Campylobacters and impaired fetal development in mice

O'sullivan, A. M.; Doré, C. J.; Coid, C. R.

doi:10.1099/00222615-25-1-7

Cited by 14 publications

(10 citation statements)

References 9 publications

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“…Earlier work in this laboratory showed that both live and heat-killed campylobacters impaired fetal development when injected into the 13-day pregnant mouse. It was suggested that endotoxin-like substances played a role in pathogenesis (O'Sullivan et al, 1988). The present report describes the effect of purified lipopolysaccharide-the endotoxin moiety (Smith, 1978hxtracted from C. fetus ss.…”

Section: Introductionmentioning

confidence: 82%

The effect of campylobacter lipopolysaccharide on fetal development in the mouse

O'sullivan

Doré

Boyle³

et al. 1988

Journal of Medical Microbiology

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Summary. Purified lipopolysaccharide (LPS) obtained from isolates of Campylobacter fetus ss. fetus and Campylobacter jejuni impaired fetal development when administered to mice on day 13 of pregnancy. Strikingly more fetal resorption was produced by C. jejuni LPS than by similar amounts of C. fetus ss. fetus LPS. Three of the four Campylobacter strains examined produced LPS that had no effect on maternal health, but LPS from one C. jejuni strain killed all of the mice to which it was administered.

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Section: Introductionmentioning

confidence: 82%

The effect of campylobacter lipopolysaccharide on fetal development in the mouse

O'sullivan

Doré

Boyle³

et al. 1988

Journal of Medical Microbiology

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“…Other Campylobacter spp. including C. fetus and C. jejuni have also been reported to be associated with miscarriages, premature labor and severe perinatal infection in both humans as well as in animals (Allos, 2001; O'Sullivan et al, 1988; Simor et al, 1986; Wong et al, 1990). It is then plausible that C. rectus may be an important contributor to adverse pregnancy outcomes due to its ability to disseminate systemically during pregnancy.…”

Section: Introductionmentioning

confidence: 99%

Characterization of the invasive and inflammatory traits of oral Campylobacter rectus in a murine model of fetoplacental growth restriction and in trophoblast cultures

Arce

Diaz

Barros

et al. 2010

Journal of Reproductive Immunology

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Campylobacter species (C. jejuni, C. fetus) are enteric abortifacient bacteria in humans and ungulates. Campylobacter rectus is a periodontal pathogen associated with human fetal exposure and adverse pregnancy outcomes including preterm delivery. Experiments in pregnant mice have demonstrated that C. rectus can translocate from a distant site of infection to the placenta to induce fetal growth restriction and impair placental development. However, placental tissues from human, small-forgestational age deliveries have not been reported to harbor C. rectus despite evidence of maternal infection and fetal exposure by fetal IgM response. This investigation examined the temporal relationship between the placental translocation of C. rectus and the effects on fetal growth in mice. BALB/c mice were infected at gestational day E7.5 to examine placental translocation of C. rectus by immunohistology. C. rectus significantly decreased fetoplacental weight at E14.5 and at E16.5. C. rectus was detected in 63% of placentas at E14.5, but not at E16.5. In in vitro trophoblast invasion assays, C. rectus was able to effectively invade human trophoblasts (BeWo) but not murine trophoblasts (SM9-1), and showed a trend for more invasiveness than C. jejuni. C. rectus challenge significantly upregulated both mRNA and protein levels of IL-6 and TNFα in a dose-dependent manner in human trophoblasts, but did not increase cytokine expression in murine cells, suggesting a correlation between invasion and cytokine activation. In conclusion, the trophoblast-invasive trait of C. rectus that appears limited to human trophoblasts may play a role in facilitating bacterial translocation and placental inflammation during early gestation.

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“…In mice, the products of other infectious agents associated with resorptions and fetal growth impairment (in particular, periodontal member of the Campylobacter genus [25,26]) have been proposed to act through lipopolysaccharide (LPS)-stimulated TNF-α production to produce resorptions [27]. Whereas these infections are typically chronic and involve intrauterine colonization, it is possible that, in the gram positive listeriae, wall teichoic acid and lipoteichoic acid may act similarly to LPS.…”

Section: Discussionmentioning

confidence: 99%

Extrauterine Listeriosis in the Gravid Mouse Influences Embryonic Growth and Development

et al. 2013

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Gravid mice and other rodents inoculated with Listeria monocytogenes typically fail to clear an intrauterine infection and either succumb or expel their intrauterine contents. We took advantage of this property to investigate the effects of an extrauterine infection on parameters of pregnancy success. Pregnant mice were selected for our study if they showed no clinical signs of listeriosis following oral inoculation at 7.5 gestational days (gd), and had no detectable intrauterine colony forming units (cfu) at near term (18.5 gd). The range of oral doses employed was 106-108 cfu per mouse for two listerial serotype strains (4nonb and 1/2a). At all doses, inoculation resulted in a decrease in average near-term (18.5 gd) fetal weight per litter compared to sham inoculated controls. Additionally, embryonic death (indicated by intrauterine resorptions) was exhibited by some inoculated mice but was absent in all sham inoculated animals. In parallel experiments designed to detect possible loss of placental function, gravid uteruses were examined histopathologically and microbiologically 96 h after oral inoculation. Placental lesions were associated with high (> 106), but not low (< 102) or absent intrauterine cfu. In vitro, mouse embryonic trophoblasts were indistinguishable from mouse enterocytes in terms of their sensitivity to listerial exposure. A model consistent with our observations is one in which products (host or bacterial) generated during an acute infection enter embryos transplacentally and influences embryonic survival and slows normal growth in utero.

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Campylobacters and impaired fetal development in mice

Cited by 14 publications

References 9 publications

The effect of campylobacter lipopolysaccharide on fetal development in the mouse

The effect of campylobacter lipopolysaccharide on fetal development in the mouse

Characterization of the invasive and inflammatory traits of oral Campylobacter rectus in a murine model of fetoplacental growth restriction and in trophoblast cultures

Extrauterine Listeriosis in the Gravid Mouse Influences Embryonic Growth and Development

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