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Open Access Highly Accessed Research article

Role of gamma-delta T cells in host response against Staphylococcus aureus-induced pneumonia

Ping Cheng1, Tao Liu1, Wei-Ying Zhou2, Yuan Zhuang1, Liu-sheng Peng1, Jin-yu Zhang1, Zhi-Nan Yin3, Xu-hu Mao1, Gang Guo1, Yun Shi1* and Quan-ming Zou1*

Author Affiliations

1 Department of Clinical Microbiology and Immunology, Faculty of Medical Laboratory Science, Third Military Medical University and National Engineering Technological Research Center of Immunological Biologicals, Chongqing 400038, China

2 Department of Pharmacology, College of Pharmacy, The Third Military Medical University, Chongqing, China

3 College of Life Sciences, Nankai University, Tianjin, China

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BMC Immunology 2012, 13:38  doi:10.1186/1471-2172-13-38

Published: 9 July 2012

Abstract

Background

Staphylococcus aureus is the major cause of hospital-acquired and community-acquired pneumonia. Host defense to S.aureus 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 S.aureus-induced pneumonia. In this study, we examined the response and the role of γδ T cells to pulmonary S.aureus infection.

Results

Mice infected with S. aureus 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−/− mice exhibited impaired neutrophil recruitment and reduced cytokine production at the site of infection. The γδ T cells in response to pulmonary S. aureus 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 S. aureus-infected lungs.

Conclusions

Accumulation of γδ T cells in the lungs to S. aureus 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.