The effect of campylobacter lipopolysaccharide on fetal development in the mouse

O'sullivan, A. M.; Doré, C. J.; Boyle, S.; Coid, C. R.; Johnson, Alan P.

doi:10.1099/00222615-26-2-101

Cited by 23 publications

(11 citation statements)

References 9 publications

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“…In addition LPS may also affect directly the embryo since it is able to cross the placental barrier. In fact, it was demonstrated that, in rat, maternal LPS administration induces an increased expression of IL-1 and TNF-mRNA in the fetal brain [21], as well as it was reported that maternal bacterial infection or LPS administration induces preterm labor and delivery or foetal death and abortion [22][23][24][25]. We have previously demonstrated in an avian model that LPS is able to affect both the mechanical activity of the embryonal heart and the viability of cultured cardiomyocytes [26] and that the presence of CD14 on embryo cardiomyocytes surface plays a pivotal role in the LPS up-take and subsequent functional responses [27].…”

Section: Introductionmentioning

confidence: 99%

Inflammatory Responses in Embryonal Cardiomyocytes Exposed to LPS Challenge. An In Vitro Model of Deciphering the Effects of LPS on the Heart

Panaro¹,

Acquafredda²,

Cavallo³

et al. 2010

CPD

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This study is focused on the links between the major products of inflammation and cell damage induced by the administration of lipopolysaccharide (LPS) from Salmonella typhimurium in embryonal cardiomyocytes. LPS treatment for 72 hours induced transcription factor NF-kappaB activation, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 expression, nitric oxide (NO) and tumor necrosis factor (TNF)-alpha release. Moreover, LPS administration induced a significant cell loss, reversed by the NO-synthases inhibitor, suggesting a relationship between cell damage and iNOS-dependent NO overproduction. Cell death was reversed by the specific NF-kappaB inhibitor, TPCK, whereas COX-2 specific inhibitor determined an increase of cell damage in terms of apoptosis, as observed by YO-PRO immunostaining, DNA laddering analysis and caspase-3 activation. Overall these findings evidenced a selective role for NF-kappaB in mediating NO-induced cell damage and a protective action by COX-2 in LPS-treated embryonal cardiomyocytes. The reflection of these experiments on human cardiac pathology will be discussed.

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Section: Introductionmentioning

confidence: 99%

Inflammatory Responses in Embryonal Cardiomyocytes Exposed to LPS Challenge. An In Vitro Model of Deciphering the Effects of LPS on the Heart

Panaro¹,

Acquafredda²,

Cavallo³

et al. 2010

CPD

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“…Humans are constantly exposed to low levels of LPS through microbial infections. Systemic maternal LPS exposure has been previously shown to be associated with adverse fetal developmental outcomes such as embryonic resorption, intrauterine fetal death, and preterm labor in animals (6). In addition, microbial invasion of the placenta is reported to cause chorioamniotitis and preterm labor in human patients (1).…”

mentioning

confidence: 99%

Attenuation of Lipopolysaccharide-Induced Inflammatory Response and Phospholipids Metabolism at the Feto-Maternal Interface by N-Acetyl Cysteine

Paintlia

Singh

et al. 2008

Pediatr Res

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Maternal microbial infections cause adverse fetal developmental outcomes including embryonic resorption, intrauterine fetal death, and preterm labor. Recent studies demonstrated that oxidativestress plays an important role in chorioamniotitis pathogenesis. Herein we investigated the effect of N-acetyl cysteine (NAC) on lipopolysaccharide (LPS)-induced preterm labor and fetal demise in murine model. Lipopolysaccharide exposure at embryonic day 18 demonstrated an increase in the abortion rate and fetal demise in pregnant rats. This was associated with increase in an inflammatory response (cytokines, chemokines, and iNOS expression) and infiltration of leukocytes (monocytes and polymorphonuclear cells) in the placenta. There was increased expression of cytosolic and secretary phospholipase A2 with increased secretion of prostaglandin-2 and leukotriene B4 in the placenta, suggestive of increased metabolism of phospholipids. In addition, expression of cycloxygenase-2 and malondialdehyde production (oxidative-stress marker) was increased in the placenta. Conversely, NAC pretreatment abolished these effects of LPS in the placenta. Collectively, these data provide evidence that LPS-induced increased inflammation and metabolism of phospholipids at the feto-maternal interface (placenta) is critical for preterm labor and fetal demise during maternal microbial infections which could be blocked by antioxidant-based therapies. (Pediatr Res 64: [334][335][336][337][338][339] 2008)

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“…, 2006). In animal models, C. jejuni and C. fetus infections result in impaired fetal development and IUGR (O’Sullivan et al. , 1988a,b).…”

Section: Discussionmentioning

confidence: 99%

Toll‐like receptor 4 mediates intrauterine growth restriction after systemic Campylobacter rectus infection in mice

Arce

Caron

Barros

et al. 2012

Molecular Oral Microbiology

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Summary Campylobacter rectus is associated with fetal exposure and low-birth weight in humans. C. rectus also invades placental tissues and induces fetal intrauterine growth-restriction (IUGR) in mice, along with Toll-like receptors (TLR4) overexpression, suggesting that TLR4 may mediate placental immunity and IUGR in mice. To test this hypothesis we examined the effect of in vitroTLR4 neutralization in trophoblastic proinflammatory activity and studied the IUGR phenotype in a congenic TLR4-mutant mouse strain after in vivo C. rectus infection. Human trophoblasts were pretreated with TLR4 neutralizing antibodies and infected with C. rectus; pro-inflammatory cytokine production was assessed by cytokine multiplexing assays. Neutralizing TLR4 antibodies significantly impaired the production of pro-inflammatory cytokines in trophoblastic cells after infection in a dose-dependent manner. We used a subcutaneous chamber model to provide a C. rectus challenge in BALB/cAnPt (TLR4Lps-d) and wild-type(WT) females. Females were mated with WT or TLR4Lps-dmales once/week; pregnant mice were infected at (E)7.5 and sacrificed at (E)16.5 to establish IUGR phenotypes. Maternal C. rectus infection significantly decreased fetal weight/length in infected WT when compared to sham WT controls(P<0.05, ANOVA). However, infected TLR4Lps-d−/− mice did not show statistically significant differences in fetal weight and length when compared to WT controls(P>0.05). Furthermore, heterozygous TLR4Lps-d −/+fetuses showed IUGR phenotype rescue. We concluded that TLR4 is an important mediator of trophoblastic proinflammatory responses and TLR4-deficient fetuses do not develop IUGR phenotypes after C. rectus infection, suggesting that placental cytokine activation is likely to be mediated by TLR4 during low birth weight/preterm delivery pathogenesis.

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The effect of campylobacter lipopolysaccharide on fetal development in the mouse

Cited by 23 publications

References 9 publications

Inflammatory Responses in Embryonal Cardiomyocytes Exposed to LPS Challenge. An In Vitro Model of Deciphering the Effects of LPS on the Heart

Inflammatory Responses in Embryonal Cardiomyocytes Exposed to LPS Challenge. An In Vitro Model of Deciphering the Effects of LPS on the Heart

Attenuation of Lipopolysaccharide-Induced Inflammatory Response and Phospholipids Metabolism at the Feto-Maternal Interface by N-Acetyl Cysteine

Toll‐like receptor 4 mediates intrauterine growth restriction after systemic Campylobacter rectus infection in mice

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