Placental Pathology of the Pregnant Mouse Inoculated with<i>Brucella abortus</i>Strain 2308

Tobias, L.; Cordes, D. O.; Schurig, Gerhardt G.

doi:10.1177/030098589303000204

Cited by 56 publications

(76 citation statements)

References 23 publications

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“…At the placental level, the onset of yeast cell phagocytosis by leukocytes and trophoblast cells began as early as 3 h after inoculation. The yeast cell phagocytosis was faster than that described for pathogenic bacteria such as Coxiella burnetti, Chlamydia psittaci, Listeria monocytogenes and Brucella abortus (Redline & Lu 1988, Baumgartner & Bachman 1992, Tobias et al 1993, Buendia et al 1998. It is possible that these microorganisms have defense mechanisms for avoiding immediate recognition by the immunological defense system of the host organism.…”

Section: Discussionmentioning

confidence: 87%

Phagocytosis as a potential mechanism for microbial defense of mouse placental trophoblast cells

Amarante-Paffaro¹,

Queiroz²,

Corrêa³

et al. 2004

Reproduction

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Trophoblast giant cells are active phagocytes during implantation and post-implantation. Phagocytosis decreases during placental maturation as the phagocytic function of nutrition is gradually replaced by the direct uptake of nutrients by the labyrinth zone trophoblast. We hypothesize that, after placental maturation, trophoblast cells maintain phagocytic functions for purposes other than nutrition. This study employs histological techniques to examine the ability of trophoblast cells to phagocytose microorganisms (yeast or bacteria) -in vivo in females receiving thioglycolate to activate macrophages and in vitro in the presence of phagocytic promoters such as interferon-g and complement component C3. Placental trophoblast cells from the second half of gestation show basal phagocytosis that can be dramatically up-regulated by these promoters when microorganisms are inoculated into pregnant animals or introduced into culture systems. Stimulated trophoblast cells phagocytosed organisms more rapidly and in greater numbers than non-stimulated trophoblast exposed to the same numbers of organisms. Taken together, our results indicate that trophoblast cells do not lose their ability to phagocytose during the placentation process, which may imply that trophoblast cells participate in embryonic and fetal innate immune defense through elimination of microorganisms present at the maternal-fetal interface.

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Section: Discussionmentioning

confidence: 87%

Phagocytosis as a potential mechanism for microbial defense of mouse placental trophoblast cells

Amarante-Paffaro¹,

Queiroz²,

Corrêa³

et al. 2004

Reproduction

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“…Splenomegaly is a well-known clinical manifestation associated with Brucella infection that correlates with increased numbers of mononuclear cells and appears to be dependent on the bacterial burden (9,(17)(18)(19)28). Splenomegaly was evident after aerosol exposure with both B. abortus, with which splenomegaly was delayed until approximately 6 weeks postexposure, and B. melitensis, with which splenomegaly was evident earlier at 4 weeks postexposure.…”

Section: Discussionmentioning

confidence: 99%

Aerosol Infection of BALB/c Mice with Brucella melitensis and Brucella abortus and Protective Efficacy against Aerosol Challenge

2007

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Brucellosis is a zoonotic disease with a worldwide distribution that can be transmitted via intentional or accidental aerosol exposure. In order to engineer superior vaccine strains against Brucella species for use in animals as well as in humans, the possibility of challenge infection via aerosol needs to be considered to properly evaluate vaccine efficacy. In this study, we assessed the use of an aerosol chamber to infect deep lung tissue of mice to elicit systemic infections with either Brucella abortus or B. melitensis at various doses. The results reveal that B. abortus causes a chronic infection of lung tissue in BALB/c mice and peripheral organs at low doses. In contrast, B. melitensis infection diminishes more rapidly, and higher infectious doses are required to obtain infection rates in animals similar to those of B. abortus. Whether this difference translates to severity of human infection remains to be elucidated. Despite these differences, unmarked deletion mutants BA⌬asp24 and BM⌬asp24 consistently confer superior protection to mice against homologous and heterologous aerosol challenge infection and should be considered viable candidates as vaccine strains against brucellosis.

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“…However, the placentas of these uninfected fetuses presented mild vascular lesions. This suggests that the placenta is probably a site of Bartonella multiplication as for the murine model of brucellosis (36).…”

Section: Susceptibilitymentioning

confidence: 99%

Kinetics ofBartonella birtlesiiInfection in Experimentally Infected Mice and Pathogenic Effect on Reproductive Functions

et al. 2001

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The kinetics of infection and the pathogenic effects on the reproductive function of laboratory mice infected with Bartonella birtlesii recovered from an Apodemus species are described. B. birtlesii infection, as determined by bacteremia, occurred in BALB/c mice inoculated intravenously. Inoculation with a low-dose inoculum (1.5 ؋ 10 3 CFU) induced bacteremia in only 75% of the mice compared to all of the mice inoculated with higher doses (>1.5 ؋ 10 4 ). Mice became bacteremic for at least 5 weeks (range, 5 to 8 weeks) with a peak ranging from 2 ؋ 10 3 to 10 5 CFU/ml of blood. The bacteremia level was significantly higher in virgin females than in males but the duration of bacteremia was similar. In mice infected before pregnancy (n ‫؍‬ 20), fetal loss was evaluated by enumerating resorption and fetal death on day 18 of gestation. The fetal death and resorption percentage of infected mice was 36.3% versus 14.5% for controls (P < 0.0001). Fetal suffering was evaluated by weighing viable fetuses. The weight of viable fetuses was significantly lower for infected mice than for uninfected mice (P < 0.0002). Transplacental transmission of Bartonella was demonstrated since 76% of the fetal resorptions tested was culture positive for B. birtlesii. The histopathological analysis of the placentas of infected mice showed vascular lesions in the maternal placenta, which could explain the reproductive disorders observed. BALB/c mice appeared to be a useful model for studying Bartonella infection. This study provides the first evidence of reproductive disorders in mice experimentally infected with a Bartonella strain originating from a wild rodent.

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Placental Pathology of the Pregnant Mouse Inoculated withBrucella abortusStrain 2308

Cited by 56 publications

References 23 publications

Phagocytosis as a potential mechanism for microbial defense of mouse placental trophoblast cells

Phagocytosis as a potential mechanism for microbial defense of mouse placental trophoblast cells

Aerosol Infection of BALB/c Mice with Brucella melitensis and Brucella abortus and Protective Efficacy against Aerosol Challenge

Kinetics ofBartonella birtlesiiInfection in Experimentally Infected Mice and Pathogenic Effect on Reproductive Functions

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