Top > JDR > Mouse Model of Abortion Induced by Brucella abortus Infection

single-dr.php

JDR Vol.7 No.3 pp. 313-318
(2012)
doi: 10.20965/jdr.2012.p0313

Review:

Views over last 60 days: 424

Mouse Model of Abortion Induced by Brucella abortus Infection

Masahisa Watarai

The United Graduate School of Veterinary Science, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8515, Japan

Received:
June 17, 2011
Accepted:
December 2, 2011
Published:
April 1, 2012
Creative Commons License
Keywords:
IFN-γ, RANTES, abortion, Brucella abortus, mouse
Abstract
The mechanisms of abortion induced by bacterial infection are largely unknown. We found that Brucella abortus, a causative agent of brucellosis and a facultative intracellular pathogen, caused abortion in pregnant mice. High rates of abortion are observed for bacterial infection on day 4.5 of gestation, but not for other days. Regardless of whether fetuses are aborted or not, the transmission of bacteria to the fetus and bacterial replication in the placenta are observed. There is a higher degree of bacterial colonization in the placenta than in other organs and many bacteria are detected in trophoblast giant cells in the placenta. The intracellular growth-defective virB4 mutant and attenuated vaccine strain S19 do not induce abortion. In the case of abortion, the induction of IFN-γ and RANTES production is observed at day 7.5 of gestation – the placental development period – for infection by the wild type strain but not by the virB4 mutant or S19. B. abortus-infected pregnant IFN-γ knockoutmice die within 15 days of infection, but nonpregnant IFN-γ knockout mice remain alive. The neutralization of IFN-γ or RANTES, in which production is induced by infection with B. abortus serves to prevent abortion. These results indicate that abortion induced by B. abortus infection is regulated by IFN-γ during the period of placental development, and the production and function of RANTES are correlated with IFN-γ.
Cite this article as:
M. Watarai, “Mouse Model of Abortion Induced by Brucella abortus Infection,” J. Disaster Res., Vol.7 No.3, pp. 313-318, 2012.
Data files:
References
  1. [1] M. N. Seleem, S. M. Boyle, and N. Sriranganathan, “Brucellosis: a re-emerging zoonosis,” Veterinary Microbiology, Vol.140, pp. 392-298, 2010.
  2. [2] G. Pappas, “The changing Brucella ecology: novel reservoirs, new threats,” Int. J. of Antimicrobial Agents, Vol.36, Supplement 1, pp. S8-S11, 2010.
  3. [3] F. M. Enright, “The pathogenesis and pathibiology of Brucella infection in domestic animals,” In Animal Brucellosis, K. Nielsen, and J. R. Duncan (Eds.), pp. 301-320. CRC Press, Boca Raton, FL, USA, 1990.
  4. [4] L. Tobias, D. O. Cordes, and G. G. Schurig, “Placental pathology of the pregnant mouse inoculated with Brucella abortus strain 2308,” Veterinary Pathology, Vol.30 pp. 119-129, 1993.
  5. [5] R. A. Ugalde, “Intracellular lifestyle of Brucella spp. common genes with other animal pathogens, plant pathogens, and endosymbionts,” Microbes and Infection, Vol.1 pp. 1211-1219, 1999.
  6. [6] R. M. Roop 2nd, J. M. Gaines, E. S. Anderson, C. C. Caswell, and D. W. Martin, “Survival of the fittest: how Brucella strains adapt to their intracellular niche in the host,” Medical Microbiology and Immunology, Vol.198, pp. 221-238, 2009.
  7. [7] P. J. Christie and J. P. Vogel “Bacterial type IV secretion: conjugation systems adapted to deliver effector molecules to host cells,” Trends in Microbiology, Vol.8, pp. 354-360, 2000.
  8. [8] R. M. Delrue, M. Martinez-Lorenzo, P. Lestrate, I. Danese, V. Bielarz, P. Mertens, X. De Bolle, A. Tibor, J. P. Gorvel, and J. J. Letesson, “Identification of Brucella spp. genes involved in intracellular trafficking,” Cellular Microbiology, Vol.3 pp. 487-497, 2001.
  9. [9] E. D. Weinberg, “Pregnancy-associated immune suppression: risks and mechanisms,” Microbial Pathogenesis, Vol.3, pp. 393-397, 1987.
  10. [10] M. Sano, M. Mitsuyama, Y. Watanabe, and K. Nomoto, “Impairment of T cell-mediated immunity to Listeria monocytogenes in pregnant mice,” Microbiology and Immunology, Vol.30, pp. 165-176, 1986.
  11. [11] Y. Zhan and C. Cheers, “Endogenous gamma interferon mediates resistance to Brucella abortus infection,” Infection and Immunity, Vol.61, pp. 4899-4901, 1993.
  12. [12] M. G. Stevens, G. W. Pugh Jr., and L. B. Tabatabai, “Effects of γ-interferon and indomethacin in preventing Brucella abortus infections in mice,” Infection and Immunity, Vol.60, pp. 4407-4409, 1992.
  13. [13] S. Kim, D. S. Lee, K. Watanabe, H. Furuoka, H. Suzuki, and M. Watarai, “Interferon-γ promotes abortion due to Brucella infection in pregnant mice,” BMC Microbiology, Vol.5, p. 22, 2005.
  14. [14] N. Bosseray and M. Plommet, “Brucella suis S2, Brucella melitensis Rev. 1 and Brucella abortus S19 living vaccines: residual virulence and immunity induced against three Brucella species challenge strains in mice,” Vaccine Vol.8 pp. 462-468, 1990.
  15. [15] H. E. Quinn, J. T. Ellis, and N. C. Smith, “Neospora caninum: a cause of immune-mediated failure of pregnancy?” Trends in Parasitology, Vol.18, pp. 391-394, 2002.
  16. [16] K. Watanabe, N. Iwai, M. Tachibana, H. Furuoka, H. Suzuki, and M. Watarai, “Regulated upon activation normal T-call expressed and secreted (RANTES) contributes to abortion caused by Brucella abortus infection in pregnant mice,” J. of Veterinary Medical Science, Vol.70, pp. 681-686, 2008.
  17. [17] R. Raghupathy, “Th1-type immunity is incompatible with successful pregnancy,” Immunology Today Vol.18, pp. 478-482, 1997.
  18. [18] H. Smith, A. E. Williams, J. H. Pearce, J. Keppie, P. W. Harris-Smith, R. B. Fitz-George, and K. Witt, “Foetal erythritol: a cause of the localization of Brucella abortus in bovine contagious abortion,” Nature Vol.193, pp. 47-49, 1962.
  19. [19] J. Keppie, A. E. Williams, K. Witt, and H. Smith, “The role of erythritol in tissue localization of the brucellae.,” British J. of Experimental Pathology, Vol.46, pp. 104-108, 1965.
  20. [20] M. J. Soares, B. M. Chapman, C. A. Rasmussen, G. Dai, T. Kamei, and K. E. Orwig, “Differentiation of trophoblast endocrine cells,” Placenta Vol.17, pp. 277-289, 1996.
  21. [21] J. C. Cross, “Genetic insights into trophoblast differentiation and placental morphogenesis,” Seminars in Cell and Developmental Biology, Vol. 11, pp. 105-113, 2000.
  22. [22] R. Ain, L. N. Canham, and M. J. Soares, “Gestation stagedependent intrauterine trophoblast cell invasion in the rat and mouse: novel endocrine phenotype and regulation,” Developmental Biology, Vol.260, pp. 176-190, 2003.
  23. [23] T. L. Thirkill, K. Lowe, H. Vedagiri, T. N. Blankenship, A. Barakat, and G. Douglas, “Macaque trophoblast migration is regulated by RANTES,” Experimental Cell Research, Vol.305, pp. 355-364, 2005.
  24. [24] R. Ramhorst, G. Gutierrez, A. Corigliano, G. Junovich, and L. Fainboim, “Implication of RANTES in the modulation of alloimmune response by progesterone during pregnancy,” American J. of Reproductive Immunology, Vol.57, pp. 147-152, 2007.
  25. [25] B. G. Dorner, A. Scheffold, M. S. Rolph, M. B. Huser, S. H. E. Kaufmann, A. Radbruch, I. E. A. Flesch, and R. A. Kroczek, “MIP-1α, MIP-1β, RANTES, and ATAC/lymphotactin function together with IFN-γ as type 1 cytokines,” Proc. of the National Academy of Sciences of the United States of America Vol.99, pp. 6181-6186, 2002.

Creative Commons License  This article is published under a Creative Commons Attribution-NoDerivatives 4.0 Internationa License.

*This site is desgined based on HTML5 and CSS3 for modern browsers, e.g. Chrome, Firefox, Safari, Edge, Opera.

Last updated on Apr. 19, 2024