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Programming of the lung by early-life infection

Published online by Cambridge University Press:  14 February 2012

P. M. Hansbro*
Affiliation:
Centre for Asthma and Respiratory Disease and Hunter Medical Research Institute, The University of Newcastle, Newcastle, Australia
M. R. Starkey
Affiliation:
Centre for Asthma and Respiratory Disease and Hunter Medical Research Institute, The University of Newcastle, Newcastle, Australia
R. Y. Kim
Affiliation:
Centre for Asthma and Respiratory Disease and Hunter Medical Research Institute, The University of Newcastle, Newcastle, Australia
R. L. Stevens
Affiliation:
Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, Massachusetts, USA
P. S. Foster
Affiliation:
Centre for Asthma and Respiratory Disease and Hunter Medical Research Institute, The University of Newcastle, Newcastle, Australia
J. C. Horvat
Affiliation:
Centre for Asthma and Respiratory Disease and Hunter Medical Research Institute, The University of Newcastle, Newcastle, Australia
*
*Address for correspondence: Professor P. M. Hansbro, Infection and Immunity, The David Maddison Clinical Sciences Building, The University of Newcastle, Cnr King and Watt Sts, Newcastle, NSW 2300, Australia. (Email Philip.Hansbro@newcastle.edu.au)

Abstract

Many important human diseases, such as asthma, have their developmental origins in early life. Respiratory infections in particular may alter the course of asthma and may either protect against or promote the development of this disease. It is likely that the nature of the effects depends on the type and age of infection and is determined by the impact of infection on the immune and respiratory systems. Immunity in early life is plastic and can be moulded by antigen encounter, which may enhance or reinforce the asthmatic phenotype of early life, or induce protective responses. Chlamydial respiratory infections have specific effects and may increase asthma severity in early life by promoting systemic interleukin 13 responses and causing permanent changes in lung structure. Respiratory viral infections, such as those of respiratory syncytial virus and rhinovirus, promote pro-asthmatic responses in early life that contribute to the induction of asthma. By contrast, probiotics or infection or exposure to certain bacteria, such as Streptococcus pneumoniae, may have protective effects in asthma by increasing the numbers and activity of regulatory T cells. Here, we review the impact of infections on the developmental origins of asthma. Understanding these effects may lead to new therapeutic approaches for asthma that either target deleterious infections or utilize beneficial ones.

Type
Review
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2012

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