The clinical significance of plasma interleukin-17 in patients with acute respiratory distress syndrome_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

CHEN Yan ^1,2 , HUANG Bin ³ , LI Mengqin ⁴ , QI Di ² , ZHAO Yan ² ,  WANG Daoxin ²

1. Department of Respiratory and Critical Care Medicine, The Second Clinical School of North Sichuan Medical College, Nanchong, Sichuan 637000, P. R. China;
2. Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, P. R. China;
3. Department of General Surgery, The Second Clinical School of North Sichuan Medical College, Nanchong, Sichuan 637000, P. R. China;
4. Department of Emergency, The affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P. R. China;

Corresponding author：

WANG Daoxin, Email: wangdaoxin1@163.com

Keywords：

Acute respiratory distress syndrome; Interleukin-17; Interleukin-6; Prognosis

DOI：

10.7507/1671-6205.201912042

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Objective To investigate the clinical signification of plasma interleukin-17 (IL-17) 1evel in patients with acute respiratory distress syndrome (ARDS).Methods Forty-five adult ARDS patients and 22 healthy controls were enrolled in this study. The plasma cytokine levels of IL-17, IL-6 and IL-10 were measured by enzyme linked immunosorbent assay. Meanwhile, the baseline data of demographic and clinical tests including oxygenation index, procalcitonin and brain natriuretic peprtide were collected, the acute physiological and chronic health Ⅱ (APACHEⅡ) score and sequential organ failure assessment (SOFA) score were recorded. The main outcome was defined as hospital mortality within 28-day follow-up.Results The plasma concentration of IL-17, IL-6 were higher in the ARDS patients (P<0.05) compared with the controls and the mean levels of IL-17, IL-6 and the APACHEⅡ score and the SOFA score in the non-survivors was higher than those in the survivors (P<0.05). In particular, there was a significant correlation between the plasma levels of IL-17 and IL-6 (P<0.05). Logistic regression and COX multivariate survival analysis suggested that age and SOFA score may be prognostic factors for ARDS.Conclusions The plasma concentration of IL-17 is significantly increased in ARDS patients, and its expression is linearly related to the proinflammatory factor IL-6. Both are important inflammatory markers in the acute phase of ARDS and may be important disease severity and prognostic indicators in addition to age and SOFA score.

Citation： CHEN Yan, HUANG Bin, LI Mengqin, QI Di, ZHAO Yan, WANG Daoxin. The clinical significance of plasma interleukin-17 in patients with acute respiratory distress syndrome. Chinese Journal of Respiratory and Critical Care Medicine, 2021, 20(6): 396-402. doi: 10.7507/1671-6205.201912042 Copy

1.	Chen W, Chen YY, Tsai CF, et al. Incidence and outcomes of acute respiratory distress syndrome: A Nationwide Registry- Based Study in Taiwan, 1997 to 2011. Medicine, 2015, 94(43): e1849.
2.	Chu CQ, Wittmer S, Dalton DK. Failure to suppress the expansion of the activated CD4 T cell population in interferon γ-deficient mice leads to exacerbation of experimental autoimmune encephalomyelitis. J Exp Med, 2000, 192(1): 123-128.
3.	Basso AS, Cheroutre H, Mucida D. More stories on Th17 cells. Cell Res, 2009, 19(4): 399-411.
4.	Fouser LA, Wright JF, Dumissi-Joannopoulos K, et al. Th17 cytokines and their emerging roles inflammation and autoimmunity. Immunol Rev, 2008, 226(1): 87-102.
5.	Laurence A, O'Shea JJ. T(H)-17 differentiation: of mice and men. Nat Immunol, 2007, 8: 903-905.
6.	Shimizu J, Yamazaki S, Takahashi T, et al. Stimulation of CD25⁺CD4⁺ regulatory T cells through GITR breaks immunological self-tolerance. Nat Immunol, 2002, 3(2): 135-142.
7.	Hsieh CS, Zheng Y, Liang Y, et al. An intersection between the self-reactive regulatory and nonregulatory T cell receptor repertoires. Nat Immunol, 2006, 7(4): 401-410.
8.	Strauss L, Bergmann C, Szczepanski M, et al. A unique subset of CD4⁺CD25highFOXP3⁺ T cells secreting interleukin-10 and transforming growth factor-β1 mediates suppression in the tumor microenvironment. Clin Cancer Res, 2007, 13(15): 4345-4354.
9.	Ivanov II, McKenzie BS, Zhou L, et al. The orphan nuclear receptor RORγt directs the differentiation program of proinflammatory IL-17⁺ T helper cells. Cell, 2006, 126(6): 1121-1133.
10.	Kramer JM, Gaffen SL. Interleukin-17: a new paradigm in inflammation, autoimmunity, and therapy. J Periodontol, 2007, 78(6): 1083-1093.
11.	Iwakura Y, Ishigame H. The IL-23/IL-17 axis in inflammation. J Clin Invest, 2006, 116(5): 1218-1122.
12.	Liu J, Zhang PS, Yu Q, et al. Losartan inhibits conventional dendritic cell maturation and Th1 and Th17 polarization responses: Novel mechanisms of preventive effects on lipopolysaccharide-induced acute lung injury. Int J Mol Med, 2012, 29(2): 269-276.
13.	You QH, Zhang D, Niu CC, et al. Expression of IL-17A and IL-17F in lipopolysaccharide-induced acute lung injury and the counteraction of anisodamine or methylprednisolone. Cytokine, 2014, 66(1): 78-86.
14.	McKenzie BS, Kastelein RA, Cua DJ. Understanding the IL-23-IL-17 immune pathway. Trends Immunol, 2006, 27(1): 17-23.
15.	Fossiez F, Djossou O, Chomarat P, et al. T cell interleukin-17 induces stromal cells to produce proinflammatory and hematopoietic cytokines. Exp Med, 1996, 183(6): 2593-2603.
16.	Silverpil E, Glader P, Hansson M, et al. Impact of interleukin-17 on macrophage phagocytosis of apoptotic neutrophils and particles. Inflammation, 2011, 34(1): 1-9.
17.	Pelletier M, Maggi L, Micheletti A, et al. Evidence for a cross-talk between human neutrophils and Th17 cells. Blood, 2010, 115(2): 335-343.
18.	Rawal G, Yadav S, Kumar R. Acute respiratory distress syndrome: an update and review. J Transl Int Med, 2018, 6(2): 74-77.
19.	Matsuda A, Motomura K, Shoda T, et al. IL-17 enhances TNF-α-induced, but not IL-1β-induced, expression of neutrophil-associated cytokines by human lung tissue cells. J Allergy Clin Immunol, 2014, 133(2): AB49.
20.	Song HW, Yang C, Liu W, et al. Interleukin-17A plays the same role on mice acute lung injury respectively induced by lipopolysaccharide and paraquat. Inflammation, 2017, 40(5): 1509-1519.
21.	Sharma AK, Mulloy DP, Le LT, et al. NADPH oxidase mediates synergistic effects of IL-17 and TNF-α on CXCL1 expression by epithelial cells after lung ischemia-reperfusion. Am J Physiol Lung Cell Mol Physiol, 2014, 306(1): L69-79.
22.	Holloway TL, Rani M, Cap AP, et al. The association between the Th-17 immune response and pulmonary complications in a trauma ICU population. Cytokine, 2015, 76(2): 328-333.
23.	Li TJ, Zhao LL, Qiu J, et al. Interleukin-17 antagonist attenuates lung inflammation through inhibition of the ERK1/2 and NFκB pathway in LPS-induced acute lung injury. Mol Med Rep, 2017, 16(2): 2225-2232.
24.	Meduri GU, Headley S, Kohler G, et al. Persistent elevation of inflammatory cytokines predicts a poor outcome in ARDS: plasma IL-1β and IL-6 levels are consistent and efficient predictors of outcome over time. Chest, 1995, 107(4): 1062.
25.	Aisiku IP, Yamal JM, Doshi P, et al. Plasma cytokines IL-6, IL-8, and IL-10 are associated with the development of acute respiratory distress syndrome in patients with severe traumatic brain injury. Critical Care, 2016, 20(1): 288.

1. Chen W, Chen YY, Tsai CF, et al. Incidence and outcomes of acute respiratory distress syndrome: A Nationwide Registry- Based Study in Taiwan, 1997 to 2011. Medicine, 2015, 94(43): e1849.
2. Chu CQ, Wittmer S, Dalton DK. Failure to suppress the expansion of the activated CD4 T cell population in interferon γ-deficient mice leads to exacerbation of experimental autoimmune encephalomyelitis. J Exp Med, 2000, 192(1): 123-128.
3. Basso AS, Cheroutre H, Mucida D. More stories on Th17 cells. Cell Res, 2009, 19(4): 399-411.
4. Fouser LA, Wright JF, Dumissi-Joannopoulos K, et al. Th17 cytokines and their emerging roles inflammation and autoimmunity. Immunol Rev, 2008, 226(1): 87-102.
5. Laurence A, O'Shea JJ. T(H)-17 differentiation: of mice and men. Nat Immunol, 2007, 8: 903-905.
6. Shimizu J, Yamazaki S, Takahashi T, et al. Stimulation of CD25⁺CD4⁺ regulatory T cells through GITR breaks immunological self-tolerance. Nat Immunol, 2002, 3(2): 135-142.
7. Hsieh CS, Zheng Y, Liang Y, et al. An intersection between the self-reactive regulatory and nonregulatory T cell receptor repertoires. Nat Immunol, 2006, 7(4): 401-410.
8. Strauss L, Bergmann C, Szczepanski M, et al. A unique subset of CD4⁺CD25highFOXP3⁺ T cells secreting interleukin-10 and transforming growth factor-β1 mediates suppression in the tumor microenvironment. Clin Cancer Res, 2007, 13(15): 4345-4354.
9. Ivanov II, McKenzie BS, Zhou L, et al. The orphan nuclear receptor RORγt directs the differentiation program of proinflammatory IL-17⁺ T helper cells. Cell, 2006, 126(6): 1121-1133.
10. Kramer JM, Gaffen SL. Interleukin-17: a new paradigm in inflammation, autoimmunity, and therapy. J Periodontol, 2007, 78(6): 1083-1093.
11. Iwakura Y, Ishigame H. The IL-23/IL-17 axis in inflammation. J Clin Invest, 2006, 116(5): 1218-1122.
12. Liu J, Zhang PS, Yu Q, et al. Losartan inhibits conventional dendritic cell maturation and Th1 and Th17 polarization responses: Novel mechanisms of preventive effects on lipopolysaccharide-induced acute lung injury. Int J Mol Med, 2012, 29(2): 269-276.
13. You QH, Zhang D, Niu CC, et al. Expression of IL-17A and IL-17F in lipopolysaccharide-induced acute lung injury and the counteraction of anisodamine or methylprednisolone. Cytokine, 2014, 66(1): 78-86.
14. McKenzie BS, Kastelein RA, Cua DJ. Understanding the IL-23-IL-17 immune pathway. Trends Immunol, 2006, 27(1): 17-23.
15. Fossiez F, Djossou O, Chomarat P, et al. T cell interleukin-17 induces stromal cells to produce proinflammatory and hematopoietic cytokines. Exp Med, 1996, 183(6): 2593-2603.
16. Silverpil E, Glader P, Hansson M, et al. Impact of interleukin-17 on macrophage phagocytosis of apoptotic neutrophils and particles. Inflammation, 2011, 34(1): 1-9.
17. Pelletier M, Maggi L, Micheletti A, et al. Evidence for a cross-talk between human neutrophils and Th17 cells. Blood, 2010, 115(2): 335-343.
18. Rawal G, Yadav S, Kumar R. Acute respiratory distress syndrome: an update and review. J Transl Int Med, 2018, 6(2): 74-77.
19. Matsuda A, Motomura K, Shoda T, et al. IL-17 enhances TNF-α-induced, but not IL-1β-induced, expression of neutrophil-associated cytokines by human lung tissue cells. J Allergy Clin Immunol, 2014, 133(2): AB49.
20. Song HW, Yang C, Liu W, et al. Interleukin-17A plays the same role on mice acute lung injury respectively induced by lipopolysaccharide and paraquat. Inflammation, 2017, 40(5): 1509-1519.
21. Sharma AK, Mulloy DP, Le LT, et al. NADPH oxidase mediates synergistic effects of IL-17 and TNF-α on CXCL1 expression by epithelial cells after lung ischemia-reperfusion. Am J Physiol Lung Cell Mol Physiol, 2014, 306(1): L69-79.
22. Holloway TL, Rani M, Cap AP, et al. The association between the Th-17 immune response and pulmonary complications in a trauma ICU population. Cytokine, 2015, 76(2): 328-333.
23. Li TJ, Zhao LL, Qiu J, et al. Interleukin-17 antagonist attenuates lung inflammation through inhibition of the ERK1/2 and NFκB pathway in LPS-induced acute lung injury. Mol Med Rep, 2017, 16(2): 2225-2232.
24. Meduri GU, Headley S, Kohler G, et al. Persistent elevation of inflammatory cytokines predicts a poor outcome in ARDS: plasma IL-1β and IL-6 levels are consistent and efficient predictors of outcome over time. Chest, 1995, 107(4): 1062.
25. Aisiku IP, Yamal JM, Doshi P, et al. Plasma cytokines IL-6, IL-8, and IL-10 are associated with the development of acute respiratory distress syndrome in patients with severe traumatic brain injury. Critical Care, 2016, 20(1): 288.

Chinese Journal of Respiratory and Critical Care Medicine

The clinical significance of plasma interleukin-17 in patients with acute respiratory distress syndrome

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