The role and mechanism of S100A8/A9 in rat model of chronic obstructive pulmonary disease_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

 CHEN Xiaoju ^1,2 , LENG Changyan ^1,3 , LIU Qin ¹ , ZHANG Wenbo ¹

1. Department of Respiratory and Critical Care Medicine, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P. R. China;
2. Department of Respiratory and Critical Care Medicine, Clinical Medical College & Affiliated Hospital of Chengdu University, Chengdu, Sichuan 610081, P. R. China;
3. Health Management Center, Sichuan Mianyang 404 Hospital, Mianyang, Sichuan 621000, P. R. China;

Corresponding?author：

CHEN Xiaoju, Email: cxj9592@163.com

Keywords：

Chronic obstructive pulmonary disease; S100A8/A9; Toll-like receptor-4; Myeloid differentiation factor 88

DOI：

10.7507/1671-6205.202103035

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Objective To investigate the role and mechanism of S100A8/A9 in rat model of chronic obstructive pulmonary disease (COPD). Methods Twelve Wistar rats were randomly divided into a normal control group and a COPD group. The COPD model was established by exposing the rats to cigarette smoke and injected lipopolysaccharide (LPS) in bronchus for 1 month. The pathological changes of the lung tissue were observed under light microscope, and the emphysema indexes of pulmonary mean linear intercept (MLI), mean alveolar numbers (MAN) and pulmonary alveolar area (PAA) were analyzed by image analysis system. The concentrations of S100A8/A9 in serum and bronchoalveolar lavage fluid (BALF) were measured by enzyme linked immunosorbent assay. The mRNA expression levels of S100A8, S100A9, Toll-like receptor-4 (TLR4) and myeloid differentiation factor 88 (MyD88) of lung tissues were measured by real time polymerase chain reaction. The protein expressions of S100A8/A9, TLR4 and MyD88 of lung tissues were detected by immunohistochemistry. Results After cigarette smoking and LPS injection for 1 month, the rat lung tissue appeared in accordance with the typical pathological changes of COPD. The MLI, MAN and PAA had obvious difference compared with the normal control group (P<0.05). The concentrations of S100A8/A9 protein in BALF and serum of the COPD group were obviously higher than those of the normal control group (P<0.05). The levels of S100A8, S100A9, TLR4 and MyD88 mRNA of lung tissues in the COPD group were obviously higher than those in the normal control group (P<0.05), and the expression levels of S100A8 and S100A9 mRNA were positively correlated with the expression levels of TLR4 and MyD88 mRNA respectively (P<0.05). The levels of S100A8/A9, TLR4 and MyD88 protein of lung tissues in COPD group were obviously higher than those in normal control group (P<0.05), and the levels of S100A8/A9 protein were positively correlated with the levels of MyD88 and TLR4 protein (P<0.05). Conclusions As a new inflammatory mediator, S100A8/A9 may be involved in the occurrence and development of COPD. By up-regulating the expression of TLR4 and MyD88, the classical TLR4-MyD88 inflammatory pathway is activated, thus promotes the occurrence and development of COPD.

Citation： CHEN Xiaoju, LENG Changyan, LIU Qin, ZHANG Wenbo. The role and mechanism of S100A8/A9 in rat model of chronic obstructive pulmonary disease. Chinese Journal of Respiratory and Critical Care Medicine, 2021, 20(12): 837-841. doi: 10.7507/1671-6205.202103035 Copy

1.	Wang S, Song R, Wang ZY, et al. S100A8/A9 in inflammation. Front Immunol, 2018, 9: 1298.
2.	Fassl SK, Austermann J, Papantonopoulon O, et al. Transcriptome assessment reveals a dominant role for TLR4 in the activation of human monocytes by the alarmin MRP8. J Immunol, 2015, 194(2): 575-583.
3.	Sumardika IW, Chen Y, Tomonobu N, et al. Neuroplastin-β mediates S100A8/A9-induced lung cancer disseminative progression. Mol Carcinog, 2019, 58(6): 980-995.
4.	Hiroshima Y, Hsu K, Tedla N, et al. S100A8/A9 and S100A9 reduce acute lung injury. Immunol Cell Biol, 2017, 95(5): 461-472.
5.	郜洪宇, 孟煥新, 侯建霞. S100A8/A9蛋白與牙周炎癥性疾病關系的研究進展. 中華口腔醫學雜志, 2020, 55(9): 679-684.
6.	Sreejit G, Latif AA, Murphy AJ, et al. Emerging roles of neutrophil-borne S100A8/A9 in cardiovascular inflammation. Pharmacol Res, 2020, 161: 105212.
7.	陳延偉. 艾文, 李一祿, 等. I-磷酸鞘氨醇在慢性阻塞性肺疾病大鼠肺部炎癥作用的研究. 武漢大學學報(醫學版), 2015, 36(1): 11-14.
8.	李曉丹, 王強. 補肺顆粒通過調控Akt通路對慢阻肺大鼠肺組織自噬和凋亡的影響. 武漢大學學報(醫學版), 2020, 41(6): 904-910.
9.	López-Campos J, Soler-Catalu?a J, Miravitlles M. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease 2019 Report: Future Challenges. Arch Bronconeumol, 2020, 56(2): 65-67.
10.	楊玲玲, 石廣軍. 依達拉奉對慢性阻塞性肺疾病模型大鼠的干預作用. 臨床肺科雜志, 2020, 25(7): 1076-1081.
11.	Pruenster M, Vogl T, Roth J, et al. S100A8/A9: from basic science to clinical application. Pharmacol Ther, 2016, 167: 120-131.
12.	Deguchi A, Tomita T, Ohto U, et al. Eritoran inhibits S100A8-mediated TLR4/MD-2 activation and tumor growth by changing the immune microenvironment. Oncogene, 2016, 35(11): 1445-1456.
13.	Ma L, Sun P, Zhang JC, et al. Proinflammatory effects of S100A8/A9 via TLR4 and RAGE signaling pathways in BV-2 microglial cells. Int J Mol Med, 2017, 40(1): 31-38.
14.	Kingsley MK, Bhat BV, Badhe BA, et al. Narciclasine improves outcome in sepsis among neonatal rats via inhibition of calprotectin and alleviating inflammatory responses. Sci Rep, 2020, 10(1): 2947.
15.	陳小菊, 向小均, 張文波, 等. 慢性阻塞性肺疾病穩定期和急性加重期血漿和誘導痰中S100A8/A9的變化及其意義. 中國呼吸與危重監護雜志, 2017, 16(5): 509-512.
16.	陳小菊, 周智, 冷長燕, 等. 鈣結合蛋白S100A8、S100A9在大鼠肺泡巨噬細胞中的表達及作用. 國際呼吸雜志, 2019, 39(8): 561-566.

1. Wang S, Song R, Wang ZY, et al. S100A8/A9 in inflammation. Front Immunol, 2018, 9: 1298.
2. Fassl SK, Austermann J, Papantonopoulon O, et al. Transcriptome assessment reveals a dominant role for TLR4 in the activation of human monocytes by the alarmin MRP8. J Immunol, 2015, 194(2): 575-583.
3. Sumardika IW, Chen Y, Tomonobu N, et al. Neuroplastin-β mediates S100A8/A9-induced lung cancer disseminative progression. Mol Carcinog, 2019, 58(6): 980-995.
4. Hiroshima Y, Hsu K, Tedla N, et al. S100A8/A9 and S100A9 reduce acute lung injury. Immunol Cell Biol, 2017, 95(5): 461-472.
5. 郜洪宇, 孟煥新, 侯建霞. S100A8/A9蛋白與牙周炎癥性疾病關系的研究進展. 中華口腔醫學雜志, 2020, 55(9): 679-684.
6. Sreejit G, Latif AA, Murphy AJ, et al. Emerging roles of neutrophil-borne S100A8/A9 in cardiovascular inflammation. Pharmacol Res, 2020, 161: 105212.
7. 陳延偉. 艾文, 李一祿, 等. I-磷酸鞘氨醇在慢性阻塞性肺疾病大鼠肺部炎癥作用的研究. 武漢大學學報(醫學版), 2015, 36(1): 11-14.
8. 李曉丹, 王強. 補肺顆粒通過調控Akt通路對慢阻肺大鼠肺組織自噬和凋亡的影響. 武漢大學學報(醫學版), 2020, 41(6): 904-910.
9. López-Campos J, Soler-Catalu?a J, Miravitlles M. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease 2019 Report: Future Challenges. Arch Bronconeumol, 2020, 56(2): 65-67.
10. 楊玲玲, 石廣軍. 依達拉奉對慢性阻塞性肺疾病模型大鼠的干預作用. 臨床肺科雜志, 2020, 25(7): 1076-1081.
11. Pruenster M, Vogl T, Roth J, et al. S100A8/A9: from basic science to clinical application. Pharmacol Ther, 2016, 167: 120-131.
12. Deguchi A, Tomita T, Ohto U, et al. Eritoran inhibits S100A8-mediated TLR4/MD-2 activation and tumor growth by changing the immune microenvironment. Oncogene, 2016, 35(11): 1445-1456.
13. Ma L, Sun P, Zhang JC, et al. Proinflammatory effects of S100A8/A9 via TLR4 and RAGE signaling pathways in BV-2 microglial cells. Int J Mol Med, 2017, 40(1): 31-38.
14. Kingsley MK, Bhat BV, Badhe BA, et al. Narciclasine improves outcome in sepsis among neonatal rats via inhibition of calprotectin and alleviating inflammatory responses. Sci Rep, 2020, 10(1): 2947.
15. 陳小菊, 向小均, 張文波, 等. 慢性阻塞性肺疾病穩定期和急性加重期血漿和誘導痰中S100A8/A9的變化及其意義. 中國呼吸與危重監護雜志, 2017, 16(5): 509-512.
16. 陳小菊, 周智, 冷長燕, 等. 鈣結合蛋白S100A8、S100A9在大鼠肺泡巨噬細胞中的表達及作用. 國際呼吸雜志, 2019, 39(8): 561-566.

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The role and mechanism of S100A8/A9 in rat model of chronic obstructive pulmonary disease

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