Mechanical ventilation modulates Toll-like receptors 2, 4, and 9 on alveolar macrophages in a ventilator-induced lung injury model

被引:38
作者
Dai, Huijun [1 ]
Pan, Linghui [1 ]
Lin, Fei [1 ]
Ge, Wanyun [1 ]
Li, Wei [1 ]
He, Sheng [1 ]
机构
[1] Guangxi Med Univ, Tumor Hosp, Dept Anesthesiol, Nanning 530021, Peoples R China
基金
中国国家自然科学基金;
关键词
Toll like receptor (TLR); myeloid differentiation factor 88 (MyD88); alveolar macrophages; ventilator-induced lung injury (VILI); RESPIRATORY-DISTRESS-SYNDROME; FACTOR-KAPPA-B; INFLAMMATORY RESPONSE; HEALTHY MICE; NLRP3; INFLAMMASOME; TLR4; ACTIVATION; INTERLEUKIN-1-BETA; PATHOGENESIS; CONTRIBUTES;
D O I
10.3978/j.issn.2072-1439.2015.02.10
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Objective: To investigate the role of Toll-like receptor 2 (TLR2), TLR4, TLR9 and myeloid differentiation factor 88 (MyD88) on alveolar macrophages in ventilator-induced lung injury (VILI). Methods: Male, adult pathogen-free Sprague-Dawley rats weighing 300-350 g were used in this study. Animals were tracheotomized and allowed to breathe spontaneously for 4 h or mechanically ventilated for 4 h with low or high tidal volume (7 or 40 mL/kg). TLR2, TLR4, and TLR9, MyD-88 and NF-kappa B of alveolar macrophages' expression under the different ventilation conditions were detected. Pulmonary permeability, lung inflammatory, IL-6 and IL-1 beta were assessed as well. Results: Rats subjected to high tidal volume showed significantly greater pulmonary permeability and lung inflammatory than the control rats. Alveolar macrophages from rats subjected to high tidal volume also showed significantly higher protein expression of TLR2 (0.59 +/- 0.049 vs. 0.35 +/- 0.036 and 0.36 +/- 0.031, both P < 0.001), TLR4 (0.845 +/- 0.0395 vs. 0.401 +/- 0.026 and 0.403 +/- 0.020, both P < 0.001), TLR9 (0.727 +/- 0.074 vs. 0.383 +/- 0.039 and 0.367 +/- 0.043, both P < 0.001), MyD-88 (1.01 +/- 0.060 vs. 0.485 +/- 0.045 and 0.507 +/- 0.046, both P < 0.001) and NF-.. (0.776 +/- 0.067 vs. 0.448 +/- 0.043 and 0.481 +/- 0.047, both P < 0.001), as well as significantly higher concentrations of IL-6 (7.32 +/- 0.24 vs. 2.42 +/- 0.13 and 2.44 +/- 0.32, both P < 0.001) and IL-1 beta (139.95 +/- 9.37 vs. 53.63 +/- 5.26 and 53.55 +/- 6.63, both P < 0.001) than the control and low tidal volume group. Conclusions: The overexpression of TLR2, TLR4, and TLR9 on alveolar macrophages and release of pro-inflammatory cytokines play a role in VILI.
引用
收藏
页码:616 / 624
页数:9
相关论文
共 41 条
[1]   Involvement of ERK, p38 and NF-κB signal transduction in regulation of TLR2, TLR4 and TLR9 gene expression induced by lipopolysaccharide in mouse dendritic cells [J].
An, HZ ;
Yu, YH ;
Zhang, MH ;
Xu, HM ;
Qi, RZ ;
Yan, XY ;
Liu, SX ;
Wang, WY ;
Guo, ZH ;
Guo, J ;
Qin, ZH ;
Cao, XT .
IMMUNOLOGY, 2002, 106 (01) :38-45
[2]   Lungs of patients with acute respiratory distress syndrome show diffuse inflammation in normally aerated regions: A [18F]-fluoro-2-deoxy-D-glucose PET/CT study [J].
Bellani, Giacomo ;
Messa, Cristina ;
Guerra, Luca ;
Spagnolli, Ester ;
Foti, Giuseppe ;
Patroniti, Nicolo ;
Fumagalli, Roberto ;
Musch, Guido ;
Fazio, Ferruccio ;
Pesenti, Antonio .
CRITICAL CARE MEDICINE, 2009, 37 (07) :2216-2222
[3]   The role of cytokines during the pathogenesis of ventilator-associated and ventilator-induced lung injury [J].
Belperio, John A. ;
Keane, Michael P. ;
Lynch, Joseph P., III ;
Strieter, Robert M. .
SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE, 2006, 27 (04) :350-364
[4]   TLRs and innate immunity [J].
Beutler, Bruce A. .
BLOOD, 2009, 113 (07) :1399-1407
[5]   Toll-like receptor signaling: a critical modulator of cell survival and ischemic injury in the heart [J].
Chao, Wei .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2009, 296 (01) :H1-H12
[6]   Hepatitis C VLPs Delivered to Dendritic Cells by a TLR2 Targeting Lipopeptide Results in Enhanced Antibody and Cell-Mediated Responses [J].
Chua, Brendon Y. ;
Johnson, Douglas ;
Tan, Amabel ;
Earnest-Silveira, Linda ;
Sekiya, Toshiki ;
Chin, Ruth ;
Torresi, Joseph ;
Jackson, David C. .
PLOS ONE, 2012, 7 (10)
[7]   Reduction in alveolar macrophages attenuates acute ventilator induced lung injury in rats [J].
Eyal, Fabien G. ;
Hamm, Charles R. ;
Parker, James C. .
INTENSIVE CARE MEDICINE, 2007, 33 (07) :1212-1218
[8]   Protection from experimental ventilator-induced acute lung injury by IL-1 receptor blockade [J].
Frank, J. A. ;
Pittet, J-F ;
Wray, C. ;
Matthay, M. A. .
THORAX, 2008, 63 (02) :147-153
[9]   Alveolar macrophages contribute to alveolar barrier dysfunction in ventilator-induced lung injury [J].
Frank, James A. ;
Wray, Charlie M. ;
McAuley, Danny F. ;
Schwendener, Reto ;
Matthay, Michael A. .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2006, 291 (06) :L1191-L1198
[10]   Interleukin-1β causes acute lung injury via αvβ5 and αvβ6 integrin-dependent mechanisms [J].
Ganter, Michael T. ;
Roux, Jeremie ;
Miyazawa, Byron ;
Howard, Marybeth ;
Frank, James A. ;
Su, George ;
Sheppard, Dean ;
Violette, Shelia M. ;
Weinreb, Paul H. ;
Horan, Gerald S. ;
Matthay, Michael A. ;
Pittet, Jean-Francois .
CIRCULATION RESEARCH, 2008, 102 (07) :804-812