| Summary: | <p>Abstract</p> <p>Background</p> <p><it>Staphylococcus aureus</it> is the major cause of hospital-acquired and community-acquired pneumonia. Host defense to <it>S.aureus</it> infection is largely mediated by the innate immune system. γδ T cells play an important role in innate immunity to many infectious diseases. However, less is known about the role of these cells during <it>S.aureus</it>-induced pneumonia. In this study, we examined the response and the role of γδ T cells to pulmonary <it>S.aureus</it> infection.</p> <p>Results</p> <p>Mice infected with <it>S. aureus</it> intranasally showed rapid γδ T cells accumulation in the lung. Deficiency of γδ T cells led to attenuated bacterial clearance and less tissue damage in lung compared with WT mice. Moreover, TCR-δ<sup>−/−</sup> mice exhibited impaired neutrophil recruitment and reduced cytokine production at the site of infection. The γδ T cells in response to pulmonary <it>S. aureus</it> infection mainly secreted IL-17 and γδ T cells deficiency reduced IL-17 production, which might regulate the production of neutrophil-inducing cytokine/chemokine in the <it>S. aureus</it>-infected lungs.</p> <p>Conclusions</p> <p>Accumulation of γδ T cells in the lungs to <it>S. aureus</it> infection is beneficial for bacteria clearance and also contributes to the tissue damage. These cells were the primary source of IL-17, which might influence the recruitment of neutrophils at the early stage of infection.</p>
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