR8-mCherry)] to
evaluate whether it also altered early infection of the respiratory epithelium.
Like Hong Kong/X31, neonatal hyperoxia increased morbidity and mortality of adult
mice infected with PR8-mCherry. Whole lung imaging and histology suggested a
modest increase in mCherry expression in adult mice exposed to neonatal hyperoxia
compared with room air-exposed animals. However, this did not reflect an increase
in airway or alveolar epithelial infection when mCherry-positive cells were
identified and quantified by flow cytometry. Instead, a modest increase in the
number of CD45-positive macrophages expressing mCherry was detected. While
neonatal hyperoxia does not alter early epithelial infection with IAV, it may
increase the activity of macrophages toward infected cells, thereby enhancing
early epithelial injury.