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.
Highlights
Acute lung injury (ALI) and its severe form acute respiratory distress syndrome (ARDS) are severe inflammatory reactions in the lung, which could cause alveolar damage and result in varied degrees of ventilation-perfusion mismatch, severe hypoxemia, decreased lung compliance and noncardiogenic pulmonary edema [1]
Our results showed that 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
We found that significantly increased plasma IL-17 in these patients compared to healthy controls (ARDS: [26.5 ± 6.02] pg/ mL vs. Healthy controls: [17.3 ± 3.07] pg/mL, p < 0.05) (Figure 1A)
Summary
Acute lung injury (ALI) and its severe form acute respiratory distress syndrome (ARDS) are severe inflammatory reactions in the lung, which could cause alveolar damage and result in varied degrees of ventilation-perfusion mismatch, severe hypoxemia, decreased lung compliance and noncardiogenic pulmonary edema [1]. It is necessary to perform the mechanisms related studies that could be helpful in the therapeutic intervention of ALI. It is generally accepted that the pathogenesis of ALI was caused by lung inflammation and cell apoptosis, including inflammatory cell accumulation, the aberrant level of proteases, reactive oxygen species (ROS), proinflammatory cytokines, dysfunction of alveolar capillary barrier, and death of pulmonary cells [6,7,8]. The exact role of IL-17 and Th17 related responses in ALI have not been defined yet
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