European Respiratory Society

Streptococcus pneumoniae infection suppresses allergic airways disease by inducing regulatory T-cells

J.A. Preston, A.N. Thorburn, M.R. Starkey, E.L. Beckett, J.C. Horvat, M.A. Wade, B.J. O'Sullivan, R. Thomas, K.W. Beagley, P.G. Gibson, P.S. Foster, P.M. Hansbro


An inverse association exists between some bacterial infections and the prevalence of asthma. We investigated whether Streptococcus pneumoniae infection protects against asthma using mouse models of ovalbumin (OVA)-induced allergic airway disease (AAD).

Mice were intratracheally infected or treated with killed S. pneumoniae before, during or after OVA sensitisation and subsequent challenge. The effects of S. pneumoniae on AAD were assessed.

Infection or treatment with killed S. pneumoniae suppressed hallmark features of AAD, including antigen-specific T-helper cell (Th) type 2 cytokine and antibody responses, peripheral and pulmonary eosinophil accumulation, goblet cell hyperplasia, and airway hyperresponsiveness. The effect of infection on the development of specific features of AAD depended on the timing of infection relative to allergic sensitisation and challenge. Infection induced significant increases in regulatory T-cell (Treg) numbers in lymph nodes, which correlated with the degree of suppression of AAD. Tregs reduced T-cell proliferation and Th2 cytokine release. The suppressive effects of infection were reversed by anti-CD25 treatment.

Respiratory infection or treatment with S. pneumoniae attenuates allergic immune responses and suppresses AAD. These effects may be mediated by S. pneumoniae-induced Tregs. This identifies the potential for the development of therapeutic agents for asthma from S. pneumoniae.


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  • Support Statement

    The study was supported by grants from the Asthma Foundation of New South Wales, the Rebecca Cooper Medical Research Foundation, the University of Newcastle Project Grant, the Hunter Medical Research Institute, the Australian Research Council and the National Health and Medical Research Council (project grants 401238 and 569219).

  • Statement of Interest

    None declared.

  • Received March 29, 2010.
  • Accepted April 30, 2010.
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