Changes of Interleukin-17 in Lung Tissue and Effects of Propofol in Rats with Acute Lung Injury_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

CHEN Wenjie , SHEN Feng , WANG Difen

Intensive Care Unit, Affiliated Hospital of Guiyang Medical College. Guiyang, Guizhou,550004, ChinaCorresponding Author: SHEN Feng, E-mail: 13511999117@ 163. com;

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Keywords：

Interleukin-17; Acute lung injury; Hydrochloric acid; Propofol; Rat

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Objective To investigate the changes of interleukin-17 ( IL-17) and the effects of propofol in rats with acute lung injury ( ALI) . Methods ALI model was established by hydrochloric acid ( HCl) inhalation in a dose of 2 mL/kg. 35 adultmale SD rats were randomly divided into seven groups, ie.a control group, a HCl group, and five propofol groups ( T24b , T12b , T0 , T1a , T3a groups, respectively) . The T0 ,T24b and T12b groups were pretreated with intraperitoneal propofol injection 0, 24 and 12 hours respectively before HCl inhalation. The T1a and T3a groups were managed by intraperitoneal propofol injection 1 and 3 hours respectively after HCl inhalation. Immunohistochemistry was used to determine the expression of IL-17 in lung tissue. ELISA was adopted to detect the levels of IL-17 and IL-8 in lung tissue homogenate as well as in bronchoalveolar lavage fluid ( BALF) , meanwhile arterial partial pressure of oxygen ( PaO2 ) and myeloperoxidase ( MPO) were measured. Results Those rats in the HCl group appeared respiratory distress, cyanosis, pulmonary edema, and inflammatory cells infiltration in lung tissues after HCl inhalation.The IL-17 levels in lung tissue homogenate as well as in BALF were higher in the HCl group than those in the control group( all P lt; 0. 01) . IL-17 was mainly expressed in alveolar epithelial cells and mononuclear cells in the ALI rats and its expression level was higher than that in the control group. IL-17 concentration in lung tissue homogenate was both correlated with IL-8 concentration in lung tissue homogenate ( r=0. 98, P =0.003) and with the activity of MPO in lung tissue( r=0. 981, P =0. 003) in the HCl group. Mainwhile, a same significant correlation was found between IL-8 level in lung tissue homogenate and the MPO activity in the HCl group( r =0. 961, P =0. 009) . Propofol attenuated lung injury induced by HCl inhalation, especially in T24b group. The concentrations of IL-17 in lung tissue homogenate and in BALF were lower in T24b group when compared with the HCl group( P = 0. 011, P =0. 003, respectively) . Conclusions The expression of IL-17 increases in ALI rats. Pretreatment with propofol by 24 hours has obvious inhibiting effects on inflammatory reaction. Inhibiting IL-17 expression may be one of the mechanisms through which propofol inhibits the inflammatory reaction of ALI.

Citation： CHEN Wenjie,SHEN Feng,WANG Difen. Changes of Interleukin-17 in Lung Tissue and Effects of Propofol in Rats with Acute Lung Injury. Chinese Journal of Respiratory and Critical Care Medicine, 2010, 9(5): 532-536. doi: Copy

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12.	Green TR, Bennett SR, Nelson VM. Specificity and properties of propofol as an antioxidant free radical scavenger. Toxicol Appl Pharmacol, 1994 , 129: 163-169.
13.	Mikawa K, Akamatsu H, Nishina K, et al. Propofol inhibits human neutrophil functions. Anesth Analg, 1998 , 87 : 695 -700.
14.	Taniguchi T, Yamamoto K, Ohmoto N, et al. Effects of propofol on hemodynamic and inflammatory responses to endotoxemia in rats.Crit Care Med, 2000, 28 : 1101-1106.

1. Moraes TJ, Zurawska JH, Downey GP. Neutrophil granule contents in the pathogenesis of lung injury. Curr 0pin Hematol, 2006, 13: 21 -27.
2. Jones CE, Chan K. Interleukin-17 stimulates the expression of interleukin-8, growth-related oncogene-α, and granulocyte-colonystimulating factor by human airway epithelial cells. AmJRespir Cell Mol Biol. 2002, 26: 748-753.
3. Endo S, Kasai T, Inada K. Evaluation of procalcitoinin levels in patients with systemic inflammatory response syndrome as the diagnosis of infection and the severity of illness. Kansenshogaku Zasshi, 1999, 73 : 197-204.
4. 李轶聪, 李悦, 王彦松, 等. 不同次数和剂量异丙酚预处理对大鼠全脑缺血再灌注损伤的作用. 中华麻醉学杂志, 2006, 26: 720 -724.
5. 罗武生, 郭兆贵. 用髓过氧化酶法定量测定心肌组织中的中性白细胞. 中国药理学通报, 1990, 6 : 264-266.
6. 张志刚, 何权瀛, 刘新民, 等. 白细胞介素-17 在急性肺损伤发病机制中的作用. 心肺血管病杂志, 2007, 26: 38-43.
7. Kurkowska A, Noble JM, Grant IS, et al. Anti-interleukin-8 antoantibodies in patients at risk for acute respiratory distress syndrome. Crit Care Med, 2002, 30: 2335-2337.
8. Fossiez F, Djossou O, Chomarat P, et al. T cell interleukin-17 induces stromal cells to produce proinflammatory and hematopoietic cytokines. Exp Med, 1996, 183: 2593-2603.
9. Miyamoto M, Prause O, Sjostrand M, et al. Endogenous IL-17 as a mediator of neutrophil recruitment caused by endotoxin exposure in mouse airways. J Immunol, 2003, 170 : 4665 -4672 .
10. Linden A, Hoshino H, and Laan M. Airway neutrophils and interleukin-17 . Eur Respir J, 2000, 15: 973 -977.
11. Andoh A, Takaya H, Makino J, et al. Cooperation of interleukin-17 and interferon-gamma on chemokine secretion in human fetal intestinal epithelial cells. Clin Exp Immunol, 2001 , 125: 56 -63 .
12. Green TR, Bennett SR, Nelson VM. Specificity and properties of propofol as an antioxidant free radical scavenger. Toxicol Appl Pharmacol, 1994 , 129: 163-169.
13. Mikawa K, Akamatsu H, Nishina K, et al. Propofol inhibits human neutrophil functions. Anesth Analg, 1998 , 87 : 695 -700.
14. Taniguchi T, Yamamoto K, Ohmoto N, et al. Effects of propofol on hemodynamic and inflammatory responses to endotoxemia in rats.Crit Care Med, 2000, 28 : 1101-1106.

Chinese Journal of Respiratory and Critical Care Medicine

Changes of Interleukin-17 in Lung Tissue and Effects of Propofol in Rats with Acute Lung Injury

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