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

Authors: Preston, JA  Thorburn, AN  Starkey, MR  Beckett, EL  Horvat, JC  Wade, MA  O'Sullivan, BJ  Thomas, R  Beagley, KW  Gibson, PG  Foster, PS  Hansbro, PM 
Citation: Preston JA, etal., Eur Respir J. 2011 Jan;37(1):53-64. Epub 2010 Jun 4.
Pubmed: (View Article at PubMed) PMID:20525707
DOI: Full-text: DOI:10.1183/09031936.00049510

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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CRRD Object Information
CRRD ID: 5147445
Created: 2011-08-04
Species: All species
Last Modified: 2011-08-04
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.