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Sulphur dioxide suppresses inflammatory response by sulphenylating NF-κB p65 at Cys38 in a rat model of acute lung injury.

  • Chen, Siyao1, 2
  • Huang, Yaqian1
  • Liu, Zhiwei3
  • Yu, Wen1
  • Zhang, Heng4
  • Li, Kun5
  • Yu, Xiaoqi5
  • Tang, Chaoshu6, 7
  • Zhao, Bin8
  • Du, Junbao9
  • Jin, Hongfang9
  • 1 Department of Pediatrics, Peking University First Hospital, Beijing 100034, P.R. China. , (China)
  • 2 Department of the Intensive Care Unit of Cardiac Surgery, Guangdong Cardiovascular Institute, Guangdong General Hospital and Guangdong Academy of Medical Sciences, Guangzhou, P.R. China. , (China)
  • 3 Department of Emergency, Beijing Jishuitan Hospital, Beijing 100035, P.R. China. , (China)
  • 4 Department of Endocrinology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, P.R. China. , (China)
  • 5 Key Laboratory of Green Chemistry and Technology, Ministry of Education, College of Chemistry, Sichuan University, Chengdu 610064, P.R. China. , (China)
  • 6 Department of Physiology and Pathophysiology, Peking University Health Science Center, Beijing 100191, P.R. China. , (China)
  • 7 Key Laboratory of Molecular Cardiology, Ministry of Education, Beijing 100191, P.R. China. , (China)
  • 8 Department of Emergency, Beijing Jishuitan Hospital, Beijing 100035, P.R. China [email protected] [email protected] [email protected] , (China)
  • 9 Department of Pediatrics, Peking University First Hospital, Beijing 100034, P.R. China [email protected] [email protected] [email protected] , (China)
Published Article
Clinical Science
Portland Press
Publication Date
Nov 01, 2017
DOI: 10.1042/CS20170274
PMID: 28935810


The present study was designed to investigate whether endogenous sulphur dioxide (SO2) controlled pulmonary inflammation in a rat model of oleic acid (OA)-induced acute lung injury (ALI). In this model, adenovirus expressing aspartate aminotransferase (AAT) 1 was delivered to the lungs, and the levels of SO2 and proinflammatory cytokines in rat lung tissues were measured. In the human alveolar epithelial cell line A549, the nuclear translocation and DNA binding activities of wild-type (wt) and C38S (cysteine-to-serine mutation at p65 Cys38) NF-κB p65 were detected. GFP-tagged C38S p65 was purified from HEK 293 cells and the sulphenylation of NF-κB p65 was studied. OA caused a reduction in SO2/AAT pathway activity but increased pulmonary inflammation and ALI. However, either the presence of SO2 donor, a combination of Na2SO3 and NaHSO3, or AAT1 overexpression in vivo successfully blocked OA-induced pulmonary NF-κB p65 phosphorylation and consequent inflammation and ALI. Either treatment with an SO2 donor or overexpression of AAT1 down-regulated OA-induced p65 activity, but AAT1 knockdown in alveolar epithelial cells mimicked OA-induced p65 phosphorylation and inflammation in vitro Mechanistically, OA promoted NF-κB nuclear translocation, DNA binding activity, recruitment to the intercellular cell adhesion molecule (ICAM)-1 promoter, and consequent inflammation in epithelial cells; these activities were reduced in the presence of an SO2 donor. Furthermore, SO2 induced sulphenylation of p65, which was blocked by the C38S mutation on p65 in epithelial cells. Hence, down-regulation of SO2/AAT is involved in pulmonary inflammation during ALI. Furthermore, SO2 suppressed inflammation by sulphenylating NF-κB p65 at Cys38.

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