山羊TNF和PTPRT基因变异的检测及其与布鲁氏菌病感染风险的相关性

IF 3.7 3区医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Cytokine Pub Date : 2025-03-20 DOI:10.1016/j.cyto.2025.156913

Zhengxuan Zhang , Congliang Wang , Minying Ju , Zhaofei Ren , Xiaoyu Liu , Yanyan Li , Xiaomin Du , Rongrong Li , Wangye Liu , Haijing Zhu

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引用次数: 0

摘要

布鲁氏菌是一种胞内兼性球虫，可引起布鲁氏菌病，对畜牧业和公共卫生构成重大威胁，筛选与布鲁氏菌病抗性相关的候选基因被认为是控制该病传播和感染的有效策略。在此背景下，我们检测了陕北白绒山羊（SWBC）体内肿瘤坏死因子（TNF）和蛋白酪氨酸磷酸酶受体T（PTPRT）基因的InDel基因变异，并分析了其多态性与山羊感染布鲁氏菌病风险的相关性。结果表明，TNF rs6691919和PTPRT rs639317914位点在所研究的山羊群体中存在多态性。这两个位点都出现了 13 bp 的 InDel 缺失，并产生了三种基因型：插入/插入（II）、插入/缺失（ID）和缺失/缺失（DD），其中 II 基因型和 I 等位基因出现的频率较高。多态性信息含量（PIC）值表明，两个 InDel 变异位点都具有中等程度的多态性（0.25 0.05）。生物信息学分析表明，rs6691919 和 rs639317914 位点分别与转录因子上游转录因子 1（USF1）和 Nescient helix-loop-helix 1（NHLH1）特异性结合。总之，我们的研究结果表明，TNF rs6691919 和 PTPRT rs639317914 位点的多态性不会影响山羊对布氏杆菌病的抵抗力。然而，研究这些多态位点与转录因子的特异性结合可能是探索家畜布鲁氏菌病抗性机制的一个新途径。

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Detection of genetic variants in TNF and PTPRT genes in goats and correlation with the risk of brucellosis infections

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Detection of genetic variants in TNF and PTPRT genes in goats and correlation with the risk of brucellosis infections

Brucella, an intracellular facultative coccidia, causes brucellosis, which poses a significant threat to livestock farming and public health, and screening for candidate genes associated with resistance to brucellosis is considered an effective strategy for controlling the transmission and infection of this disease. In this context, we detected InDel genetic variants of the tumor necrosis factor (TNF) and protein tyrosine phosphatase receptor T (PTPRT) genes in the Shaanbei White Cashmere (SWBC) goat and analyzed the correlation between their polymorphisms and the risk of brucellosis infection in goats. The results indicated that the TNF rs669191919 and PTPRT rs639317914 loci were polymorphic in the examined goat populations. Both loci exhibited a 13 bp InDel deletion and resulted in three genotypes: insertion/insertion (II), insertion/deletion (ID), and deletion/deletion (DD), with II genotypes and I alleles occurring at higher frequencies. The polymorphism information content (PIC) values suggested that both InDel variant loci were moderately polymorphic (0.25 < PIC <0.50). Furthermore, association analysis revealed that none of the four established genetic models codominant, dominant, recessive, and allele showed an association between the polymorphisms at the rs669191919 and rs639317914 loci and the risk of brucellosis in goats (P > 0.05). Bioinformatics analyses indicated that the rs669191919 and rs639317914 loci specifically bind to the transcription factors upstream transcription factor 1 (USF1) and nescient helix-loop-helix 1 (NHLH1), respectively. In summary, our findings suggest that polymorphisms at the TNF rs669191919 and PTPRT rs639317914 loci do not influence resistance to brucellosis in goats. However, investigations into the specific binding of these polymorphic loci to transcription factors may represent a novel avenue for exploring the mechanisms underlying resistance to brucellosis in livestock.

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来源期刊

Cytokine 医学-免疫学

CiteScore

7.60

自引率

2.60%

发文量

262

审稿时长

48 days

期刊介绍： The journal Cytokine has an open access mirror journal Cytokine: X, sharing the same aims and scope, editorial team, submission system and rigorous peer review. * Devoted exclusively to the study of the molecular biology, genetics, biochemistry, immunology, genome-wide association studies, pathobiology, diagnostic and clinical applications of all known interleukins, hematopoietic factors, growth factors, cytotoxins, interferons, new cytokines, and chemokines, Cytokine provides comprehensive coverage of cytokines and their mechanisms of actions, 12 times a year by publishing original high quality refereed scientific papers from prominent investigators in both the academic and industrial sectors. We will publish 3 major types of manuscripts: 1) Original manuscripts describing research results. 2) Basic and clinical reviews describing cytokine actions and regulation. 3) Short commentaries/perspectives on recently published aspects of cytokines, pathogenesis and clinical results.