Effects of Single Immunoglobin IL-1 Receptor Related Protein on Inflammation Induced by Cigarette Smoke Extract in A549 Cells_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

ZhaoWei ^1,2 , WangXiaoping ¹ , ZhouYongan ¹ , KanXiaolong ¹ , NiYunfeng ¹ ,  TianFeng ¹

1. Department of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, Shanxi, 710032, China;
2. ;

Corresponding author：

TianFeng, Email: doctianfg@hotmail.com

Keywords：

Single immunoglobin IL-1 receptor related protein; Cigarette smoke extract; A549 cells

DOI：

10.7507/1671-6205.2015014

Video：

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Objective To investagte the effects of single immunoglobin IL-1 receptor related protein (SIGIRR) on inflammation induced by cigarette smoke extract (CSE) in A549 cells derived from mouse alveolar epithelial cells. Methods A549 cells were divided into a control group and an over-expressed SIGIRR group. Eukaryotic expression vectors pcDNA3.1(+) constructed with SIGIRR cDNA were transiently transfected into A549 cells, in which SIGIRR was forced to be over-expressed. The expression level of SIGIRR after transfection was detected with Western blot and RT-PCR method. After stimulated by CSE in both groups, the protein level of IL-6 was detected by ELISA, the transcriptional activity of cyclooxygenase-2(COX-2) was detected by dual-luciferase reporter assay system, and the release of reactive oxygen species (ROS) was measured by chemiluminescence method. Results The expression level of SIGIRR increased significantly in A549 cells transfected with SIGIRR vectors. The COX-2 expression and the levels of ROS and IL-6 were significantly increased in the control group after CSE stimulation. Nevertheless, in the over-expressed SIGIRR group, the COX-2 expression and the release of ROS was reduced while the protein level of IL-6 was down-regulated compared with the control group(P < 0.05). Conclusions Up-regulated SIGIRR expression can suppress the levels of ROS, COX-2 and IL-6 in A549 cells stimulated by CSE. It suggests that SIGIRR can inhibit airway inflammation caused by smoking.

Citation： ZhaoWei, WangXiaoping, ZhouYongan, KanXiaolong, NiYunfeng, TianFeng. Effects of Single Immunoglobin IL-1 Receptor Related Protein on Inflammation Induced by Cigarette Smoke Extract in A549 Cells. Chinese Journal of Respiratory and Critical Care Medicine, 2015, 14(1): 60-63. doi: 10.7507/1671-6205.2015014 Copy

1.	Lin CC, Lee IT, Yang YL, et al.Induction of COX-2/PGE(2)/IL-6 is crucial for cigarette smoke extract-induced airway inflammation:Role of TLR4-dependent NADPH oxidase activation.Free Radic Biol Med, 2010, 48:240-254.
2.	Laqente V, Planquois JM, Leclerc O, et al.Oxidative stress is an important component of airway inflammation in mice exposed to cigarette smoke or lipopolysaccharide.Clin Exp Pharmacol Physiol, 2008, 35:601-605.
3.	Lin CC, Hsiao LD, Chien CS, et al.Tumor necrosis factor-alpha-induced cyclooxygenase-2 expression in human tracheal smooth muscle cells:involvement of p42/p44 and p38 mitogen-activated protein kinases and nuclear factor-kappaB.Cell Signal, 2004, 16:597-607.
4.	Rahman I, Adcock IM.Oxidative stress and redox regulation of lung inflammation in COPD.Eur Respir J, 2006, 28:219-242.
5.	Brusselle GG, Bracke KR, Maes T, et al.Murine models of COPD.Pulm Pharmacol Ther, 2006, 19:155-165.
6.	黄勋, 梁晓华, 田丰, 等.SIGIRR对HMGB1诱导的A549细胞炎性反应的影响.中国呼吸与危重监护杂志, 2011, 10:577-580.
7.	田丰, 王云杰, 赵晋波, 等.SIGIRR在人正常肺组织及脂多糖诱导的肺泡上皮细胞急性损伤中的表达.中国呼吸与危重监护杂志, 2009, 8:242-246.
8.	Doz E, Noulin N, Boichot E, et al.Cigarette smoke-induced pulmonary inflammation is TLR4/MyD88 and IL-1R1/MyD88 signaling dependent.J Immunol, 2008, 180:1169-1178.
9.	Togbe D, Schnyder-Candrian S, Schnyder B, et al.TLR4 gene dosage contributes to endotoxin-induced acute respiratory inflammation.J Leukoc Biol, 2006, 80:451-457.
10.	Akira S, Takeda K.Toll-like receptor signalling.Nat Rev Immunol, 2004, 4:499-511.
11.	Pace E, Ferraro M, Siena L, et al.Cigarette smoke increases Toll-like receptor 4 and modifies lipopolysaccharide-mediated responses in airway epithelial cells.Immunology, 2008, 124:401-411.
12.	Foronjy RF, Mirochnitchenko O, Propokenko O, et al.Superoxide dismutase expression attenuates cigarette smoke-or elastase-generated emphysema in mice.Am J Respir Crit Care Med, 2006, 173:623-631.
13.	Son YH, Jeong YT, Lee KA, et al.Roles of MAPK and NF-kappaB in interleukin-6 induction by lipopolysaccharide in vascular smooth muscle cells.J Cardiovasc Pharmacol, 2008, 51:71-77.
14.	Feng T, Yunfeng N, Jinbo Z, et al.Single immunolobulin IL-1 receptor-related protein attenuates the lipopolysaccharide-induced inflammatory response in A549 cells.Chem Biol Interact, 2010, 183:442-449.
15.	Garlanda C, Anders HJ, Mantovani A.TIR8/SIGIRR:an IL-1R/TLR family member with regulatory functions in inflammation and T cell polarization.Trends Iummunol, 2009, 30:439-446.
16.	Qin J, Qian Y, Yao J, et al.SIGIRR inhibits interleukin-1 receptor-and toll-like receptor 4-mediated signaling through different mechanisms.J Biol Chem, 2005, 280:25233-25241.

1. Lin CC, Lee IT, Yang YL, et al.Induction of COX-2/PGE(2)/IL-6 is crucial for cigarette smoke extract-induced airway inflammation:Role of TLR4-dependent NADPH oxidase activation.Free Radic Biol Med, 2010, 48:240-254.
2. Laqente V, Planquois JM, Leclerc O, et al.Oxidative stress is an important component of airway inflammation in mice exposed to cigarette smoke or lipopolysaccharide.Clin Exp Pharmacol Physiol, 2008, 35:601-605.
3. Lin CC, Hsiao LD, Chien CS, et al.Tumor necrosis factor-alpha-induced cyclooxygenase-2 expression in human tracheal smooth muscle cells:involvement of p42/p44 and p38 mitogen-activated protein kinases and nuclear factor-kappaB.Cell Signal, 2004, 16:597-607.
4. Rahman I, Adcock IM.Oxidative stress and redox regulation of lung inflammation in COPD.Eur Respir J, 2006, 28:219-242.
5. Brusselle GG, Bracke KR, Maes T, et al.Murine models of COPD.Pulm Pharmacol Ther, 2006, 19:155-165.
6. 黄勋, 梁晓华, 田丰, 等.SIGIRR对HMGB1诱导的A549细胞炎性反应的影响.中国呼吸与危重监护杂志, 2011, 10:577-580.
7. 田丰, 王云杰, 赵晋波, 等.SIGIRR在人正常肺组织及脂多糖诱导的肺泡上皮细胞急性损伤中的表达.中国呼吸与危重监护杂志, 2009, 8:242-246.
8. Doz E, Noulin N, Boichot E, et al.Cigarette smoke-induced pulmonary inflammation is TLR4/MyD88 and IL-1R1/MyD88 signaling dependent.J Immunol, 2008, 180:1169-1178.
9. Togbe D, Schnyder-Candrian S, Schnyder B, et al.TLR4 gene dosage contributes to endotoxin-induced acute respiratory inflammation.J Leukoc Biol, 2006, 80:451-457.
10. Akira S, Takeda K.Toll-like receptor signalling.Nat Rev Immunol, 2004, 4:499-511.
11. Pace E, Ferraro M, Siena L, et al.Cigarette smoke increases Toll-like receptor 4 and modifies lipopolysaccharide-mediated responses in airway epithelial cells.Immunology, 2008, 124:401-411.
12. Foronjy RF, Mirochnitchenko O, Propokenko O, et al.Superoxide dismutase expression attenuates cigarette smoke-or elastase-generated emphysema in mice.Am J Respir Crit Care Med, 2006, 173:623-631.
13. Son YH, Jeong YT, Lee KA, et al.Roles of MAPK and NF-kappaB in interleukin-6 induction by lipopolysaccharide in vascular smooth muscle cells.J Cardiovasc Pharmacol, 2008, 51:71-77.
14. Feng T, Yunfeng N, Jinbo Z, et al.Single immunolobulin IL-1 receptor-related protein attenuates the lipopolysaccharide-induced inflammatory response in A549 cells.Chem Biol Interact, 2010, 183:442-449.
15. Garlanda C, Anders HJ, Mantovani A.TIR8/SIGIRR:an IL-1R/TLR family member with regulatory functions in inflammation and T cell polarization.Trends Iummunol, 2009, 30:439-446.
16. Qin J, Qian Y, Yao J, et al.SIGIRR inhibits interleukin-1 receptor-and toll-like receptor 4-mediated signaling through different mechanisms.J Biol Chem, 2005, 280:25233-25241.

Chinese Journal of Respiratory and Critical Care Medicine

Effects of Single Immunoglobin IL-1 Receptor Related Protein on Inflammation Induced by Cigarette Smoke Extract in A549 Cells

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