Mastitis and Fertility in Cattle – Possible Involvement of Inflammation or Immune Activation in Embryonic Mortality*

American Journal of Reproductive Immunology - Tập 51 Số 4 - Trang 294-301 - 2004
Peter J. Hansen1, Paolete Soto1, R.P. Natzke1
1Department of Animal Sciences, University of Florida, Gainesville, FL, USA

Tóm tắt

Causes for pre‐implantation embryo loss, which can be as high as 50% or more of fertilized embryos, are multifactorial and largely undescribed. Studies in cattle using mastitis as a model indicate that one cause of early embryonic loss is infectious disease or activation of immune responses at sites outside the reproductive tract. Infection of the mammary gland in dairy cattle is associated with a reduction in pregnancy rate (proportion of inseminated cows that become pregnant) and an increase in the number of inseminations required to establish pregnancy. Also, intravenous challenge with bacterial peptidoglycan and polysaccharide at ∼days 3–5 after breeding reduced subsequent pregnancy rate in sheep that had been previously immunized against the same material. The mechanism by which extrauterine activation of immune and inflammatory responses leads to embryonic loss is not clear although cytokines probably play a crucial role. Effects could be exerted at the level of the hypothalamic–pituitary axis, ovary, reproductive tract or embryo. Interferon (IFN)‐α, for example, which can reduce pregnancy rate in cattle when injected around 13–19 days after breeding, increases body temperature, inhibits secretion of luteinizing hormone, and reduces circulating concentrations of progesterone. Other cytokines or products of cytokine activation could cause embryonic loss by causing hyperthermia (as elevated temperature blocks oocyte function and embryonic development), exerting toxic effects on the corpus luteum [for example, IFN‐γ, tumor necrosis factor‐α (TNF‐α) and prostaglandin F2α], stimulating endometrial prostaglandin synthesis [TNF‐α and interleukin(IL)‐1β], reducing endometrial cell proliferation (IL‐1β), and interfering with oocyte maturation and embryonic development (TNF‐α, nitric oxide, and prostaglandin F2α). Although largely neglected by reproductive immunologists, study of the involvement of the immune system in pre‐implantation embryonic loss is likely to lead to new methods for enhancing fertility.

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Tài liệu tham khảo

Kline J, 1989, Conception to Birth Epidemiology of Prenatal Development

10.1017/S1357729800051845

10.3168/jds.S0022-0302(01)70207-X

10.3168/jds.S0022-0302(98)75690-5

10.3168/jds.S0022-0302(01)70172-5

Holaskova I, 2002, Effect of peptidoglycan‐polysacharide complex (PG‐PS) of streptococcal cell wall on reproductive efficiency and mastitis in sheep, Am J Reprod Immunol, 47, 361

10.1016/0378-4320(89)90045-6

10.1016/0093-691X(88)90169-0

10.3168/jds.S0022-0302(93)77629-8

10.1002/(SICI)1098-2795(199702)46:2<138::AID-MRD4>3.0.CO;2-R

10.1002/mrd.90017

10.2527/jas1963.223713x

10.1016/S0093-691X(99)91889-7

10.3168/jds.S0022-0302(02)74086-1

10.3168/jds.S0022-0302(01)74568-7

10.1053/rvsc.2001.0514

10.1016/S0739-7240(00)00079-5

10.1017/S0022029900004489

10.1016/S0034-5288(02)00147-9

10.1016/S0034-5288(97)90209-5

10.1292/jvms.63.675

10.2527/1999.7792523x

10.3168/jds.S0022-0302(02)74246-X

10.3168/jds.S0022-0302(99)75512-8

Giri SN, 1984, Role of prostaglandins in pathogenesis of bovine mastitis induced by Escherichia coli endotoxin, Am J Vet Res, 45, 586

10.1016/S0378-4320(99)00089-5

10.1034/j.1600-0897.2003.00101.x

10.1210/en.134.1.206

10.1095/biolreprod60.2.479

Pampfer S, 1997, Increased cell death in rat blastocyst exposed to maternal diabetes in utero and to high glucose or tumor necrosis factor‐α in vitro, Development, 124, 4827, 10.1242/dev.124.23.4827

10.1111/j.8755-8920.2001.450602.x

10.1095/biolreprod54.3.531

10.1016/S0090-6980(98)00063-X

10.1034/j.1600-0897.2003.00085.x

Fazio RA, 1997, Embryonic development of frozen‐thawed bovine embryos cultured in vitro in response to elevated concentrations of prostaglandin F2α, Biol Reprod, 56, 187 (abstract)

10.1002/(SICI)1098-2795(199805)50:1<45::AID-MRD6>3.0.CO;2-X

10.1002/1098-2795(200103)58:3<262::AID-MRD3>3.0.CO;2-8

10.1016/S0015-0282(01)01780-0

10.1146/annurev.pharmtox.39.1.191

10.1095/biolreprod62.5.1116

10.1071/RD9951037

10.1016/S0090-6980(98)00050-1

10.1159/000016347

10.3168/jds.S0022-0302(90)78713-9

10.1016/0093-691X(90)90541-Z

10.1055/s-2007-1002160

10.1111/j.1749-6632.2000.tb05368.x

10.1677/joe.0.1330175

10.3168/jds.S0022-0302(82)82303-5

10.1095/biolreprod29.1.25

10.1210/endo-112-5-1782

Peter AT, 1989, Suppression of preovulatory luteinizing hormone surges in heifers after intrauterine infusions of Escherichia coli endotoxin, Am J Vet Res, 50, 368

10.1016/0890-6238(94)00068-9

10.1016/S0739-7240(01)00098-4

10.1095/biolreprod50.1.38

10.1095/biolreprod44.2.357

10.1530/rep.0.1210753

10.1055/s-2000-12567

Kauma SW, 2000, Cytokines in implantation, J Reprod Fertil Suppl, 55, 31

10.1126/science.1071601

Thatcher WW, 1995, Maternal recognition of pregnancy, J Reprod Fertil Suppl, 49, 15

10.1210/endo-122-5-2342

10.2527/1992.7051471x

10.3168/jds.S0022-0302(90)79042-X

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American Journal of Reproductive Immunology

Tập 51 Số 4

294-301

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