Abstract
An inverse association exists between some bacterial infections and the prevalence of asthma. We investigated whether Streptococcus pneumoniae (Spn) infection protects against asthma using mouse models of ovalbumin (OVA)-induced allergic airway disease (AAD).
Mice were intratracheally infected, or treated with killed Spn, before, during or after OVA sensitisation and subsequent challenge. The effects of Spn on AAD were assessed.
Infection, or treatment with killed Spn suppressed hallmark features of AAD including; antigen-specific T helper cell type 2 (Th2) cytokine and antibody responses, peripheral and pulmonary eosinophil accumulation, goblet cell hyperplasia, and airway hyper-responsiveness (AHR). 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 Spn attenuates allergic immune responses and suppresses AAD. These effects may be mediated by Spn-induced Tregs. This identifies the potential for the development of therapeutic agents for asthma from Spn.
Footnotes
- ERS
