期刊论文详细信息
BMC Veterinary Research
Parity-dependent association between TNF-α and LTF gene polymorphisms and clinical mastitis in dairy cattle
Tomasz Strabel3  Joanna Szyda2  Katarzyna Wojdak-Maksymiec1 
[1] Faculty of Biotechnology and Husbandry, Department of Animal Genetics and Breeding, West Pomeranian University of Technology in Szczecin, ul. Doktora Judyma 6, 71-466 Szczecin, Poland;Wroclaw University of Environmental and Life Sciences, Kozuchowska 7, 51-631 Wroclaw, Poland;Poznan University of Life Sciences, Wolynska 33, 60-637 Poznan, Poland
关键词: Inflamm-ageing;    Immunity;    Lactoferrin;    Tumor necrosis factor;    Mastitis;   
Others  :  1119524
DOI  :  10.1186/1746-6148-9-114
 received in 2013-04-29, accepted in 2013-06-04,  发布年份 2013
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【 摘 要 】

Background

One major problem in dairy cattle husbandry is the prevalence of udder infections. In today’s breeding programmes, top priority is being given to making animal evaluation more cost-effective and reliable and less time-consuming. We proposed tumor necrosis factor α (TNF-α), lactoferrin (LTF) and macrophage-expressed lysozyme (mLYZ) genes as potential DNA markers in the improvement of immunity to mastitis.

This study included 588 Polish Holstein-Friesian cows kept on one farm located in the north-western region of Poland. All clinical cases of mastitis in the herd under study were recorded by a qualified veterinarian employed by the farm. The following indicators were applied to determine udder immunity to mastitis in the cows under study: morbidity rate (MR), duration of mastitis (DM) and extent of mastitis (EM). TNF-α, mLYZ and LTF genotypes were identified by real-time PCR method, using SimpleProbe technology. Due to the very low frequency of mLYZ allele T, the gene was excluded from further analysis.

A statistical analysis of associations between TNF-α and LTF genes and immunity to mastitis were performed using three models: 1) a parity-averaged model including only additive effects of the genes; 2) a parity-averaged model including both additive and epistatic effects of the genes; and 3) a parity-specific model including only additive effects of the genes.

Results

With the first and second models it was revealed that the genes effects on the applied indicators of immunity to mastitis were non-significant whereas with the third one the effects were found to be statistically significant. Particularly noteworthy was the finding that the effects of TNF-α and LTF varied depending on age (parity). The alleles which were linked to high immunity to mastitis in lower parities appeared to be less favourable in higher parities.

Conclusions

These interactions might be related to inflamm-ageing, that is an increased susceptibility to infection due to immune system deregulation that progresses with age. Such pattern of interactions makes it impossible to use the genes in question in marker-assisted selection aimed at reducing heritable susceptibility to mastitis. This is because the immune mechanisms behind resistance to infections proved to be too complex.

【 授权许可】

   
2013 Wojdak-Maksymiec et al.; licensee BioMed Central Ltd.

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【 参考文献 】
  • [1]Togashi K, Lin CY: Theoretical efficiency of multiple-trait quantitative trait loci-assisted selection. J Anim Breed Genet 2010, 127(1):53-63.
  • [2]Ashwell MS, Heyen DW, Sonstegard TS, Van Tassell CP, Da Y, Van Raden PM, Ron M, Weller JI, Lewin HA: Detection of quantitative trait loci affecting milk production, health, and reproductive traits in Holstein cattle. J Dairy Sci 2004, 87(2):468-475.
  • [3]Sharma BS, Jansen GB, Karrow NA, Kelton D, Jiang Z: Detection and characterization of amplified fragment length polymorphism markers for clinical mastitis in Canadian Holsteins. J Dairy Sci 2006, 89(9):3653-3663.
  • [4]Lund MS, Guldbrandtsen B, Buitenhuis AJ, Thomsen B, Bendixen C: Detection of quantitative trait loci in Danish Holstein cattle affecting clinical mastitis, somatic cell score, udder conformation traits, and assessment of associated effects on milk yield. J Dairy Sci 2008, 91(10):4028-4036.
  • [5]Benedict CA, Banks TA, Ware CF: Death and survival: viral regulation of TNF signaling pathways. Curr Opin Immunol 2003, 15:59-65.
  • [6]Bradley JR: TNF-mediated inflammatory disease. J Pathol, Special Issue: Molecular and cellular themes in inflammation and immunology 2008, 214(2):149-160.
  • [7]Lester DH, Russell GC, Barendse W, Williams JL: The use of gradient gel electrophoresis in mapping the bovine tumor necrosis factor α locus. Mamm Genome 1996, 7:250-252.
  • [8]Bannerman DD: Pathogen-dependent induction of cytokines and other soluble inflammatory mediators during intramammary infection of dairy cows. J Anim Sci 2009, 87(13 suppl):10-25.
  • [9]Orsi N: The antimicrobial activity of lactoferrin: current status and perspectives. Biometals 2004, 17:189-196.
  • [10]Jenssen H, Hancock RE: Antimicrobial properties of lactoferrin. Biochimie 2009, 91(1):19-29.
  • [11]Legrand D, Mazurier J: A critical review of the roles of host lactoferrin in immunity. Biometals 2010, 23(3):365-376.
  • [12]Jabeen T, Sharma S, Singh N, Bhushan A, Singh TP: Structure of the zinc-saturated C-terminal lobe of bovine lactoferrin at 2.0 A resolution. Acta Crystallogr D: Biol Crystallogr 2005, 61(8):107-115.
  • [13]Zimecki M, Artym J, Chodaczek G, Kocięba M, Kruzel ML: Protective effects of lactoferrin in Escherichia coli-induced bacteremia in mice: relationship to reduced serum TNF alpha level and increased turnover of neutrophils. Infl Amm Res 2004, 53:292-296.
  • [14]Ward PP, Uribe-Luna S, Conneely OM: Lactoferrin and host defence. Bioch Cel Biol 2002, 80:95-102.
  • [15]Teng CT: Lactoferrin gene expression and regulation: an overview. Biochem Cell Biol 2002, 80:7-16.
  • [16]Ibrahim HR, Matsuzaki T, Aoki T: Genetic evidence that antibacterial activity of lysozyme is independent of its catalytic function. FEBS Lett 2001, 506:27-32.
  • [17]Ibrahim HR, Thomas U, Pellegrini A: A helix-loop helix peptide at the upper lip of the active site cleft of lysozyme confers potent antimicrobial activity with membrane permeabilization action. J Biol Chem 2001, 276:43767-43774.
  • [18]Imoto T: Lysozyme.   2009,  : .
  • [19]Brunner RM, Henke M, Guérin G, Goldammer T, Seyfert HM, Schwerin M: The macrophage expressed variant of the bovine lysozyme-encoding gene maps to chromosome 5q23. Mamm Genome 1994, 5(12):834.
  • [20]Pareek CS, Seyfert H-M, Walawski K, Pareek RS, Schwerin M: The 5′-promoter and coding region of the macrophage expressed lysozyme encoding-gene do not reveal variants associated with high serum lytic activity in Polish Black-and-White cattle. J Anim Breed Genet 2003, 120:132-136.
  • [21]Gomez CR, Boehmer ED, Kovacs EJ: The aging innate immune system. Curr Opin Immunol 2005, 17:457-462.
  • [22]Effros RB: Genetic alterations in the ageing immune system: impact on infection, and cancer. Mech Ageing Dev 2003, 124:71-77.
  • [23]Franceschi C, Capri M, Monti D, Giunta S, Olivieri F, Sevini F, Panourgia MP, Invidia L, Celani L, Scurti M, Cevenini E, Castellani GC, Salvioli S: Inflammaging and anti-inflammaging: a systemic perspective on aging and longevity emerged from studies in humans. Mech Ageing Dev 2007, 128:92-105.
  • [24]Castle SC: Clinical Relevance of Age-Related Immune Dysfunction. Clin Infect Dis 2000, 31:578-585.
  • [25]Franceschi C, Bonafe M, Valensin S, Olivieri F, De Luca M, Ottaviani E, De Benedictis G: Inflamm-aging. An evolutionary perspective on immunosenescence. Ann NY Acad Sci 2000, 908:244-254.
  • [26]De Martinis M, Franceschi C, Monti D, Ginaldi L: Inflamm-ageing and lifelong antigenic load as major determinants of ageing rate and longevity. FEBS Lett 2005, 579:2035-2039.
  • [27]Fulop T, Larbi A, Wikby A, Mocchegiani E, Hirokawa K, Pawelec G: Dysregulation of T-cell function in the elderly: scientific basis and clinical implications. Drugs Aging 2005, 22:589-603.
  • [28]Petropoulou C, Chondrogianni N, Simőes D, Agiostratidou G, Drosopoulos N, Kotsota V, Gonos ES: Aging and longevity. A paradigm of complementation between homeostatic mechanisms and genetic control? Ann NY Acad Sci 2000, 908:133-142.
  • [29]Gavazzi G, Krause K-H: Ageing and infection. Lancet Infect Dis 2002, 2:659-666.
  • [30]Bjornsson HT, Sigurdsson MI, Fallin MD, Irizarry RA, Aspelund T, Cui H, Yu W, Rongione MA, Ekström TJ, Harris TB, Launer LJ, Eiriksdottir G, Leppert MF, Sapienza C, Gudnason V, Feinberg AP: Intra-individual change over time in DNA methylation with familial clustering. JAMA 2008, 299:2877-2883.
  • [31]Gowers IR, Walters K, Kiss-Toth E, Read RC, Duff GW, Wilson AG: Age-related loss of CpG methylation in the tumour necrosis factor promoter. Cytokine 2011, 56(3):792-797.
  • [32]Larbi A, Franceschi C, Mazzatti D, Solana R, Wikby A, Pawelec G: Aging of the immune system as a prognostic factor for human longevity. Physiology (Bethesda) 2008, 23(2):64-74.
  • [33]Zimecki M, Artym J, Kocieba M: Endogenous steroids are responsible for lactoferrin-induced myelopoiesis in mice. Pharmacol Rep 2009, 61(4):705-710.
  • [34]Actor JK, Hwang S-A, Kruzel ML: Lactoferrin as a natural immune modulator. Current pharmaceutical design. Curr Pharm Des 2009, 15(17):1956-1973.
  • [35]Kruzel ML, Bacsi A, Choudhury B, Sur S, Boldogh I: Lactoferrin decreases pollen antigen-induced allergic airway inflammation in a murine model of asthma. Immunology 2006, 119:159-166.
  • [36]Britigan BE, Lewis TS, Waldschmidt M, McCormick ML, Krieg AM: Lactoferrin binds CpG-containing oligonucleotides and inhibits their immunostimulatory effects on human B cells. J Immunol 2001, 167(5):2921-2928.
  • [37]Carrieri G, Marzi E, Olivieri F, Marchegiani F, Cavallone L, Cardelli M, Giovagnetti S, Stecconi R, Molendini C, Trapassi C, De Benedictis G, Kletsas D, Franceschi C: The G/C915 polymorphism of transforming growth factor beta1 is associated with human longevity: a study in Italian centenarians. Aging Cell 2004, 3:443-448.
  • [38]Lang PO, Mitchell WA, Lapenna A, Pitts D, Aspinall R: Immunological pathogenesis of main age-related diseases and frailty: Role of immunosenescence. Eur Geriatric Med 2010, 1:112-121.
  • [39]Vasto S, Candore G, Balistreri CR, Caruso M, Colonna-Romano G, Grimaldi MP, Listi F, Nuzzo D, Lio D, Caruso C: Inflammatory networks in ageing, age-related diseases and longevity. Mech Ageing Dev 2007, 128:83-91.
  • [40]Franceschi C, Bonafe M, Valensin S: Human immunosenescence: the prevailing of innate immunity, the failing of clonotypic immunity, and the filling of immunological space. Vaccine 2000, 18:1717-1720.
  • [41]Caruso C, Candore G, Colonna-Romano G, Lio D, Franceschi C: Inflammation and life-span. Science 2005, 307:208-209.
  • [42]Wick G, Berger P, Jansen-Durr P, Grubeck-Loebenstein B: A Darwinian-evolutionary concept of age-related diseases. Exp Gerontol 2003, 38:13-25.
  • [43]Crimmins EM, Finch CE: Infection, inflammation, height and longevity. PNAS 2006, 1003:498-503.
  • [44]Seyfert HM, Kühn C: Characterization of a first bovine lactoferrin gene variant, based on an EcoRI polymorphism. Anim Genet 1994, 25:54.
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