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Tobacco smoking aggravates airway inflammation by upregulating endothelin-2 and activating the c-Jun amino terminal kinase pathway in asthma.
Int Immunopharmacol 2019; 77:105916II

Abstract

BACKGROUND

Asthma is closely associated with tobacco smoking (TS) and is more difficult to effectively treat after exposure to TS.

OBJECTIVE

To observe the effects of TS on the expression of endothelin-2 (ET-2) and airway inflammation in asthmatic rats and to explore the related mechanisms.

METHODS

We established an animal model of asthma with ovalbumin (OVA)/Al(OH)3 and subjected different animal groups to TS and/or dexamethasone/bosentan. The differences in the inflammatory cell infiltration, the pathological changes to the bronchial wall and the bronchial smooth muscle thickness, and the expression of ET-2, c-Jun amino terminal kinase (JNK1/2), malondialdehyde (MDA), and glutathione peroxidase (GSH) in the lung tissue and of interleukin (IL)-7 in bronchoalveolar lavage fluid (BALF) were assessed.

RESULTS

Exposure to TS or OVA caused an obvious increase in the inflammatory cells in the BALF over what was observed in the control group. In asthma models, the expression of ET-1, JNK1/2, MDA, and GSH in the lung tissues, as well as that of IL-17 in the BALF, was increased. After treatment with dexamethasone/bosentan, the expression of IL-17, JNK1/2, MDA, and GSH decreased compared to the smoking group; airway inflammation and the staining intensity in the lung tissue were also reduced.

CONCLUSION

TS exposure can clearly exacerbate airway inflammation in asthmatic rats, while bosentan can alleviate airway inflammation through regulation of the ET-2/JNK1/2 signalling pathway.

Authors+Show Affiliations

Department of Respiratory Medicine, Affiliated Hospital of Jining Medical University, Jining, Shandong 272029, China.Department of Respiratory Medicine, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221000, China.Department of Respiratory Medicine, Affiliated Hospital of Jining Medical University, Jining, Shandong 272029, China.Department of Respiratory Medicine, Zhengzhou Center Hospital Affiliated to Zhengzhou University, Zhengzhou, Henan 450000, China.Department of Respiratory Medicine, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221000, China.Department of Respiratory Medicine, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221000, China.Department of Respiratory Medicine, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221000, China. Electronic address: chenbi207@163.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31629215

Citation

Guo, Maoqing, et al. "Tobacco Smoking Aggravates Airway Inflammation By Upregulating Endothelin-2 and Activating the c-Jun Amino Terminal Kinase Pathway in Asthma." International Immunopharmacology, vol. 77, 2019, p. 105916.
Guo M, Liu Y, Han X, et al. Tobacco smoking aggravates airway inflammation by upregulating endothelin-2 and activating the c-Jun amino terminal kinase pathway in asthma. Int Immunopharmacol. 2019;77:105916.
Guo, M., Liu, Y., Han, X., Han, F., Zhu, J., Zhu, S., & Chen, B. (2019). Tobacco smoking aggravates airway inflammation by upregulating endothelin-2 and activating the c-Jun amino terminal kinase pathway in asthma. International Immunopharmacology, 77, p. 105916. doi:10.1016/j.intimp.2019.105916.
Guo M, et al. Tobacco Smoking Aggravates Airway Inflammation By Upregulating Endothelin-2 and Activating the c-Jun Amino Terminal Kinase Pathway in Asthma. Int Immunopharmacol. 2019 Oct 16;77:105916. PubMed PMID: 31629215.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Tobacco smoking aggravates airway inflammation by upregulating endothelin-2 and activating the c-Jun amino terminal kinase pathway in asthma. AU - Guo,Maoqing, AU - Liu,Yanan, AU - Han,Xiao, AU - Han,Fangfang, AU - Zhu,Jiechen, AU - Zhu,Shuyang, AU - Chen,Bi, Y1 - 2019/10/16/ PY - 2019/05/24/received PY - 2019/09/04/revised PY - 2019/09/13/accepted PY - 2019/10/20/pubmed PY - 2019/10/20/medline PY - 2019/10/20/entrez KW - Asthma KW - Bosentan KW - Endothelin KW - JNK1/2 KW - Tobacco SP - 105916 EP - 105916 JF - International immunopharmacology JO - Int. Immunopharmacol. VL - 77 N2 - BACKGROUND: Asthma is closely associated with tobacco smoking (TS) and is more difficult to effectively treat after exposure to TS. OBJECTIVE: To observe the effects of TS on the expression of endothelin-2 (ET-2) and airway inflammation in asthmatic rats and to explore the related mechanisms. METHODS: We established an animal model of asthma with ovalbumin (OVA)/Al(OH)3 and subjected different animal groups to TS and/or dexamethasone/bosentan. The differences in the inflammatory cell infiltration, the pathological changes to the bronchial wall and the bronchial smooth muscle thickness, and the expression of ET-2, c-Jun amino terminal kinase (JNK1/2), malondialdehyde (MDA), and glutathione peroxidase (GSH) in the lung tissue and of interleukin (IL)-7 in bronchoalveolar lavage fluid (BALF) were assessed. RESULTS: Exposure to TS or OVA caused an obvious increase in the inflammatory cells in the BALF over what was observed in the control group. In asthma models, the expression of ET-1, JNK1/2, MDA, and GSH in the lung tissues, as well as that of IL-17 in the BALF, was increased. After treatment with dexamethasone/bosentan, the expression of IL-17, JNK1/2, MDA, and GSH decreased compared to the smoking group; airway inflammation and the staining intensity in the lung tissue were also reduced. CONCLUSION: TS exposure can clearly exacerbate airway inflammation in asthmatic rats, while bosentan can alleviate airway inflammation through regulation of the ET-2/JNK1/2 signalling pathway. SN - 1878-1705 UR - https://www.unboundmedicine.com/medline/citation/31629215/Tobacco_smoking_aggravates_airway_inflammation_by_upregulating_endothelin-2_and_activating_the_c-Jun_amino_terminal_kinase_pathway_in_asthma L2 - https://linkinghub.elsevier.com/retrieve/pii/S1567-5769(19)31124-5 DB - PRIME DP - Unbound Medicine ER -