Inflammatory responses to acute pneumovirus infection in neonatal mice

<p>Abstract</p> <p>Background</p> <p>The innate immune responses of neonates differ dramatically from those of adults. Here we examine the acute inflammatory responses of neonatal and weanling mice infected with pneumonia virus of mice (PVM), a rodent pathogen (family &...

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Main Authors: Rosenberg Helene F, Percopo Caroline M, Ptaschinski Catherine, Bonville Cynthia A, Domachowske Joseph B
Format: Article
Language:English
Published: BMC 2010-11-01
Series:Virology Journal
Online Access:http://www.virologyj.com/content/7/1/320
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spelling doaj-a7e30f1ceed74b0b8896e473579225552020-11-24T21:32:26ZengBMCVirology Journal1743-422X2010-11-017132010.1186/1743-422X-7-320Inflammatory responses to acute pneumovirus infection in neonatal miceRosenberg Helene FPercopo Caroline MPtaschinski CatherineBonville Cynthia ADomachowske Joseph B<p>Abstract</p> <p>Background</p> <p>The innate immune responses of neonates differ dramatically from those of adults. Here we examine the acute inflammatory responses of neonatal and weanling mice infected with pneumonia virus of mice (PVM), a rodent pathogen (family <it>Paramyxoviridae</it>, genus Pneumovirus) that replicates the sequelae of severe respiratory syncytial virus infection.</p> <p>Results</p> <p>We demonstrate that virus replication proceeds indistinguishably in all age groups (inoculated at 1, 2, 3 and 4 weeks of age), although inflammatory responses vary in extent and character. Some of the biochemical mediators detected varied minimally with age at inoculation. Most of the mediators evaluated demonstrated elevated expression over baseline correlating directly with age at the time of virus inoculation. Among the latter group are CCL2, CCL3, and IFN-γ, all cytokines previously associated with PVM-induced inflammatory pathology in mature mice. Likewise, we detect neutrophil recruitment to lung tissue in all age groups, but recruitment is most pronounced among the older (3 - 4 week old) mice. Interestingly, all mice exhibit failure to thrive, lagging in expected weight gain for given age, including the youngest mice that present little overt evidence of inflammation.</p> <p>Conclusions</p> <p>Our findings among the youngest mice may explain in part the phenomenon of atypical or minimally symptomatic respiratory infections in human neonates, which may be explored further with this infection model.</p> http://www.virologyj.com/content/7/1/320
collection DOAJ
language English
format Article
sources DOAJ
author Rosenberg Helene F
Percopo Caroline M
Ptaschinski Catherine
Bonville Cynthia A
Domachowske Joseph B
spellingShingle Rosenberg Helene F
Percopo Caroline M
Ptaschinski Catherine
Bonville Cynthia A
Domachowske Joseph B
Inflammatory responses to acute pneumovirus infection in neonatal mice
Virology Journal
author_facet Rosenberg Helene F
Percopo Caroline M
Ptaschinski Catherine
Bonville Cynthia A
Domachowske Joseph B
author_sort Rosenberg Helene F
title Inflammatory responses to acute pneumovirus infection in neonatal mice
title_short Inflammatory responses to acute pneumovirus infection in neonatal mice
title_full Inflammatory responses to acute pneumovirus infection in neonatal mice
title_fullStr Inflammatory responses to acute pneumovirus infection in neonatal mice
title_full_unstemmed Inflammatory responses to acute pneumovirus infection in neonatal mice
title_sort inflammatory responses to acute pneumovirus infection in neonatal mice
publisher BMC
series Virology Journal
issn 1743-422X
publishDate 2010-11-01
description <p>Abstract</p> <p>Background</p> <p>The innate immune responses of neonates differ dramatically from those of adults. Here we examine the acute inflammatory responses of neonatal and weanling mice infected with pneumonia virus of mice (PVM), a rodent pathogen (family <it>Paramyxoviridae</it>, genus Pneumovirus) that replicates the sequelae of severe respiratory syncytial virus infection.</p> <p>Results</p> <p>We demonstrate that virus replication proceeds indistinguishably in all age groups (inoculated at 1, 2, 3 and 4 weeks of age), although inflammatory responses vary in extent and character. Some of the biochemical mediators detected varied minimally with age at inoculation. Most of the mediators evaluated demonstrated elevated expression over baseline correlating directly with age at the time of virus inoculation. Among the latter group are CCL2, CCL3, and IFN-γ, all cytokines previously associated with PVM-induced inflammatory pathology in mature mice. Likewise, we detect neutrophil recruitment to lung tissue in all age groups, but recruitment is most pronounced among the older (3 - 4 week old) mice. Interestingly, all mice exhibit failure to thrive, lagging in expected weight gain for given age, including the youngest mice that present little overt evidence of inflammation.</p> <p>Conclusions</p> <p>Our findings among the youngest mice may explain in part the phenomenon of atypical or minimally symptomatic respiratory infections in human neonates, which may be explored further with this infection model.</p>
url http://www.virologyj.com/content/7/1/320
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AT percopocarolinem inflammatoryresponsestoacutepneumovirusinfectioninneonatalmice
AT ptaschinskicatherine inflammatoryresponsestoacutepneumovirusinfectioninneonatalmice
AT bonvillecynthiaa inflammatoryresponsestoacutepneumovirusinfectioninneonatalmice
AT domachowskejosephb inflammatoryresponsestoacutepneumovirusinfectioninneonatalmice
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