Lipid Peroxidation and Antioxidant System in Erythrocytes of Brucella Vaccinated and Challenged Goats

Amit Kumar, V. Gupta, A. Verma, M. Rajesh, Il., A. Rahal, S. Yadav
{"title":"Lipid Peroxidation and Antioxidant System in Erythrocytes of Brucella Vaccinated and Challenged Goats","authors":"Amit Kumar, V. Gupta, A. Verma, M. Rajesh, Il., A. Rahal, S. Yadav","doi":"10.15406/IJVV.2017.04.00092","DOIUrl":null,"url":null,"abstract":"Brucellosis is a reemerging worldwide zoonotic disease and the occurrence of the disease in humans is largely dependent on the animal reservoir [1]. In human it is mainly caused by Brucella melitensis. The highest rate of human infection is mainly in those areas where rates of brucellosis in sheep and goats are high [2,3] as sheep and goats are main reservoir of B. melitensis [4]. The prevention and control of B. melitensis in sheep and goats can be the best fitted model to control human brucellosis. For the purpose it is important to understand the patho-physiological interface involved in the course of disease in sheep or goats as virulence of Brucella species varies according to species, strain and the number of brucellae in inoculums [5,6]. Moreover, being intra cellular parasite, the pathogenic potential of Brucella spp. is highly dependent on its ability to enter and survive within host cells particularly polymorphonuclear cells and macrophages [7]. Further for the survival of Brucella spp. in the harsh environmental stress encountered in route of entry to their replicative niche, include interactive reactive oxygen species, acidic pH, and nutrient deprivation as a key determinant of Brucella virulence [8,9]. The capacity of Brucella to induce disease is dependent on their ability to overcome host cellular response and to replicate within both host phagocytes [10]. In general the intracellular environment of any phagocytic cells is potentially hostile for microbes and, threat their viability by oxidative (MyeloperoxidaseH2O2halide) or non-oxidative (cationic protein, lysozyme, lactoferritin and proteases [11]. Depending upon the type of adjuvants or immunomodulators used in any vaccine macrophages and dendritic cells are recruited and activated for antigen processing to generate free reactive radicals resulting in inflammatory sequelae [12]. Superoxide dismutase (SOD), Catalase, and glutathione peroxidase are integral part of intracellular defense systems and antioxidant mechanism [13]. Cytotoxic effects of oxidants involve DNA damage, protein oxidation, lipid peroxidation with inhibition of cellular metabolic pathways [12]. The establishment of Brucella infection has been correlated with induced oxidative stress and lipid peroxidation in human [8], mice [11]; cattle [14]; rat [15] and in pregnant goats [16]. Thus the aim of the present study was to assess erythrocyte redox parameters viz., lipid peroxidation, Glutathion (GSH) formation and activity of catalase, SOD and Glutathion-STransferase (GST) in clinically healthy goats during Rev.1 vaccination and challenge.","PeriodicalId":17656,"journal":{"name":"Journal of Vaccines and Vaccination","volume":"99 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2017-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"7","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Vaccines and Vaccination","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15406/IJVV.2017.04.00092","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 7

Abstract

Brucellosis is a reemerging worldwide zoonotic disease and the occurrence of the disease in humans is largely dependent on the animal reservoir [1]. In human it is mainly caused by Brucella melitensis. The highest rate of human infection is mainly in those areas where rates of brucellosis in sheep and goats are high [2,3] as sheep and goats are main reservoir of B. melitensis [4]. The prevention and control of B. melitensis in sheep and goats can be the best fitted model to control human brucellosis. For the purpose it is important to understand the patho-physiological interface involved in the course of disease in sheep or goats as virulence of Brucella species varies according to species, strain and the number of brucellae in inoculums [5,6]. Moreover, being intra cellular parasite, the pathogenic potential of Brucella spp. is highly dependent on its ability to enter and survive within host cells particularly polymorphonuclear cells and macrophages [7]. Further for the survival of Brucella spp. in the harsh environmental stress encountered in route of entry to their replicative niche, include interactive reactive oxygen species, acidic pH, and nutrient deprivation as a key determinant of Brucella virulence [8,9]. The capacity of Brucella to induce disease is dependent on their ability to overcome host cellular response and to replicate within both host phagocytes [10]. In general the intracellular environment of any phagocytic cells is potentially hostile for microbes and, threat their viability by oxidative (MyeloperoxidaseH2O2halide) or non-oxidative (cationic protein, lysozyme, lactoferritin and proteases [11]. Depending upon the type of adjuvants or immunomodulators used in any vaccine macrophages and dendritic cells are recruited and activated for antigen processing to generate free reactive radicals resulting in inflammatory sequelae [12]. Superoxide dismutase (SOD), Catalase, and glutathione peroxidase are integral part of intracellular defense systems and antioxidant mechanism [13]. Cytotoxic effects of oxidants involve DNA damage, protein oxidation, lipid peroxidation with inhibition of cellular metabolic pathways [12]. The establishment of Brucella infection has been correlated with induced oxidative stress and lipid peroxidation in human [8], mice [11]; cattle [14]; rat [15] and in pregnant goats [16]. Thus the aim of the present study was to assess erythrocyte redox parameters viz., lipid peroxidation, Glutathion (GSH) formation and activity of catalase, SOD and Glutathion-STransferase (GST) in clinically healthy goats during Rev.1 vaccination and challenge.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
布氏菌免疫和攻毒山羊红细胞脂质过氧化和抗氧化系统的研究
布鲁氏菌病是一种在世界范围内再次出现的人畜共患疾病,该疾病在人类中的发生在很大程度上取决于动物宿主[1]。人类主要由布鲁氏菌引起。人类感染率最高的地区主要是绵羊和山羊布鲁氏菌病发病率高的地区[2,3],因为绵羊和山羊是山羊布鲁氏菌的主要宿主[4]。绵羊和山羊的梅利特白杆菌的预防和控制可以作为控制人类布鲁氏菌病的最佳模型。为此,了解绵羊或山羊疾病过程中涉及的病理生理界面是很重要的,因为布鲁氏菌的毒力根据接种的布鲁氏菌的种类、菌株和数量而变化[5,6]。此外,作为细胞内寄生虫,布鲁氏菌的致病潜力高度依赖于其进入宿主细胞,特别是多形核细胞和巨噬细胞内存活的能力[7]。此外,布鲁氏菌在进入其繁殖生态位的过程中遇到的恶劣环境胁迫下的生存,包括相互作用的活性氧、酸性pH和营养剥夺,这是布鲁氏菌毒力的关键决定因素[8,9]。布鲁氏菌诱导疾病的能力取决于其克服宿主细胞反应和在宿主吞噬细胞内复制的能力[10]。一般来说,任何吞噬细胞的细胞内环境对微生物都是潜在的敌对环境,并通过氧化(髓过氧化物酶eh2o2卤化物)或非氧化(阳离子蛋白、溶菌酶、乳铁蛋白和蛋白酶)威胁微生物的生存能力[11]。根据任何疫苗中使用的佐剂或免疫调节剂的类型,巨噬细胞和树突状细胞被招募和激活,进行抗原加工,产生游离活性自由基,导致炎症后遗症[12]。超氧化物歧化酶(SOD)、过氧化氢酶和谷胱甘肽过氧化物酶是细胞内防御系统和抗氧化机制的重要组成部分[13]。氧化剂的细胞毒性作用包括DNA损伤、蛋白质氧化、脂质过氧化以及细胞代谢途径的抑制[12]。在人[8]、小鼠[11]中,布鲁氏菌感染的建立与诱导的氧化应激和脂质过氧化有关;牛[14];大鼠[15]和怀孕山羊[16]。因此,本研究的目的是评估临床健康山羊在Rev.1疫苗接种和攻击期间红细胞氧化还原参数,即脂质过氧化,谷胱甘肽(GSH)形成以及过氧化氢酶,SOD和谷胱甘肽转移酶(GST)的活性。
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 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Differential Transcription Profiling in Bone Marrow Mononuclear Cells Between Myasthenia Gravis Patients With or Without Thymoma Rapid screening for variants of concern in routine SARS-CoV-2 PCR diagnostics Mast Cells and COVID-19: a case report implicating a role of mast cell activation in the prevention and treatment of Covid-19 Evaluating Child Malnutrition in Southern Belize Using an Anthropologic Screening Tool Sero-prevalence and risk factors for sheeppox in Kordofan states in Sudan
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1