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Oncotarget. 2017 Oct 4;8(55):93704-93711. doi: 10.18632/oncotarget.21474. eCollection 2017 Nov 7.

Role of IL-17 in LPS-induced acute lung injury: an in vivo study.

Author information

1
Department of Respiratory Medicine, The First Affiliated Hospital of Soochow University, Suzhou 215006, China.
2
Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou 215006, China.
3
Clinical Immunology Laboratory of Jiangsu Province, Suzhou 215006, China.

Abstract

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.

KEYWORDS:

IL-17; PI3K pathway; RORγt; acute lung injury; acute respiratory distress syndrome

Conflict of interest statement

CONFLICTS OF INTEREST The authors declare that they have no conflicts of interest.

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