Involvement of a capsaicin-sensitive TRPV1-independent mechanism in lipopolysaccharide-induced fever in chickens

被引:12
作者
Mahmoud, Motamed Elsayed
Shimizu, Yasutake
Shiina, Takahiko
Nikami, Hideki
Dosoky, Reem Mahmoud
Ahmed, Moustafa Mohamed
Takewaki, Tadashi
机构
[1] Gifu Univ, United Grad Sch Vet Sci, Dept Vet Basic Sci, Physiol Lab, Gifu 5011193, Japan
[2] Gifu Univ, Life Sci Res Ctr, Gifu 5011193, Japan
[3] Assiut Univ, Fac Vet Med, Dept Anim Hyg Anim Behav, Assiut, Egypt
来源
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-MOLECULAR & INTEGRATIVE PHYSIOLOGY | 2007年 / 148卷 / 03期
关键词
capsaicin; capsazepine; chicken; fever; LPS; TRPVI;
D O I
10.1016/j.cbpa.2007.07.012
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
It has been demonstrated that capsaicin blocks lipopolysaccharide (LPS)-induced fever in mammals. In this study, we investigated TRPVI (transient receptor potential ion channel of vanilloid subtype-D-independent action of capsaicin on LPS-induced fever in chickens. The chicken is a valuable model for this purpose because chicken TRPV1 has been shown to be insensitive to capsaicin and thus the effects of capsaicin can be attributed to TRPV1-independent mechanisms. Administration of capsaicin (10 mg/kg, iv) to conscious unrestrained chicks at 5 days of age caused a transient decrease in body temperature. This effect of capsaicin was not observed in chicks that had been pretreated twice with capsaicin, indicating that the capsaicin-sensitive pathway can be desensitized. LPS (2 mg/kg, ip) induced fever that lasted for about 2.5 h, but fever was not induced in chicks that had been pretreated with capsaicin for 2 days. The preventive effect of capsaicin on LPS-induced fever was not blocked by capsazepine, an antagonist for TRPVI, but the antagonist per se blocked the febrile response to LPS. These findings suggest that a capsaicin-sensitive TRPV1-independent mechanism may be involved in LPS-induced fever. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:578 / 583
页数:6
相关论文
共 37 条
[31]   Adenosine 5′-monophosphate ameliorates D-galactosamine/lipopolysaccharide-induced liver injury through an adenosine receptor-independent mechanism in mice [J].
Y Zhan ;
Z Wang ;
P Yang ;
T Wang ;
L Xia ;
M Zhou ;
Y Wang ;
S Wang ;
Z Hua ;
J Zhang .
Cell Death & Disease, 2014, 5 :e985-e985
[32]   Adenosine 5′-monophosphate ameliorates D-galactosamine/lipopolysaccharide-induced liver injury through an adenosine receptor-independent mechanism in mice [J].
Zhan, Y. ;
Wang, Z. ;
Yang, P. ;
Wang, T. ;
Xia, L. ;
Zhou, M. ;
Wang, Y. ;
Wang, S. ;
Hua, Z. ;
Zhang, J. .
CELL DEATH & DISEASE, 2014, 5 :e985-e985
[33]   PARTICIPATION OF INTERLEUKIN-1 AND TUMOR-NECROSIS-FACTOR IN THE RESPONSES OF THE SYMPATHETIC NERVOUS-SYSTEM DURING LIPOPOLYSACCHARIDE-INDUCED FEVER [J].
SAIGUSA, T .
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 1990, 416 (03) :225-229
[34]   Capsaicin mimics mechanical load-induced intracellular signaling events Involvement of TRPV1-mediated calcium signaling in induction of skeletal muscle hypertrophy [J].
Ito, Naoki ;
Ruegg, Urs T. ;
Kudo, Akira ;
Miyagoe-Suzuki, Yuko ;
Takeda, Shin'ichi .
CHANNELS, 2013, 7 (03) :221-224
[35]   The Neurokinin-1 Receptor Contributes to the Early Phase of Lipopolysaccharide-Induced Fever via Stimulation of Peripheral Cyclooxygenase-2 Protein Expression in Mice [J].
Pakai, Eszter ;
Tekus, Valeria ;
Zsiboras, Csaba ;
Rumbus, Zoltan ;
Olah, Emoke ;
Keringer, Patrik ;
Khidhir, Nora ;
Matics, Robert ;
Deres, Laszlo ;
Ordog, Katalin ;
Szentes, Nikolett ;
Pohoczky, Krisztina ;
Kemeny, Agnes ;
Hegyi, Peter ;
Pinter, Erika ;
Garami, Andras .
FRONTIERS IN IMMUNOLOGY, 2018, 9
[36]   Capsaicin Protects Against Lipopolysaccharide-Induced Acute Lung Injury Through the HMGB1/NF-κB and PI3K/AKT/mTOR Pathways [J].
Chen, Hui ;
Li, Na ;
Zhan, Xiang ;
Zheng, Ting ;
Huang, Xinzhou ;
Chen, Qianglin ;
Song, Zihao ;
Yang, Fei ;
Nie, Hao ;
Zhang, Yanxiang ;
Zheng, Bing ;
Gong, Quan .
JOURNAL OF INFLAMMATION RESEARCH, 2021, 14 :5291-5304
[37]   Lipopolysaccharide-induced down-regulation of organic anion transporting polypeptide 4 (Oatp4; Slc21a10) is independent of tumor necrosis factor-α, interleukin-1β, interleukin-6, or inducible nitric oxide synthase [J].
Li, N ;
Klaassen, CD .
TOXICOLOGICAL SCIENCES, 2005, 83 (01) :197-203