摘要
随着畜牧业集约化生产水平的不断提高,动物炎症带来的经济损失逐渐受到重视。细胞表面Toll样受体(TLRs)可以通过活化胞浆内核转录因子-κB(NF-κB),诱导核苷酸结合寡聚域样受体蛋白3(NLRP3)炎性小体表达,加剧炎症反应。本文就NLRP3炎性小体与炎症疾病,褪黑素对TLRs、NF-κB和NLRP3炎性小体的作用以及炎症对动物生产的影响作一综述。
With the continuous improvement of intensive production level of animal husbandry,the economic losses caused by animal inflammation have been paid more and more attention. Toll-like receptors on cell surface can induce the expression of nucleotide-binding oligomeric domain-like receptor protein-3 inflammatory corpuscle by activating intracytoplasmic nuclear transcription factor-kappa B,and aggravate the inflammatory response. This article reviews the nucleotide-binding oligomeric receptor protein-3 inflammatory corpuscle and inflammatory diseases,the effects of melatonin on Toll-like receptors,nuclear transcription factor-kappa B and nucleotide-binding oligomeric receptor protein-3 inflammatory corpuscle,and the effects of inflammation on animal production.[Chinese Journal of Animal Nutrition,2019,31( 5) : 2069-2075]
引文
[1] LEVY M,THAISS C A,ELINAV E. Taming the inflammasome[J].Nature M edicine,2015,21(3):213-215.
[2] ZHOU R B,YAZDI A S,MENU P,et al. A role for mitochondria in NLRP3 inflammasome activation[J].Nature,2011,469(7329):221-225.
[3] SABROE I,PARKER L C,DOWER S K,et al. The role of TLR activation in inflammation[J]. Journal of Pathology,2010,214(2):126-135.
[4] LATZ E,XIAO T S,STUTZ A.Activation and regulation of the inflammasomes[J].Nature Review s Immunology,2013,13(6):397-411.
[5] HERNANDEZ-CUELLAR E,TSUCHIYA K,HARA H,et al. Cutting edge:nitric oxide inhibits the NLRP3inflammasome[J]. Journal of Immunology,2012,189(11):5113-5117.
[6] RATHINAM V A K,VANAJA S K,FITZGERALD K A. Regulation of inflammasome signaling[J]. Nature Immunology,2012,13(4):333-342.
[7] LEE S,SUH G Y,RYTER S W,et al.Regulation and function of the nucleotide binding domain leucine-rich repeat-containing receptor,pyrin domain-containing-3inflammasome in lung disease[J]. American Journal of Respiratory Cell and M olecular Biology,2016,54(2):151-60.
[8] MARTINEZ G J,ROBERTSON S,BARRACLOUGH J,et al.Colchicine acutely suppresses local cardiac production of inflammatory cytokines in patients w ith an acute coronary syndrome[J]. Journal of the American Heart Association,2015,4(8):e002128.
[9] KIM S,JOE Y,JEONG S O,et al.Endoplasmic reticulum stress is sufficient for the induction of IL-1βproduction via activation of the NF-κB and inflammasome pathw ays[J]. Innate Immunity,2014,20(8):799-815.
[10] OVERLEY-ADAMSON B,ARTLETT C M,STEPHENS C,et al. Targeting the unfolded protein response,XBP1,and the NLRP3 inflammasome in fibrosis and cancer[J]. Cancer Biology&Therapy,2014,15(4):452-462.
[11] FANN D Y W,SANTRO T,MANZANERO S,et al.Intermittent fasting attenuates inflammasome activity in ischemic stroke[J].Experimental Neurology,2014,257:114-119.
[12] HOEGEN T,TREMEL N,KLEIN M,et al. The NLRP3 inflammasome contributes to brain injury in pneumococcal meningitis and is activated through ATP-dependent lysosomal cathepsin B release[J].The Journal of Immunology,2011,187(10):5440-5451.
[13] LI J,WANG Y L,WANG Y P,et al.Pharmacological activation of AM PK prevents Drp1-mediated mitochondrial fission and alleviates endoplasmic reticulum stress-associated endothelial dysfunction[J].Journal of M olecular and Cellular Cardiology,2015,86:62-74.
[14] BECKER C E,O’NEILL L A J. Inflammasomes in inflammatory disorders:the role of TLRs and their interactions w ith NLRs[J].Seminars in Immunopathology,2007,29(3):239-248.
[15] TAKEDA K,KAISHO T,AKIRA S. Toll-like receptors[J]. Annual Review of Immunology,2003,21(1):335-376.
[16] AKIRA S,TAKEDA K. Toll-like receptor signalling[J].Nature Reviews Immunology,2004,4(7):499-511.
[17]陈洁,姜虹.TLR4信号通路与炎性反应[J].医学综述,2009,15(19):2902-2904.
[18] FITZGERALD K A,MCWHIRTER S M,FAIA K L,et al.IKKεepsilon and TBK1 are essential components of the IRF3 signaling pathw ay[J]. Nature Immunology,2003,4(5):491-496.
[19] SHIBOLET O,PODOLSKY D K. TLRs in the Gut.Ⅳ.negative regulation of Toll-like receptors and intestinal homeostasis:addition by subtraction[J]. American Journal of Physiology:Gastrointestinal and Liver Physiology,2007,292(6):1469-1473.
[20] QIAO Y,WANG P,QI J N,et al. TLR-induced NF-κB activation regulates NLRP3 expression in murine macrophages[J].FEBS Letters,2012,586(7):1022-1026.
[21] BOARU S G,BORKHAM-KAMPHORST E,VAN DE LEUR E,et al. NLRP3 inflammasome expression is driven by NF-κB in cultured hepatocytes[J]. Biochemical and Biophysical Research Communications,2015,458(3):700-706.
[22] ORTIZ F,ACUNA-CASTROVIEJO D,DOERRIER C,et al. M elatonin blunts the mitochondrial/NLRP3connection and protects against radiation-induced oral mucositis[J]. Journal of Pineal Research,2015,58(1):34-49.
[23] GARCIA J A,VOLT H,VENEGAS C,et al. Disruption of the NF-κB/NLRP3 connection by melatonin requires retinoid-related orphan receptor-αand blocks the septic response in mice[J].FASEB Journal,2015,29(9):3863-3875.
[24] ZHANG Y,LI X R,GRAILER J J,et al.Melatonin alleviates acute lung injury through inhibiting the NLRP3 inflammasome[J]. Journal of Pineal Research,2016,60(4):405-414.
[25] DONG Y S,FAN C X,HU W,et al.Melatonin attenuated early brain injury induced by subarachnoid hemorrhage via regulating NLRP3 inflammasome and apoptosis signaling[J]. Journal of Pineal Research,2016,60(3):253-262.
[26] KANG J W,KOH E J,LEE S M. Melatonin protects liver against ischemia and reperfusion injury through inhibition of Toll-like receptor signaling pathw ay[J].Journal of Pineal Research,2011,50(4):403-411.
[27] CHUFFA L G A,FIORUCI-FONTANELLI B A,M ENDES L O,et al. M elatonin attenuates the TLR4-mediated inflammatory response through M yD88-and TRIF-dependent signaling pathw ays in an in vivo model of ovarian cancer[J].BM C Cancer,2015,15:34.
[28] BEKYAROVA G,BRATCHKOVA Y,TANCHEVA S,et al.Effective melatonin protection of burn-induced hepatic disorders in rats[J]. Central European Journal of M edicine,2012,7(4):533-538.
[29] MUXEL S M,PIRES-LAPA M A,MONTEIRO A W A,et al. NF-κB drives the synthesis of melatonin in RAW 264. 7 macrophages by inducing the transcription of the arylalkylamine-N-acetyltransferase(AANAT)gene[J].PLoS One,2012,7(12):e52010.
[30] CARRILLO-VICO A,LARDONE P J,ALVAREZSANCHEZ N,et al. M elatonin:buffering the immune system[J]. International Journal of M olecular Sciences,2013,14(4):8638-8683.
[31] MANCHESTER L C,COTO-MONTES A,BOGA J A,et al.M elatonin:an ancient molecule that makes oxygen metabolically tolerable[J]. Journal of Pineal Research,2015,59(4):403-419.
[32] MALDONADO M D, GARCIA-MORENO H,GONZALEZ-YANES C,et al.Possible involvement of the inhibition of NF-κB factor in anti-inflammatory actions that melatonin exerts on mast cells[J].Journal of Cellular Biochemistry,2016,117(8):1926-1933.
[33] AKASHI M,TAKUMI T.The orphan nuclear receptor RORαregulates circadian transcription of the mammalian core-clock Bmal1[J].Nature Structural&M olecular Biology,2005,12(5):441-448.
[34] CRUMBLEY C,WANG Y J,KOJETIN D J,et al.Characterization of the core mammalian clock component,NPAS2,as a REV-ERBα/RORαtarget gene[J].Journal of Biological Chemistry,2010,285(46):35386-35392.
[35] SPENGLER M L,KUROPATWINSKI K K,COMAS M,et al. Core circadian protein CLOCK is a positive regulator of NF-κB-mediated transcription[J]. Proceedings of the National Academy of Sciences of the United States of America,2012,109(37):E2457-E2465.
[36] RAHIM I,DJERDJOURI B,SAYED R K,et al.Melatonin administration to w ild-type mice and nontreated NLRP3 mutant mice share similar inhibition of the inflammatory response during sepsis[J]. Journal of Pineal Research,2017,63(1):e12410.
[37] ACUNACA-STROVIEJO D, REITER R J,M ENENDEZ-PELAEZ A,et al. Characterization of high-affinity melatonin binding sites in purified cell nuclei of rat liver[J]. Journal of Pineal Research,1994,16(2):100-112.
[38] WIESENBERG I,MISSBACH M,CARLBERG C.The potential role of the transcription factor RZR/ROR as a mediator of nuclear melatonin signaling[J].Restorative Neurology&Neuroscience,1998,12(2/3):143-150.
[39] BROOM L J,KOGUT M H. Inflammation:friend or foe for animal production?[J]. Poultry Science,2017,97(2):510-514.
[40] JIANG Z,SCHATZMAYR G,MOHNL M,et al. Net effect of an acute phase response-partial alleviation w ith probiotic supplementation[J]. Poultry Science,2010,89(1):28-33.
[41] CHANDRA R K. Nutrition and the immune system[J]. Proceedings of the Nutrition Society,1993,52(1):77-84.
[42] LABUSSIERE E,DUBOIS S,GILBERT H,et al.Effect of inflammation stimulation on energy and nutrient utilization in piglets selected for low and high residual feed intake[J].Animal,2015,9(10):1653-1661.
[43] BALLINGER B A,AZOOZ O,EL-HAJ T,et al.Grow th failure occurs through a decrease in insulinlike grow th factor 1 w hich is independent of undernutrition in a rat model of colitis[J]. Gut,2000,46(5):695-700.
[44] SAWCZENKO A,AZOOZ O,PARASZCZUK J,et al. Intestinal inflammation-induced grow th retardation acts through IL-6 in rats and depends on the-174 IL-6G/C polymorphism in children[J].Proceedings of the National Academy of Sciences of the United States of America,2005,102(37):13260-13265.
[45] CONNOR E E,BALDWIN R L,BLANTON J R,Jr,et al. Grow th and development symposium:understanding and mitigating the impacts of inflammation on animal grow th and development[J].Journal of Animal Science,2012,90(5):1436-1437.
[46] SANDBERG F B,EMMANS G C,KYRIAZAKIS I.The effects of pathogen challenges on the performance of nave and immune animals:the problem of prediction[J].Animal,2007,1(1):67-86.
[47] WEBEL D M,JOHNSON R W,BAKER D H. Lipopolysaccharide-induced reductions in food intake do not decrease the efficiency of lysine and threonine utilization for protein accretion in chickens[J].The Journal of Nutrition,1998,128(10):1760-1766.