Streptococcus pneumoniae infection suppresses allergic airways disease by inducing regulatory T-cells
Streptococcus pneumoniae infection suppresses allergic airways disease by inducing regulatory T-cells
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DOI：
10.1183/09031936.00049510
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发表时间：
2011-01-01
影响因子：
24.3
通讯作者：
Hansbro, P. M.
中科院分区：
文献类型：
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作者：
Preston, J. A.;Thorburn, A. N.;Hansbro, P. M.
某些细菌感染与哮喘患病率之间存在负相关关系。我们使用卵清蛋白 (OVA) 诱导的过敏性气道疾病 (AAD) 小鼠模型研究了肺炎链球菌感染是否可以预防哮喘。在 OVA 致敏和随后的攻击之前、期间或之后，对小鼠进行气管内感染或用灭活的肺炎链球菌进行治疗。评估了肺炎链球菌对 AAD 的影响。感染或用灭活的肺炎链球菌治疗可抑制 AAD 的标志性特征，包括抗原特异性 T 辅助细胞 (Th) 2 型细胞因子和抗体反应、外周和肺部嗜酸性粒细胞积聚、杯状细胞增生和气道高反应性。感染对 AAD 特定特征发展的影响取决于感染相对于过敏致敏和激发的时间。感染导致淋巴结中调节性 T 细胞 (Treg) 数量显着增加，这与 AAD 的抑制程度相关。 Tregs 减少了 T 细胞增殖和 Th2 细胞因子释放。抗 CD25 治疗可逆转感染的抑制作用。呼吸道感染或肺炎链球菌治疗会减弱过敏性免疫反应并抑制 AAD。这些作用可能是由肺炎链球菌诱导的 Tregs 介导的。这确定了开发肺炎链球菌哮喘治疗剂的潜力。
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.