Relationship of bovine TNF-α gene polymorphisms with the risk of bovine tuberculosis in Holstein cattle

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  • CHENG Yafen
    School of Veterinary Medicine, National Taiwan University, No. 1, Sec. 4, Roosevelt Rd., Taipei 10617, Taiwan Centers for Disease Control, Ministry of Health and Welfare, No. 6, Linsen S. Rd., Taipei 10050, Taiwan
  • HUANG ChenShen
    School of Veterinary Medicine, National Taiwan University, No. 1, Sec. 4, Roosevelt Rd., Taipei 10617, Taiwan Animal Health Research Institute, Council of Agriculture, Executive Yuan, No. 376, Zhongzheng Rd., New Taipei City 25158, Taiwan
  • TSAI Hsiang-Jung
    School of Veterinary Medicine, National Taiwan University, No. 1, Sec. 4, Roosevelt Rd., Taipei 10617, Taiwan Animal Health Research Institute, Council of Agriculture, Executive Yuan, No. 376, Zhongzheng Rd., New Taipei City 25158, Taiwan

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  • Relationship of bovine <i>TNF-α</i> gene polymorphisms with the risk of bovine tuberculosis in Holstein cattle

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Many studies suggest significant genetic variation in the resistance of cattle and humans to infection with Mycobacterium bovis (M. bovis), the causative agent of zoonotic tuberculosis. TNF-α promotes inflammation and induces apoptosis in response to mycobacterial infection. The aim of the present study was to investigate the influence of single nucleotide polymorphisms of the TNF-α gene on bovine tuberculosis (bTB) susceptibility. We genotyped the TNF-α gene in 74 bTB-infected Holstein cows and 90 healthy control animals. The influence in the exon 3 region of TNF-α polymorphisms on bTB susceptibility was subsequently investigated by association analysis. Our finding demonstrated that the g.27534932A>C polymorphism of the TNF-α is associated with bTB in Holstein cattle. The susceptibility of cattle with the g.27534932A>C genotype compared with the CC genotype was 4.11-fold (95% CI, 1.27–13.36; P=0.02) higher. The g.27534932A>C polymorphism located in exon 3 of the TNF-α gene, and the functional consequence was missense. The deduced amino acid sequence for the protein product revealed an arginine to serine conversion at position 159, which may affect initiation of protein synthesis and disrupt normal TNF-α function that protects animals against mycobacterial infection. A significant association was observed with the A allele as a risk factor for bTB susceptibility (OR, 3.84; 95% CI, 1.21–12.17; P=0.02). In conclusion, this is the first report showing that the g.27534932A>C polymorphism may contribute to TNF-α-mediated bTB susceptibility.

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