Neonatal pneumococcal colonisation caused by Influenza A infection alters lung function in adult mice

Meaghan FitzPatrick, Simon G Royce, Shenna Langenbach, Jonathan McQualter, Patrick C. Reading, Odilia Wijburg, Gary P. Anderson, Alastair Stewart, Jane Bourke, Steven Bozinovski

Research output: Contribution to journalArticleResearchpeer-review

3 Citations (Scopus)

Abstract

There is emerging epidemiological data to suggest that upper respiratory tract bacterial colonisation in infancy may increase the risk of developing respiratory dysfunction later in life, and respiratory viruses are known to precipitate persistent colonisation. This study utilized a neonatal mouse model of Streptococcus pneumonia (SP) and influenza A virus (IAV) co-infection, where bronchoalveolar leukocyte infiltration had resolved by adulthood. Only co-infection resulted in persistent nasopharyngeal colonisation over 40 days and a significant increase in airway resistance in response to in vivo methacholine challenge. A significant increase in hysteresivity was also observed in IAV and co-infected mice, consistent with ventilatory heterogeneity and structural changes in the adult lung. Airway hyper-responsiveness was not associated with a detectable increase in goblet cell transdifferentiation, peribronchial smooth muscle bulk or collagen deposition in regions surrounding the airways. Increased reactivity was not observed in precision cut lung slices challenged with methacholine in vitro. Histologically, the airway epithelium appeared normal and expression of epithelial integrity markers (ZO-1, occludin-1 and E-cadherin) were not altered. In summary, neonatal co-infection led to persistent nasopharyngeal colonisation and increased airway responsiveness that was not associated with detectable smooth muscle or mucosal epithelial abnormalities, however increased hysteresivity may reflect ventilation heterogeneity.
Original languageEnglish
Article number22751
Pages (from-to)1 - 12
Number of pages12
JournalScientific Reports
Volume6
DOIs
Publication statusPublished - 2016

Cite this

FitzPatrick, M., Royce, S. G., Langenbach, S., McQualter, J., Reading, P. C., Wijburg, O., ... Bozinovski, S. (2016). Neonatal pneumococcal colonisation caused by Influenza A infection alters lung function in adult mice. Scientific Reports, 6, 1 - 12. [22751]. https://doi.org/10.1038/srep22751
FitzPatrick, Meaghan ; Royce, Simon G ; Langenbach, Shenna ; McQualter, Jonathan ; Reading, Patrick C. ; Wijburg, Odilia ; Anderson, Gary P. ; Stewart, Alastair ; Bourke, Jane ; Bozinovski, Steven. / Neonatal pneumococcal colonisation caused by Influenza A infection alters lung function in adult mice. In: Scientific Reports. 2016 ; Vol. 6. pp. 1 - 12.
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title = "Neonatal pneumococcal colonisation caused by Influenza A infection alters lung function in adult mice",
abstract = "There is emerging epidemiological data to suggest that upper respiratory tract bacterial colonisation in infancy may increase the risk of developing respiratory dysfunction later in life, and respiratory viruses are known to precipitate persistent colonisation. This study utilized a neonatal mouse model of Streptococcus pneumonia (SP) and influenza A virus (IAV) co-infection, where bronchoalveolar leukocyte infiltration had resolved by adulthood. Only co-infection resulted in persistent nasopharyngeal colonisation over 40 days and a significant increase in airway resistance in response to in vivo methacholine challenge. A significant increase in hysteresivity was also observed in IAV and co-infected mice, consistent with ventilatory heterogeneity and structural changes in the adult lung. Airway hyper-responsiveness was not associated with a detectable increase in goblet cell transdifferentiation, peribronchial smooth muscle bulk or collagen deposition in regions surrounding the airways. Increased reactivity was not observed in precision cut lung slices challenged with methacholine in vitro. Histologically, the airway epithelium appeared normal and expression of epithelial integrity markers (ZO-1, occludin-1 and E-cadherin) were not altered. In summary, neonatal co-infection led to persistent nasopharyngeal colonisation and increased airway responsiveness that was not associated with detectable smooth muscle or mucosal epithelial abnormalities, however increased hysteresivity may reflect ventilation heterogeneity.",
author = "Meaghan FitzPatrick and Royce, {Simon G} and Shenna Langenbach and Jonathan McQualter and Reading, {Patrick C.} and Odilia Wijburg and Anderson, {Gary P.} and Alastair Stewart and Jane Bourke and Steven Bozinovski",
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FitzPatrick, M, Royce, SG, Langenbach, S, McQualter, J, Reading, PC, Wijburg, O, Anderson, GP, Stewart, A, Bourke, J & Bozinovski, S 2016, 'Neonatal pneumococcal colonisation caused by Influenza A infection alters lung function in adult mice', Scientific Reports, vol. 6, 22751, pp. 1 - 12. https://doi.org/10.1038/srep22751

Neonatal pneumococcal colonisation caused by Influenza A infection alters lung function in adult mice. / FitzPatrick, Meaghan; Royce, Simon G; Langenbach, Shenna; McQualter, Jonathan; Reading, Patrick C.; Wijburg, Odilia; Anderson, Gary P.; Stewart, Alastair ; Bourke, Jane; Bozinovski, Steven.

In: Scientific Reports, Vol. 6, 22751, 2016, p. 1 - 12.

Research output: Contribution to journalArticleResearchpeer-review

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T1 - Neonatal pneumococcal colonisation caused by Influenza A infection alters lung function in adult mice

AU - FitzPatrick, Meaghan

AU - Royce, Simon G

AU - Langenbach, Shenna

AU - McQualter, Jonathan

AU - Reading, Patrick C.

AU - Wijburg, Odilia

AU - Anderson, Gary P.

AU - Stewart, Alastair

AU - Bourke, Jane

AU - Bozinovski, Steven

PY - 2016

Y1 - 2016

N2 - There is emerging epidemiological data to suggest that upper respiratory tract bacterial colonisation in infancy may increase the risk of developing respiratory dysfunction later in life, and respiratory viruses are known to precipitate persistent colonisation. This study utilized a neonatal mouse model of Streptococcus pneumonia (SP) and influenza A virus (IAV) co-infection, where bronchoalveolar leukocyte infiltration had resolved by adulthood. Only co-infection resulted in persistent nasopharyngeal colonisation over 40 days and a significant increase in airway resistance in response to in vivo methacholine challenge. A significant increase in hysteresivity was also observed in IAV and co-infected mice, consistent with ventilatory heterogeneity and structural changes in the adult lung. Airway hyper-responsiveness was not associated with a detectable increase in goblet cell transdifferentiation, peribronchial smooth muscle bulk or collagen deposition in regions surrounding the airways. Increased reactivity was not observed in precision cut lung slices challenged with methacholine in vitro. Histologically, the airway epithelium appeared normal and expression of epithelial integrity markers (ZO-1, occludin-1 and E-cadherin) were not altered. In summary, neonatal co-infection led to persistent nasopharyngeal colonisation and increased airway responsiveness that was not associated with detectable smooth muscle or mucosal epithelial abnormalities, however increased hysteresivity may reflect ventilation heterogeneity.

AB - There is emerging epidemiological data to suggest that upper respiratory tract bacterial colonisation in infancy may increase the risk of developing respiratory dysfunction later in life, and respiratory viruses are known to precipitate persistent colonisation. This study utilized a neonatal mouse model of Streptococcus pneumonia (SP) and influenza A virus (IAV) co-infection, where bronchoalveolar leukocyte infiltration had resolved by adulthood. Only co-infection resulted in persistent nasopharyngeal colonisation over 40 days and a significant increase in airway resistance in response to in vivo methacholine challenge. A significant increase in hysteresivity was also observed in IAV and co-infected mice, consistent with ventilatory heterogeneity and structural changes in the adult lung. Airway hyper-responsiveness was not associated with a detectable increase in goblet cell transdifferentiation, peribronchial smooth muscle bulk or collagen deposition in regions surrounding the airways. Increased reactivity was not observed in precision cut lung slices challenged with methacholine in vitro. Histologically, the airway epithelium appeared normal and expression of epithelial integrity markers (ZO-1, occludin-1 and E-cadherin) were not altered. In summary, neonatal co-infection led to persistent nasopharyngeal colonisation and increased airway responsiveness that was not associated with detectable smooth muscle or mucosal epithelial abnormalities, however increased hysteresivity may reflect ventilation heterogeneity.

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JO - Scientific Reports

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SN - 2045-2322

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