The responses of γδ T‐cells against acute Pseudomonas aeruginosa pulmonary infection in mice via interleukin‐17

Abstract Interleukin (IL)‐17‐producing T‐lymphocytes play a crucial role in inflammation, yet the potential roles of the cells in acute bacterial pulmonary infection remain unclear. Here, we investigated the role of IL‐17‐producing γδ T‐cells in a mouse model of acute Pseudomonas aeruginosa pulmonary infection. Results showed that augmentation of IL‐17, IL‐22 and IL‐23 was associated with the development of acute bacterial pulmonary infection. However, IL‐17 was markedly reduced following the blockade of γδ T‐cell activity in vivo. The levels of the chemokines, including granulocyte colony‐stimulating factor (G‐CSF), keratinocyte chemoattractant (KC), macrophage inflammatory protein‐1α (MIP‐1) and macrophage inflammatory protein (MIP‐2), were also noticeably decreased in the anti‐γδ T Cell Receptor(TCR) mice after 8 h infection. Following the depletion of γδ T‐cells, the bacterial load was consistently increased. Anti‐TCRγδ‐treated mice had changes similar to those in the the anti‐IL‐17‐treated mice. The mRNA and protein levels of IL‐22 and IL‐23, and the mRNA level of RORγt were all markedly decreased in the anti‐TCRγδ mice. Overall, our results demonstrated that at the early stage of acute P. aeruginosa pulmonary infection, γδ T‐cells are the major source of IL‐17 and play a pivotal role in the host immune response and defense against bacteria.
Source: FEMS Immunology and Medical Microbiology - Category: Microbiology Authors: Tags: Research Article Source Type: research