Azithromycin inhibits neutrophil accumulation in airways by affecting interleukin-17 downstream signals

作者：Nguyen Van Luu; Yang Jiong^*; Qu Xue-ju; Guo Ming; Wang Xin; Xian Qiao-yang; Tang Zhi-jiao; Huang Zhi-xiang; Wang Yong

来源：Chinese Medical Journal, 2012, 125(3): 491-495.

DOI：10.3760/cma.j.issn.0366-6999.2012.03.017

• azithromycin
• macrolides
• neutrophils
• interleukin-17

Background Azithromycin can reduce neutrophil accumulation in neutrophilic pulmonary diseases. However, the precise mechanism behind this action remains unknown. Our experiment assessed whether azithromycin inhibits neutrophil accumulation in the airways by affecting interleukin-17 (IL-17) downstream signals.
Methods Mice were pretreated with azithromycin before murine IL-17A (mIL-17) stimulation. After the mIL-17 stimulation, the levels of six neutrophil-mobilizing cytokines were determined by enzyme-linked immunosorbent assay (ELISA) tests in bronchoalveolar lavage (BAL) fluid; IL-6, CXC chemokine ligand-1 (CXCL-1), CXCL-5, macrophage inflammatory protein-2 (MIP-2), granulocyte colony-stimulating factor (G-CSF), and granulocyte macrophage colony-stimulating factor (GM-CSF). The number of neutrophils in BAL fluid were evaluated by cytospin preparations.
Results (1) Azithromycin pretreatment significantly inhibited both the release of three neutrophil-mobilizing cytokines (MIP-2, CXCL-5 and GM-CSF) and the accumulation of neutrophils in airways caused by mIL-17 stimulation. (2) The levels of three neutrophil-mobilizing cytokines (IL-6, MIP-2 and GM-CSF) were positively correlated with the numbers of neutrophil in BAL fluid.
Conclusions Azithromycin can inhibit neutrophil accumulation in the airways by affecting IL-17 downstream signals. This finding suggests that macrolide antibiotic application might be useful in prevention of neutrophilic pulmonary diseases characterized by high levels of IL-17. Chin Med J 2012;125(3):491-495

• 出版日期2012-2-5
• 单位武汉大学