Abstract:Objective To study the effects of the change in transient receptor potential vanilloid 1 (TRPV1) channel activity on the degree of airway inflammation in asthmatic mice. Methods BALB/c mice were randomly divided into control, asthma, capsaicin (TRPV1 agonist), capsazepine (TRPV1 antagonist), and dexamethasone groups. The asthmatic mouse model was established by intraperitoneal injection of mixed ovalbumin-aluminium hydroxide solution and ultrasonic atomization with OVA for sensitization and challenge. The capsaicin, capsazepine, and dexamethasone groups were given intraperitoneal injection of capsaicin (30 μg/kg), capsazepine (10 μmol/kg), and dexamethasone (2 mg/kg) respectively, at 30 minutes before challenge. Hematoxylin and eosin staining was used to observe the degree of pulmonary inflammation. ELISA was used to measure the content of interleukin-8 (IL-8) and interleukin-13 (IL-13) in bronchoalveolar lavage fluid (BALF). Real-Time PCR was used to measure the relative content of TRPV1 mRNA in lung tissue. Results Compared with the asthma group, the capsazepine and dexamethasone groups showed reduced pulmonary inflammation, while the capsaicin group showed aggravated pulmonary inflammation. Compared with the control group, the asthma and capsaicin groups showed increases in the content of IL-13 and IL-8 in BALF and the mRNA expression of TRPV1 in lung tissue (P < 0.05). Compared with the asthma group, the capsazepine and dexamethasone groups showed reductions in the content of IL-13 and IL-8 in BALF and the mRNA expression of TRPV1 in lung tissue (P < 0.05). The capsaicin group showed increases in the content of IL-13 and IL-8 in BALF (P < 0.05). Conclusions TRPV1 channel agonist and antagonist can influence the degree of airway inflammation in asthmatic mice. Dexamethasone may reduce airway inflammation through regulating TRPV1 level.
FENG Shuang,ZHANG Yuan-Yuan,GAO Wen-Juan et al. Role of transient receptor potential vanilloid 1 in airway inflammation in asthmatic mice[J]. CJCP, 2016, 18(9): 874-878.
Zholos AV. TRP channels in respiratory pathophysiology:the role of oxidative, chemical irritant and temperature stimuli[J]. Curr Neuropharmacol, 2015, 13(2):279-291.
[3]
Chen CL, Li H, Xing XH, et al. Effect of TRPV1 gene mutation on bronchial asthma in children before and after treatment[J]. Allergy Asthma Proc, 2015, 36(2):e29-e36.
[4]
Locke NR, Royce SG, Wainewright JS, et al. Comparison of airway remodeling in acute, subacute, and chronic models of allergic airways disease[J]. Am J Respir Cell Mol Biol, 2007, 36(5):625-632.
[5]
Delescluse I, Mace H, Adcock JJ. Inhibition of airway hyperresponsiveness by TRPV1 antagonists (SB-705498 and PF-04065463) in the unanaesthetized ovalbumin-sensitized guinea pig[J]. Br J Pharmacol, 2012, 166(6):1822-1832.
[6]
Cantero-Recasens G, Gonzalez JR, Fandos C, et al. Loss of function of transient receptor potential vanilloid 1(TRPV1) genetic variant is associated with lower risk of active childhood asthma[J]. J Biol Chem, 2010, 285(36):27532-27535.
[7]
Ma J, Altomare A, Guarino M, et al. HCl-induced and ATPdependent upregulation of TRPV1 receptor expression and cytokine production by human esophageal epithelial cells[J]. Am J Physiol Gastrointest Liver Physiol, 2012, 303(5):G635-G645.
[8]
Wang Z, Yang Y, Yang H, et al. NF-κB feedback control of JNK1 activation modulates TRPV1-induced increases in IL-6 and IL-8 release by human corneal epithelial cells[J]. Mol Vis, 2011, 17:3137-3146.
[9]
Tsilogianni Z, Hillas G, Bakakos P, et al. Sputum interleukin-13 as a biomarker for the evaluation of asthma control[J]. Clin Exp Allergy, 2016, 46(7):923-931.
[10]
Dunn R, Szefler SJ. Severe asthma in pediatric patients. Pathophysiology and unmet needs[J]. Ann Am Thorac Soc, 2016, 13 Suppl 1:S103-S104.