Research advances in role of inflammasome in traumatic brain injury

doi:10.3877/cma.j.issn.2095-123X.2024.03.009

Abstract

Abstract:

Traumatic brain injury (TBI) is characterized by high incidence, high disability and high mortality. Neuroinflammatory response plays an important role in the pathological process of secondary brain injury. Moderate neuroinflammatory response can promote the removal of cell debris after tissue injury and accelerate the repair of injured neurons, but excessive neuroinflammatory response can also aggravate cell injury and lead to neurological symptoms and neurodegeneration. The inflammasome is a protease complex that is an important component of the neuroinflammatory response. In recent years, with the deepening of the research on inflammasome, inflammasome has been considered as a potential biomarker and therapeutic target for TBI. This review focuses on the role of inflammasome in TBI and its potential as a new generation biomarker and therapeutic target in TBI.

Key words: Inflammasome, Traumatic brain injury, Pyroptosis, Biomarkers, Therapeutic targets

Yan Wang, Haiqian Liang, Shanshan Guo. Research advances in role of inflammasome in traumatic brain injury[J]. Chinese Journal of Brain Diseases and Rehabilitation(Electronic Edition), 2024, 14(03): 177-181.

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References 43

[1]	Wanner IB, Anderson MA, Song B, et al. Glial scar borders are formed by newly proliferated, elongated astrocytes that interact to corral inflammatory and fibrotic cells via STAT3-dependent mechanisms after spinal cord injury[J]. J Neurosci, 2013, 33(31): 12870-12886. DOI: 10.1523/jneurosci.2121-13.2013.
[2]	阎朝龙,闫惠颖. NLRP3炎性小体在创伤性脑损伤中的作用[J].医学研究生学报, 2021, 34(4): 418-423. DOI: 10.16571/j.cnki.1008-8199.2021.04.017.
[3]	Bayen E, Ruet A, Jourdan C, et al. Lawsuit and traumatic brain injury: the relationship between long-lasting sequelae and financial compensation in litigants. Results from the PariS-TBI study[J]. Front Neurol, 2019, 10: 320. DOI: 10.3389/fneur.2019.00320.
[4]	Lozano D, Gonzales-Portillo GS, Acosta S, et al. Neuroinflammatory responses to traumatic brain injury: etiology, clinical consequences, and therapeutic opportunities[J]. Neuropsychiatr Dis Treat, 2015, 11: 97-106. DOI: 10.2147/ndt.S65815.
[5]	Simon DW, McGeachy MJ, Bayır H, et al. The far-reaching scope of neuroinflammation after traumatic brain injury[J]. Nat Rev Neurol, 2017, 13(3): 171-191. DOI: 10.1038/nrneurol.2017.13.
[6]	McKee CA, Lukens JR. Emerging roles for the immune system in traumatic brain injury[J]. Front Immunol, 2016, 7: 556. DOI: 10.3389/fimmu.2016.00556.
[7]	Donat CK, Scott G, Gentleman SM, et al. Microglial activation in traumatic brain injury[J]. Front Aging Neurosci, 2017, 9: 208. DOI: 10.3389/fnagi.2017.00208.
[8]	宋鸽,刘晓银,史新宇,等.创伤性脑损伤相关神经炎症的研究进展[J].天津医药, 2020, 48(5): 449-454. DOI: 10.11958/20193631.
[9]	Brown GC, Vilalta A, Fricker M. Phagoptosis-cell death by phagocytosis-plays central roles in physiology, host defense and pathology[J]. Curr Mol Med, 2015, 15(9): 842-851. DOI: 10.2174/156652401509151105130628.
[10]	Rathbone AT, Tharmaradinam S, Jiang S, et al. A review of the neuro- and systemic inflammatory responses in post concussion symptoms: introduction of the "post-inflammatory brain syndrome" PIBS[J]. Brain Behav Immun, 2015, 46: 1-16. DOI: 10.1016/j.bbi.2015.02.009.
[11]	Collins-Praino LE, Corrigan F. Does neuroinflammation drive the relationship between tau hyperphosphorylation and dementia development following traumatic brain injury?[J]. Brain Behav Immun, 2017, 60: 369-382. DOI: 10.1016/j.bbi.2016.09.027.
[12]	Malik A, Kanneganti TD. Inflammasome activation and assembly at a glance[J]. J Cell Sci, 2017, 130(23): 3955-3963. DOI: 10.1242/jcs.207365.
[13]	Bauernfried S, Scherr MJ, Pichlmair A, et al. Human NLRP1 is a sensor for double-stranded RNA[J]. Science, 2021, 371(6528): eabd0811. DOI: 10.1126/science.abd0811.
[14]	Chavarría-Smith J, Vance RE. The NLRP1 inflammasomes[J]. Immunol Rev, 2015, 265(1): 22-34. DOI: 10.1111/imr.12283.
[15]	陶丙岩,刘羽阳,张泽瀚,等. NLRP3、AIM2炎症小体在创伤性脑损伤中作用的研究进展[J].解放军医学院学报, 2022, 43(9): 993-997. DOI: 10.3969/j.issn.2095-5227.2022.09.015.
[16]	Broz P, Dixit VM. Inflammasomes: mechanism of assembly, regulation and signalling[J]. Nat Rev Immunol, 2016, 16(7): 407-420. DOI: 10.1038/nri.2016.58.
[17]	Sundaram B, Kanneganti TD. Advances in understanding activation and function of the NLRC4 inflammasome[J]. Int J Mol Sci, 2021, 22(3): 1048. DOI: 10.3390/ijms22031048.
[18]	Ghimire L, Paudel S, Jin L, et al. The NLRP6 inflammasome in health and disease[J]. Mucosal Immunol, 2020, 13(3): 388-398. DOI: 10.1038/s41385-020-0256-z.
[19]	Adamczak SE, de Rivero Vaccari JP, Dale G, et al. Pyroptotic neuronal cell death mediated by the AIM2 inflammasome[J]. J Cereb Blood Flow Metab, 2014, 34(4): 621-629. DOI: 10.1038/jcbfm.2013.236.
[20]	Schimmel SJ, Acosta S, Lozano D. Neuroinflammation in traumatic brain injury: a chronic response to an acute injury[J]. Brain Circ, 2017, 3(3): 135-142. DOI: 10.4103/bc.bc_18_17.
[21]	de Rivero Vaccari JP, Lotocki G, Alonso OF, et al. Therapeutic neutralization of the NLRP1 inflammasome reduces the innate immune response and improves histopathology after traumatic brain injury[J]. J Cereb Blood Flow Metab, 2009, 29(7): 1251-1261. DOI: 10.1038/jcbfm.2009.46.
[22]	Silverman WR, de Rivero Vaccari JP, Locovei S, et al. The pannexin 1 channel activates the inflammasome in neurons and astrocytes[J]. J Biol Chem, 2009, 284(27): 18143-18151. DOI: 10.1074/jbc.M109.004804.
[23]	Liu HD, Li W, Chen ZR, et al. Expression of the NLRP3 inflammasome in cerebral cortex after traumatic brain injury in a rat model[J]. Neurochem Res, 2013, 38(10): 2072-2083. DOI: 10.1007/s11064-013-1115-z.
[24]	Irrera N, Pizzino G, Calò M, et al. Lack of the Nlrp3 inflammasome improves mice recovery following traumatic brain injury[J]. Front Pharmacol, 2017, 8: 459. DOI: 10.3389/fphar.2017.00459.
[25]	孙硕,何鑫.创伤性脑损伤与神经炎性反应[J].中国微侵袭神经外科杂志, 2020, 25(5): 232-235. DOI: 10.11850/j.issn.1009-122X.2020.05.012.
[26]	Du H, Li CH, Gao RB, et al. Ablation of GSDMD attenuates neurological deficits and neuropathological alterations after traumatic brain injury[J]. Front Cell Neurosci, 2022, 16: 915969. DOI: 10.3389/fncel.2022.915969.
[27]	Liu W, Chen Y, Meng J, et al. Ablation of caspase-1 protects against TBI-induced pyroptosis in vitro and in vivo[J]. J Neuroinflammation, 2018, 15(1): 48. DOI: 10.1186/s12974-018-1083-y.
[28]	Kwan J, Horsfield G, Bryant T, et al. IL-6 is a predictive biomarker for stroke associated infection and future mortality in the elderly after an ischemic stroke[J]. Exp Gerontol, 2013, 48(9): 960-965. DOI: 10.1016/j.exger.2013.07.003.
[29]	Cyr B, Hadad R, Keane RW, et al. The role of non-canonical and canonical inflammasomes in inflammaging[J]. Front Mol Neurosci, 2022, 15: 774014. DOI: 10.3389/fnmol.2022.774014.
[30]	Korley FK, Jain S, Sun X, et al. Prognostic value of day-of-injury plasma GFAP and UCH-L1 concentrations for predicting functional recovery after traumatic brain injury in patients from the US TRACK-TBI cohort: an observational cohort study[J]. Lancet Neurol, 2022, 21(9): 803-813. DOI: 10.1016/s1474-4422(22)00256-3.
[31]	O'Brien WT, Pham L, Symons GF, et al. The NLRP3 inflammasome in traumatic brain injury: potential as a biomarker and therapeutic target[J]. J Neuroinflammation, 2020, 17(1): 104. DOI: 10.1186/s12974-020-01778-5.
[32]	Pérez-Bárcena J, Crespí C, Frontera G, et al. Levels of caspase-1 in cerebrospinal fluid of patients with traumatic brain injury: correlation with intracranial pressure and outcome[J]. J Neurosurg, 2020, 134(5): 1644-1649. DOI: 10.3171/2020.2.Jns193079.
[33]	Kerr N, Lee SW, Perez-Barcena J, et al. Inflammasome proteins as biomarkers of traumatic brain injury[J]. PLoS One, 2018, 13(12): e0210128. DOI: 10.1371/journal.pone.0210128.
[34]	Johnson NH, Hadad R, Taylor RR, et al. Inflammatory biomarkers of traumatic brain injury[J]. Pharmaceuticals (Basel), 2022, 15(6): 660. DOI: 10.3390/ph15060660.
[35]	张芮筝,栾永,宋辛叶.创伤性脑损伤相关生物标志物的研究进展[J].大连医科大学学报, 2022, 44(6): 523-528. DOI: 10.11724/jdmu.2022.06.09.
[36]	de Rivero Vaccari JP, Dietrich WD, Keane RW. Therapeutics targeting the inflammasome after central nervous system injury[J]. Transl Res, 2016, 167(1): 35-45. DOI: 10.1016/j.trsl.2015.05.003.
[37]	崔刚,王德亮,付茂武,等.创伤性脑损伤后鼠脑内RHO/ROCK信号通路与神经炎症反应及病理性损伤关系的研究[J].中华神经创伤外科电子杂志, 2022, 8(6): 324-328. DOI: 10.3877/cma.j.issn.2095-9141.2022.06.002.
[38]	Zahid A, Li B, Kombe AJK, et al. Pharmacological inhibitors of the NLRP3 inflammasome[J]. Front Immunol, 2019, 10: 2538. DOI: 10.3389/fimmu.2019.02538.
[39]	Coll RC, Hill JR, Day CJ, et al. MCC950 directly targets the NLRP3 ATP-hydrolysis motif for inflammasome inhibition[J]. Nat Chem Biol, 2019, 15(6): 556-559. DOI: 10.1038/s41589-019-0277-7.
[40]	Dempsey C, Rubio Araiz A, Bryson KJ, et al. Inhibiting the NLRP3 inflammasome with MCC950 promotes non-phlogistic clearance of amyloid-β and cognitive function in APP/PS1 mice[J]. Brain Behav Immun, 2017, 61: 306-316. DOI: 10.1016/j.bbi.2016.12.014.
[41]	Sun Z, Nyanzu M, Yang S, et al. VX765 attenuates pyroptosis and HMGB1/TLR4/NF-κB pathways to improve functional outcomes in TBI mice[J]. Oxid Med Cell Longev, 2020, 2020: 7879629. DOI: 10.1155/2020/7879629.
[42]	Kerr NA, de Rivero Vaccari JP, Abbassi S, et al. Traumatic brain injury-induced acute lung injury: evidence for activation and inhibition of a neural-respiratory-inflammasome axis[J]. J Neurotrauma, 2018, 35(17): 2067-2076. DOI: 10.1089/neu.2017.5430.
[43]	Lee SW, de Rivero Vaccari JP, Truettner JS, et al. The role of microglial inflammasome activation in pyroptotic cell death following penetrating traumatic brain injury[J]. J Neuroinflammation, 2019, 16(1): 27. DOI: 10.1186/s12974-019-1423-6.

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