Reduced inflammation and altered innate response in neonates during paramyxoviral infection
<p>Abstract</p> <p>Background</p> <p>Human infants are frequently hospitalized due to infection with the paramyxovirus respiratory syncytial virus (RSV). However, very little is known about the neonatal response to paramyxoviral infection. Here, a neonatal model of para...
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doaj-3b94c44ad3cb4173b4d51a78ffec4b952020-11-25T02:28:17ZengBMCVirology Journal1743-422X2011-12-018154910.1186/1743-422X-8-549Reduced inflammation and altered innate response in neonates during paramyxoviral infectionBhattacharya SomashubhraBeal Brandon TJanowski Ann MShornick Laurie P<p>Abstract</p> <p>Background</p> <p>Human infants are frequently hospitalized due to infection with the paramyxovirus respiratory syncytial virus (RSV). However, very little is known about the neonatal response to paramyxoviral infection. Here, a neonatal model of paramyxoviral infection is developed using the mouse pathogen Sendai virus (SeV).</p> <p>Results</p> <p>Adult mice infected with SeV developed a predominantly neutrophilic inflammatory cell influx and a concomitant reduction in lung function, as determined by oxygen saturation. In contrast, neonates with SeV had significantly reduced inflammation and normal lung function. Surprisingly, infected neonates had similar viral loads as adult mice. A reduced neutrophil influx in the neonates may be due in part to reduced expression of both CXCL2 and intracellular adhesion molecule-1 (ICAM-1). Expression of IFN-γ and TNF-α increased in a dose-dependent manner in adult lungs, but neonates did not increase expression of either of these cytokines, even at the highest doses. Importantly, the expression of the RIG-I-like receptors (RLRs) was delayed in the neonatal mice, which might have contributed to their reduced inflammation and differential cytokine expression.</p> <p>Conclusions</p> <p>Neonatal mice developed similar SeV titers and cleared the virus with similar efficiency despite developing a dramatically lower degree of pulmonary inflammation compared to adults. This suggests that inflammation in the lung may not be required to control viral replication. Future studies will be needed to determine any effect the reduced inflammation may have on the development of a protective memory response in neonates.</p> http://www.virologyj.com/content/8/1/549ViralNeonatalLungInnate |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Bhattacharya Somashubhra Beal Brandon T Janowski Ann M Shornick Laurie P |
spellingShingle |
Bhattacharya Somashubhra Beal Brandon T Janowski Ann M Shornick Laurie P Reduced inflammation and altered innate response in neonates during paramyxoviral infection Virology Journal Viral Neonatal Lung Innate |
author_facet |
Bhattacharya Somashubhra Beal Brandon T Janowski Ann M Shornick Laurie P |
author_sort |
Bhattacharya Somashubhra |
title |
Reduced inflammation and altered innate response in neonates during paramyxoviral infection |
title_short |
Reduced inflammation and altered innate response in neonates during paramyxoviral infection |
title_full |
Reduced inflammation and altered innate response in neonates during paramyxoviral infection |
title_fullStr |
Reduced inflammation and altered innate response in neonates during paramyxoviral infection |
title_full_unstemmed |
Reduced inflammation and altered innate response in neonates during paramyxoviral infection |
title_sort |
reduced inflammation and altered innate response in neonates during paramyxoviral infection |
publisher |
BMC |
series |
Virology Journal |
issn |
1743-422X |
publishDate |
2011-12-01 |
description |
<p>Abstract</p> <p>Background</p> <p>Human infants are frequently hospitalized due to infection with the paramyxovirus respiratory syncytial virus (RSV). However, very little is known about the neonatal response to paramyxoviral infection. Here, a neonatal model of paramyxoviral infection is developed using the mouse pathogen Sendai virus (SeV).</p> <p>Results</p> <p>Adult mice infected with SeV developed a predominantly neutrophilic inflammatory cell influx and a concomitant reduction in lung function, as determined by oxygen saturation. In contrast, neonates with SeV had significantly reduced inflammation and normal lung function. Surprisingly, infected neonates had similar viral loads as adult mice. A reduced neutrophil influx in the neonates may be due in part to reduced expression of both CXCL2 and intracellular adhesion molecule-1 (ICAM-1). Expression of IFN-γ and TNF-α increased in a dose-dependent manner in adult lungs, but neonates did not increase expression of either of these cytokines, even at the highest doses. Importantly, the expression of the RIG-I-like receptors (RLRs) was delayed in the neonatal mice, which might have contributed to their reduced inflammation and differential cytokine expression.</p> <p>Conclusions</p> <p>Neonatal mice developed similar SeV titers and cleared the virus with similar efficiency despite developing a dramatically lower degree of pulmonary inflammation compared to adults. This suggests that inflammation in the lung may not be required to control viral replication. Future studies will be needed to determine any effect the reduced inflammation may have on the development of a protective memory response in neonates.</p> |
topic |
Viral Neonatal Lung Innate |
url |
http://www.virologyj.com/content/8/1/549 |
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