The expression and clinical significance of neutrophil extracellular traps, interleukin 8 and interleukin 33 in plasma of patients with chronic obstructive pulmonary disease_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

FAN Ao ¹ , HUANG Zhong ^2,3 , DUAN Yuqing ¹ ,  LU Xianling ^1,3

1. First Department of Respiratory Medicine, The First Affiliated Hospital of Shihezi Medical University, Shihezi, Xinjiang 832000, P. R. China;
2. Emergency Department, The First Affiliated Hospital of Shihezi Medical University, Shihezi, Xinjiang 832000, P. R. China;
3. NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, First Affiliated Hospital, School of Medicine, Shihezi University, Shihezi, Xinjiang 832000, P. R. China;

Corresponding author：

LU Xianling, Email: luxianlingmary@163.com

Keywords：

Chronic obstructive pulmonary disease; neutrophil extracellular traps; interleukin-8; interleukin-33

DOI：

10.7507/1671-6205.202110009

Video：

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Objective To investigate the expression of double-stranded DNA (dsDNA), citrulline histone 3 (CitH3), myeloperoxidase-DNA (MPO-DNA), IL-8 and IL-33 in plasma of patients with chronic obstructive pulmonary disease (COPD) and their clinical significance. Methods Forty patients with acute exacerbation COPD (AECOPD) who were hospitalized in The First Affiliated Hospital of Shihezi University School of Medicine from October 2020 to May 2021 were recruited in the AECOPD group, and recruited in the stable COPD group when they entered the stable stage. In the same period, forty healthy individuals were recruited in the control group. General informations including pulmonary function and peripheral blood were collected from each subject. Plasma levels of CitH3, MPO-DNA, interleukin (IL)-8 and IL-33 were measured by enzyme linked immunosorbent assay and plasma levels of dsDNA were measured by PicoGreen fluorescent dye quantitative analysis. Results The levels of dsDNA, CitH3, MPO-DNA, IL-8 and IL-33 in the AECOPD group were higher than those in the stable group and the control group, with statistical significance (P<0.05), and the levels of dsDNA, CitH3, MPO-DNA and IL-33 in the stable group were higher than those in the control group, with statistical significance (P<0.05) . The levels of CitH3, MPO-DNA, IL-33 and IL-8 in the AECOPD group were positively correlated with COPD assessment test (CAT) score. MPO-DNA and IL-8 were positively correlated with CAT score, MPO-DNA was negatively correlated with FEV₁%pred, CitH3 was negatively correlated with FEV₁/FVC. The levels of IL-8 and dsDNA, CitH3 were positively correlated with the levels of MPO-DNA in the AECOPD group, and positively correlated with the levels of IL-8 and dsDNA in the stable group, but not with CitH3 and MPO-DNA. The levels of IL-33 and IL-8, dsDNA, CitH3, MPO-DNA were positively correlated in the AECOPD group, but not in the stable group. Conclusions The levels of neutrophil extracellular traps (NETs), IL-8 and IL-33 in plasma of COPD patients were increased, and the levels of NETs were correlated with pulmonary function, CAT score, IL-33 and IL-8. NETs may be involved in the development of COPD.

Citation： FAN Ao, HUANG Zhong, DUAN Yuqing, LU Xianling. The expression and clinical significance of neutrophil extracellular traps, interleukin 8 and interleukin 33 in plasma of patients with chronic obstructive pulmonary disease. Chinese Journal of Respiratory and Critical Care Medicine, 2022, 21(2): 84-89. doi: 10.7507/1671-6205.202110009 Copy

1.	Singh D, Agusti A, Anzueto A, et al. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease: the GOLD science committee report 2019. Eur Respir J, 2019, 53(5): 1900164.
2.	Trivedi A, Khan MA, Bade G, et al. Orchestration of neutrophil extracellular traps (Nets), a unique innate immune function during chronic obstructive pulmonary disease (COPD) Development. Biomedicines, 2021, 9(1): 53.
3.	Jasper AE, Mciver WJ, Sapey E, et al. Understanding the role of neutrophils in chronic inflammatory airway disease. F1000 Res, 2019, 8: F1000 Faculty Rev-557.
4.	Vorobjeva NV, Pinegin BV. Neutrophil extracellular traps: mechanisms of formation and role in health and disease. Biochemistry, 2014, 79(12): 1286-1296.
5.	Kang LJ, Yu HL, Yang X, et al. Neutrophil extracellular traps released by neutrophils impair revascularization and vascular remodeling after stroke. Nat Commun, 2020, 11(1): 2488.
6.	Sanni K, Ena G, Sanket K, et al. Quantification of NETs formation in neutrophil and its correlation with the severity of sepsis and organ dysfunction. Clin Chim Acta, 2019, 495: 606-610.
7.	Zhang SG, Jia XQ, Zhang QY, et al. Neutrophil extracellular traps activate lung fibroblast to induce polymyositis-related interstitial lung diseases via TLR9-miR-7-Smad2 pathway. J Cell Mol Med, 2020, 24(2): 1658-1669.
8.	Wright T, Gibson PG, Simpson JL, et al. Neutrophil extracellular traps are associated with inflammation in chronic airway disease. Respirology, 2016, 21(3): 467-475.
9.	Alison JD, Megan LC, Eleanor GP, et al. Neutrophil extracellular traps are associated with disease severity and microbiota diversity in patients with chronic obstructive pulmonary disease. J Allergy Clin Immunol, 2018, 141(1): 117-127.
10.	徐俊杰, 茅晓楠, 程锐, 等. 中性粒细胞胞外诱捕网与非感染性肺部疾病的研究进展. 中国呼吸与危重监护杂志, 2020, 19(5): 515-519.
11.	Shang J, Zhao JL, Wu XJ, et al. Interleukin-33 promotes inflammatory cytokine production in chronic airway inflammation. Biochem Cell Biol, 2015, 93(4): 359-366.
12.	White PC, Hirschfeld J, Milward MR, et al. Cigarette smoke modifies neutrophil chemotaxis, neutrophil extracellular trap formation and inflammatory response-related gene expression. J Periodontal Res, 2018, 53: 525-535.
13.	Rosales C, Lowell CA, Schnoor M, et al. Neutrophils: their role in innate and adaptive immunity 2017. J Immunol Res, 2017, 2017: 9748345.
14.	Uddin M, Watz H, Malmgren A, et al. NETopathic inflammation in chronic obstructive pulmonary disease and severe asthma. Front Immunol, 2019, 10: 47.
15.	Gonzalez-Aparicio M, Alfaro C. Influence of interleukin-8 and neutrophil extracellular trap (NET) formation in the tumor microenvironment: is there a pathogenic role?. J Immunol Res, 2019, 2019: 6252138.
16.	An ZJ, Li JW, Yu JB, et al. Neutrophil extracellular traps induced by IL-8 aggravate atherosclerosis via activation NF-κB signaling in macrophages. Cell Cycle, 2019, 18(21): 2928-2938.
17.	Bendib I, Granger V, Schlemmer F, et al. Neutrophil extracellular traps are elevated in patients with pneumonia-related acute respiratory distress syndrome. Anesthesiology, 2019, 130(4): 581-591.
18.	Delgado-Rizo V, Martinez-Guzman MA, Iniguez-Gutierrez L, et al. Neutrophil extracellular traps and its implications in inflammation: an overview. Front Immunol, 2017, 8: 81.
19.	Liu T, Wang FP, Wang G, et al. Role of neutrophil extracellular traps in asthma and chronic obstructive pulmonary disease. Chin Med J, 2017, 130(6): 730-736.
20.	Wu HX, Yang SF, Wu XJ, et al. Interleukin-33/ST2 signaling promotes production of interleukin-6 and interleukin-8 in systemic inflammation in cigarette smoke-induced chronic obstructive pulmonary disease mice. Biochem Biophys Res Commun, 2014, 450(1): 110-116.
21.	Wang XD, Li XY, Chen LY, et al. Interleukin-33 facilitates cutaneous defense against Staphylococcus aureus by promoting the development of neutrophil extracellular trap. Int Immunopharmacol, 2020, 81: 106256.
22.	Yazdani HO, Chen HW, Tohme S, et al. IL-33 exacerbates liver sterile inflammation by amplifying neutrophil extracellular trap formation. J Hepatol, 2018, 68(1): 130-139.

1. Singh D, Agusti A, Anzueto A, et al. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease: the GOLD science committee report 2019. Eur Respir J, 2019, 53(5): 1900164.
2. Trivedi A, Khan MA, Bade G, et al. Orchestration of neutrophil extracellular traps (Nets), a unique innate immune function during chronic obstructive pulmonary disease (COPD) Development. Biomedicines, 2021, 9(1): 53.
3. Jasper AE, Mciver WJ, Sapey E, et al. Understanding the role of neutrophils in chronic inflammatory airway disease. F1000 Res, 2019, 8: F1000 Faculty Rev-557.
4. Vorobjeva NV, Pinegin BV. Neutrophil extracellular traps: mechanisms of formation and role in health and disease. Biochemistry, 2014, 79(12): 1286-1296.
5. Kang LJ, Yu HL, Yang X, et al. Neutrophil extracellular traps released by neutrophils impair revascularization and vascular remodeling after stroke. Nat Commun, 2020, 11(1): 2488.
6. Sanni K, Ena G, Sanket K, et al. Quantification of NETs formation in neutrophil and its correlation with the severity of sepsis and organ dysfunction. Clin Chim Acta, 2019, 495: 606-610.
7. Zhang SG, Jia XQ, Zhang QY, et al. Neutrophil extracellular traps activate lung fibroblast to induce polymyositis-related interstitial lung diseases via TLR9-miR-7-Smad2 pathway. J Cell Mol Med, 2020, 24(2): 1658-1669.
8. Wright T, Gibson PG, Simpson JL, et al. Neutrophil extracellular traps are associated with inflammation in chronic airway disease. Respirology, 2016, 21(3): 467-475.
9. Alison JD, Megan LC, Eleanor GP, et al. Neutrophil extracellular traps are associated with disease severity and microbiota diversity in patients with chronic obstructive pulmonary disease. J Allergy Clin Immunol, 2018, 141(1): 117-127.
10. 徐俊杰, 茅晓楠, 程锐, 等. 中性粒细胞胞外诱捕网与非感染性肺部疾病的研究进展. 中国呼吸与危重监护杂志, 2020, 19(5): 515-519.
11. Shang J, Zhao JL, Wu XJ, et al. Interleukin-33 promotes inflammatory cytokine production in chronic airway inflammation. Biochem Cell Biol, 2015, 93(4): 359-366.
12. White PC, Hirschfeld J, Milward MR, et al. Cigarette smoke modifies neutrophil chemotaxis, neutrophil extracellular trap formation and inflammatory response-related gene expression. J Periodontal Res, 2018, 53: 525-535.
13. Rosales C, Lowell CA, Schnoor M, et al. Neutrophils: their role in innate and adaptive immunity 2017. J Immunol Res, 2017, 2017: 9748345.
14. Uddin M, Watz H, Malmgren A, et al. NETopathic inflammation in chronic obstructive pulmonary disease and severe asthma. Front Immunol, 2019, 10: 47.
15. Gonzalez-Aparicio M, Alfaro C. Influence of interleukin-8 and neutrophil extracellular trap (NET) formation in the tumor microenvironment: is there a pathogenic role?. J Immunol Res, 2019, 2019: 6252138.
16. An ZJ, Li JW, Yu JB, et al. Neutrophil extracellular traps induced by IL-8 aggravate atherosclerosis via activation NF-κB signaling in macrophages. Cell Cycle, 2019, 18(21): 2928-2938.
17. Bendib I, Granger V, Schlemmer F, et al. Neutrophil extracellular traps are elevated in patients with pneumonia-related acute respiratory distress syndrome. Anesthesiology, 2019, 130(4): 581-591.
18. Delgado-Rizo V, Martinez-Guzman MA, Iniguez-Gutierrez L, et al. Neutrophil extracellular traps and its implications in inflammation: an overview. Front Immunol, 2017, 8: 81.
19. Liu T, Wang FP, Wang G, et al. Role of neutrophil extracellular traps in asthma and chronic obstructive pulmonary disease. Chin Med J, 2017, 130(6): 730-736.
20. Wu HX, Yang SF, Wu XJ, et al. Interleukin-33/ST2 signaling promotes production of interleukin-6 and interleukin-8 in systemic inflammation in cigarette smoke-induced chronic obstructive pulmonary disease mice. Biochem Biophys Res Commun, 2014, 450(1): 110-116.
21. Wang XD, Li XY, Chen LY, et al. Interleukin-33 facilitates cutaneous defense against Staphylococcus aureus by promoting the development of neutrophil extracellular trap. Int Immunopharmacol, 2020, 81: 106256.
22. Yazdani HO, Chen HW, Tohme S, et al. IL-33 exacerbates liver sterile inflammation by amplifying neutrophil extracellular trap formation. J Hepatol, 2018, 68(1): 130-139.

Chinese Journal of Respiratory and Critical Care Medicine

The expression and clinical significance of neutrophil extracellular traps, interleukin 8 and interleukin 33 in plasma of patients with chronic obstructive pulmonary disease

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