Chinese Journal of Respiratory and Critical Care Medicine
Supervisor：Ministry of Education of the People's Republic of ChinaSponsor：West China Medical Center & West China Hospital, Sichuan University Editor-in-chief：LIN Jiangtao / LIU Chuntao Publishing period：
Monthly
ISSN：1671-6205CN：51-1631/R
1. Department of Respiratory and Critical Care Medicine, Clinical Medical College & Affiliated Hospital of Chengdu University, Chengdu, Sichuan 610081, P. R. China;
2. Department of Respiratory and Critical Care Medicine, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P. R. China;
3. Department of Respiratory and Critical Care Medicine, The First People's Hospital of Neijiang, Neijiang, Sichuan 641000, P. R. China;
Objective To observe the expression of S100A8 and S100A9 in alveolar macrophages (AMs) of chronic obstructive pulmonary disease (COPD) rats, and explore the effect on the release of inflammatory mediators from AMs in COPD rats. Methods Twelve adult male 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 intratracheal injection of endotoxin for 1 month. The pathological changes of lung tissue of rats were observed under light microscope. Total cells counts and the number of AMs, lymphocytes, neutrophils in bronchoalveolar lavage fluid (BALF) of two groups were examined by Wright's staining methods. Rat AMs from the control group and the COPD group were isolated and cultured, and then treated with different doses of S100A8 and S100A9 for 6 hours and 12 hours. The levels of interleukin (IL)-8, IL-6 and tumour necrosis factor-α (TNF-α) in the AMs supernatants were measured by enzyme linked immunosorbent assay. The expression of S100A8 and S100A9 mRNA in AMs of rats were observed by in situ hybridization. The immunohistochemical method was used to observed the expression of S100A8/A9 protein of AMs. Results After cigarette smoking combined with intratracheal injection of endotoxin for 1 month, the lung tissue of rats showed typical pathological changes of COPD. Total cell counts and the number of AMs, lymphocytes, neutrophils in BALF of the COPD rats were significantly higher than those of the normal rats (P<0.05). Among them, the increase in the number of AMs was the most obvious. Compared with the control group, the expression of S100A8 mRNA, S100A9 mRNA and S100A8/A9 protein in AMs of the COPD group were up-regulated significantly (P<0.05). After the AMs of COPD rats were treated with S100A8 and S100A9, the contents of IL-8, IL-6 and TNF-α in AMs supernatants increased significantly in a time- and dose-dependent manner. When the AMs were treated with the same dose of S100A8 and S100A9 for the same time, the levels of IL-8, IL-6 and TNF-α in the AMs supernatant of the COPD group were higher than those of the normal control group. Conclusions The expression of S100A8 and S100A9 in cultured COPD rat AMs is significantly increased. S100A8 and S100A9 can promote the secretion and release of inflammatory factors IL-6, IL-8 and TNF-α from AMs of COPD rats in a time and dose-dependent manner. The effects of S100A8 and S100A9 on the secretion of IL-6, IL-8 and TNF-α in AM of COPD rats are significantly enhanced compared with those of normal rats.
Citation：CHEN Xiaoju, ZHOU Zhi, YU Chengxiu, CHEN Yong, LIU Qin, CHEN Pei. The expression and pro-inflammatory effect of S100A8 and S100A9 in alveolar macrophages of rats with chronic obstructive pulmonary disease. Chinese Journal of Respiratory and Critical Care Medicine, 2022, 21(11): 804-809. doi: 10.7507/1671-6205.202206051Copy
Copyright ? the editorial department of Chinese Journal of Respiratory and Critical Care Medicine of West China Medical Publisher. All rights reserved
1.
Adeloye D, Song P, Zhu Y, et al. Global, regional, and national prevalence of, and risk factors for, chronic obstructive pulmonary disease (COPD) in 2019: a systematic review and modelling analysis. Lancet Respir Med, 2022, 10(5): 447-458.
2.
Fujii W, Kapellos TS, Ba?ler K, et al. Alveolar macrophage transcriptomic profiling in COPD shows major lipid metabolism changes. ERJ Open Res, 2021, 7(3): 00915-2020.
3.
Pruenster M, Vogl T, Roth J, et al. S100A8/A9: From basic science to clinical application. Pharmacol Ther, 2016, 167: 120-131.
4.
Johnstone KF, Wei YP, Bittner-Eddy PD, et al. Calprotectin (S100A8/A9) is an innate immune effector in experimental periodontitis. Infect Immun, 2021, 89(10): e0012221.
5.
Hiroshima Y, Hsu K, Tedla N, et al. S100A8/A9 and S100A9 reduce acute lung injury. Immunol Cell Biol, 2017, 95(5): 461-472.
Averill MM, Kerkhoff C, Bornfeldt KE. S100A8 and S100A9 in cardiovascular biology and disease. Arterioscler Thromb Vasc Biol, 2012, 32(2): 223-229.
14.
Sprenkeler EGG, Zandstra J, van Kleef ND, et al. S100A8/A9 is a marker for the release of neutrophil extracellular traps and induces neutrophil activation. Cells, 2022, 11(2): 236.
15.
Uspenskaya YA, Komleva YK, Pozhilenkova EA, et al. Ligands of RAGE-proteins: role in intercellular communication and pathogenesis of inflammation. Vestn Ross Akad Med Nauk, 2015, 70(6): 694-703.
16.
Fontaine M, Planel S, Peronnet E, et al. S100A8/A9 mRNA induction in an ex vivo model of endotoxin tolerance: roles of IL-10 and IFNγ. PLoS One, 2014, 9: e100909.
17.
Joly P, Marshall JC, Tessier PA, et al. S100A8/A9 and sRAGE kinetic after polytrauma; an explorative observational study. Scand J Trauma Resusc Emerg Med, 2017, 25(1): 114.
1. Adeloye D, Song P, Zhu Y, et al. Global, regional, and national prevalence of, and risk factors for, chronic obstructive pulmonary disease (COPD) in 2019: a systematic review and modelling analysis. Lancet Respir Med, 2022, 10(5): 447-458.
2. Fujii W, Kapellos TS, Ba?ler K, et al. Alveolar macrophage transcriptomic profiling in COPD shows major lipid metabolism changes. ERJ Open Res, 2021, 7(3): 00915-2020.
3. Pruenster M, Vogl T, Roth J, et al. S100A8/A9: From basic science to clinical application. Pharmacol Ther, 2016, 167: 120-131.
4. Johnstone KF, Wei YP, Bittner-Eddy PD, et al. Calprotectin (S100A8/A9) is an innate immune effector in experimental periodontitis. Infect Immun, 2021, 89(10): e0012221.
5. Hiroshima Y, Hsu K, Tedla N, et al. S100A8/A9 and S100A9 reduce acute lung injury. Immunol Cell Biol, 2017, 95(5): 461-472.
13. Averill MM, Kerkhoff C, Bornfeldt KE. S100A8 and S100A9 in cardiovascular biology and disease. Arterioscler Thromb Vasc Biol, 2012, 32(2): 223-229.
14. Sprenkeler EGG, Zandstra J, van Kleef ND, et al. S100A8/A9 is a marker for the release of neutrophil extracellular traps and induces neutrophil activation. Cells, 2022, 11(2): 236.
15. Uspenskaya YA, Komleva YK, Pozhilenkova EA, et al. Ligands of RAGE-proteins: role in intercellular communication and pathogenesis of inflammation. Vestn Ross Akad Med Nauk, 2015, 70(6): 694-703.
16. Fontaine M, Planel S, Peronnet E, et al. S100A8/A9 mRNA induction in an ex vivo model of endotoxin tolerance: roles of IL-10 and IFNγ. PLoS One, 2014, 9: e100909.
17. Joly P, Marshall JC, Tessier PA, et al. S100A8/A9 and sRAGE kinetic after polytrauma; an explorative observational study. Scand J Trauma Resusc Emerg Med, 2017, 25(1): 114.
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Citation：CHEN Xiaoju, ZHOU Zhi, YU Chengxiu, CHEN Yong, LIU Qin, CHEN Pei. The expression and pro-inflammatory effect of S100A8 and S100A9 in alveolar macrophages of rats with chronic obstructive pulmonary disease. Chinese Journal of Respiratory and Critical Care Medicine, 2022, 21(11): 804-809. doi: 10.7507/1671-6205.202206051
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