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.
This paper seems to demonstrate that IL17 plays an important role in protection in early stage Pseudomonas aeruginosa-induced disease. By depleting either IL17 or gamma delta T cells, the authors show that the effects of the cytokine and T cell subset are fully overlapping, which provides a strong argument for their conclusion, i.e. that gamma delta T cells are the source of IL17 early in infection. This is potentially a new and exciting role of gamma delta T cells in infection.