Features of humoral immunity in patients with mild traumatic brain injury

A. O. Norka, S. Vorobyev, R. Kuznetsova, M. Serebriakova, I. Kudryavtsev, S. N. Kovalenko, D. N. Monashenko, Z. Korobova
{"title":"Features of humoral immunity in patients with mild traumatic brain injury","authors":"A. O. Norka, S. Vorobyev, R. Kuznetsova, M. Serebriakova, I. Kudryavtsev, S. N. Kovalenko, D. N. Monashenko, Z. Korobova","doi":"10.46235/1028-7221-1182-foh","DOIUrl":null,"url":null,"abstract":"Traumatic brain injury (TBI) is an important problem of the healthcare system. A lPeading role in pathogenesis belongs to the action of shock wave upon skull and brain integuments, extending from the impacted site, as well as displacement and rotation of the cerebral hemispheres relative to the fixed brain stem. As a result, a cascade of metabolic, biochemical and inflammatory changes is initiated, leading to secondary damage. TBI, depending on its mechanism, severity and type, causes various primary structural and functional brain lesions at molecular, cellular, tissue and organ levels with dysregulation of all systems in the body, dependent on its degree and extent. In most cases, the brain injury increases the risk of developing epilepsy and neurodegenerative diseases such as Alzheimers disease, arkinsons disease and chronic traumatic encephalopathy (CTE), with mental health disorders. TBI is a long-term symptomatic process in patients with functional and structural damage. In response to a traumatic event, the damage-associated molecular patterns (DAMPs) encountered upon tissue damage are expressed, which cause activation of the resident brain tissue cells, and secretion of multiple chemokine and cytokine by distinct cell populations. Neutrophils migrate to focal lesions, which remove damaged cells and debris. Migration of T and B cells is observed 3-7 days after the trauma. Hence, following primary injury, due to a cascade of immune reactions, a more extensive lesion, the so-called secondary trauma, is developed. The aim of our study was to evaluate the role of immune response in pathogenesis of mild traumatic brain injury. \nAn increased number of Bm2 cells, IgDdimCD27low naive B cells and B cells with the IgDlowCD27hi (plasmablasts) phenotype was found in patients with mild brain contusion, compared to comparison group. Moreover, the number of naive mature B cells with the CD27lowCD38dim phenotype was significantly decreased compared with the controls.","PeriodicalId":21524,"journal":{"name":"Russian Journal of Immunology","volume":"79 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Russian Journal of Immunology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.46235/1028-7221-1182-foh","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Traumatic brain injury (TBI) is an important problem of the healthcare system. A lPeading role in pathogenesis belongs to the action of shock wave upon skull and brain integuments, extending from the impacted site, as well as displacement and rotation of the cerebral hemispheres relative to the fixed brain stem. As a result, a cascade of metabolic, biochemical and inflammatory changes is initiated, leading to secondary damage. TBI, depending on its mechanism, severity and type, causes various primary structural and functional brain lesions at molecular, cellular, tissue and organ levels with dysregulation of all systems in the body, dependent on its degree and extent. In most cases, the brain injury increases the risk of developing epilepsy and neurodegenerative diseases such as Alzheimers disease, arkinsons disease and chronic traumatic encephalopathy (CTE), with mental health disorders. TBI is a long-term symptomatic process in patients with functional and structural damage. In response to a traumatic event, the damage-associated molecular patterns (DAMPs) encountered upon tissue damage are expressed, which cause activation of the resident brain tissue cells, and secretion of multiple chemokine and cytokine by distinct cell populations. Neutrophils migrate to focal lesions, which remove damaged cells and debris. Migration of T and B cells is observed 3-7 days after the trauma. Hence, following primary injury, due to a cascade of immune reactions, a more extensive lesion, the so-called secondary trauma, is developed. The aim of our study was to evaluate the role of immune response in pathogenesis of mild traumatic brain injury. An increased number of Bm2 cells, IgDdimCD27low naive B cells and B cells with the IgDlowCD27hi (plasmablasts) phenotype was found in patients with mild brain contusion, compared to comparison group. Moreover, the number of naive mature B cells with the CD27lowCD38dim phenotype was significantly decreased compared with the controls.
轻度外伤性脑损伤患者体液免疫的特点
创伤性脑损伤(TBI)是医疗卫生系统的一个重要问题。在发病机制中起主导作用的是冲击波对颅骨和脑膜的作用,冲击波从撞击部位向外延伸,以及大脑半球相对于固定脑干的移位和旋转。因此,一系列代谢、生化和炎症变化被启动,导致继发性损伤。TBI根据其机制、严重程度和类型,在分子、细胞、组织和器官水平上引起各种原发性结构和功能性脑损伤,并根据其程度和程度导致体内所有系统失调。在大多数情况下,脑损伤会增加患癫痫和神经退行性疾病的风险,如阿尔茨海默病、阿金森氏病和慢性创伤性脑病(CTE),并伴有精神健康障碍。TBI是功能和结构损伤患者的一个长期症状过程。在对创伤事件的反应中,组织损伤时遇到的损伤相关分子模式(DAMPs)被表达,这导致常驻脑组织细胞的激活,并由不同的细胞群分泌多种趋化因子和细胞因子。中性粒细胞迁移到局灶性病变,清除受损细胞和碎片。外伤后3-7天观察T细胞和B细胞的迁移。因此,在原发性损伤之后,由于免疫反应的级联反应,更广泛的病变,即所谓的继发性创伤,被发展。本研究旨在探讨免疫反应在轻度外伤性脑损伤发病机制中的作用。与对照组相比,轻度脑挫伤患者的Bm2细胞、IgDdimCD27low初始B细胞和IgDlowCD27hi(浆母细胞)表型的B细胞数量增加。此外,与对照组相比,CD27lowCD38dim表型的幼稚成熟B细胞数量显著减少。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
0.40
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信