Role of IL-17 in LPS-induced acute lung injury: an in vivo study
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Qi Ding1,3, Gao-Qin Liu2, Yuan-Yuan Zeng1, Jian-Jie Zhu1, Ze-Yi Liu1, Xueguang Zhang2 and Jian-An Huang1,2
1Department of Respiratory Medicine, The First Affiliated Hospital of Soochow University, Suzhou 215006, China
2Clinical Immunology Laboratory of Jiangsu Province, Suzhou 215006, China
3Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou 215006, China
Jian-An Huang, email: firstname.lastname@example.org
Keywords: IL-17, acute respiratory distress syndrome, acute lung injury, RORγt, PI3K pathway
Received: June 28, 2017 Accepted: September 20, 2017 Published: October 04, 2017
To assess the clinical significance of IL-17 in patients with sepsis-induced acute respiratory distress syndrome (ARDS) and to investigate the effects of IL-17 blocking in a mouse model of acute lung injury (ALI). Significantly increased IL-17 level was found in patients with sepsis-related ARDS compared to healthy controls, whereas significantly increased plasma IL-17 level was also observed in non-survivors compared to that in survivors. According to the data from the mouse ALI model, we found significantly increased IL-17 level in lung tissue lysates, mouse bronchoalveolar lavage fluid (mBALF) and plasma at 6, 12 and 24 h after ALI. Histological analyses revealed that reduced sign of pathological changes and lung injury score in the lungs at 48 h after IL-17 blocking antibody administration. Reduced level of proinflammatory tumor necrosis factor α and increased level of anti-inflammatory factor interleukin-10 were found in both mBALF and plasma. Moreover, IL-17 blocking antibody administration attenuated the expression of RORγt and activity of PI3K-Akt pathway. Increased IL-17 was presented in patients with sepsis-induced ARDS and IL-17 may serve as a biomarker to indicate the severity of ARDS. Moreover, IL-17 antibody administration could relieve the ALI symptom by affecting RORγt level and PI3K pathway.
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