Toll-like Receptors in Pregnancy Disorders and Placental Dysfunction

Riley, Joan; Nelson, D. F.

doi:10.1007/s12016-009-8178-2

Cited by 70 publications

(79 citation statements)

References 103 publications

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“…4). In the downstream of TLRs, signal molecules involved in Myd88-dependent orindependent pathways regulate transcriptional factors such as nuclear factor-kB (NFkB) and activator protein 1 (AP1), leading to the initiation of transcription in the nucleus (Riley & Nelson 2010). The release of human b-defensin (hBD) 2 was found to be controlled by phosphoinositide 3 kinase (PI3K) and NFkB, whereas The values with different letters are significantly different (P!0.05).…”

Section: Discussionmentioning

confidence: 99%

Induction of avian β-defensins by CpG oligodeoxynucleotides and proinflammatory cytokines in hen vaginal cells in vitro

et al. 2013

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Immune function in the vagina of hen oviduct is essential to prevent infection by microorganisms colonizing in the cloaca. The aim of this study was to determine whether CpG oligodeoxynucleotides (CpG-ODN) stimulate the expression of avian b-defensins (AvBDs) in hen vaginal cells. Specific questions were whether CpG-ODN affects the expression of AvBDs and proinflammatory cytokines and whether the cytokines affect AvBDs expression in vaginal cells. The dispersed vaginal cells of White Leghorn laying hens were cultured and stimulated by different doses of lipopolysaccharide (LPS), CpG-ODN, interleukin 1b (IL1B), or IL6. The cultured cell population contained epithelial cells, fibroblast-like cells, and CD45-positive leukocytes. The immunoreactive AvBD3, -10, and -12 were localized in the mucosal epithelium in the section of the vagina. The expression of AvBDs, IL1B, and IL6 was analyzed by quantitative RT-PCR. RT-PCR analysis showed the expression of AvBD1, -3, -4, -5, -10, and -12 in the cultured vaginal cells without stimulation. Toll-like receptors (TLRs) 4 and 21, which recognize LPS and CpG-ODN respectively and IL1 and IL6 receptors (IL1R1 and IL6R) were also expressed in them. The expression of IL1B, IL6, and AvBD10 and -12 was upregulated by LPS, whereas only IL1B and IL6 were upregulated by CpG-ODN. IL1B stimulation upregulated AvBD1 and -3 expression, whereas IL6 stimulation did not cause changes in AvBDs expression. These results suggest that CpG-ODN derived from microbes upregulates the expression of IL1B and IL6 by interaction with TLR21 and then IL1B induces AvBD1 and -3 to prevent infection in the vagina.

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Section: Discussionmentioning

confidence: 99%

Induction of avian β-defensins by CpG oligodeoxynucleotides and proinflammatory cytokines in hen vaginal cells in vitro

et al. 2013

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“…TLR-dependent innate immunity plays a role as the first line of host defense. Activation of TLRs on trophoblast cells influences immune cell recruitment, proinflammatory cytokine secretion, and decidual responses to invading pathogens during pregnancy [48]. Importantly, recent data directly implicate signaling by TLRs at multiple maternal-fetal interfaces in the pathogenesis of several pregnancy pathologies, including preeclampsia, intrauterine growth restriction, and preterm labor [48].…”

Section: Toll-like Receptors (Tlrs)mentioning

confidence: 99%

Inflammatory pattern recognition receptors and their ligands: factors contributing to the pathogenesis of preeclampsia

et al. 2011

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“…Recently, increasing numbers of studies have demonstrated that TLR2 and TLR4 are involved in the development of the host innate inflammatory response in I/R-induced pathology, very likely through their interaction with endogenous agonists (Arumugam et al 2009). TLR4 (which can bind bacterial lipopolysaccharide (LPS)) is widely expressed in the placenta (Riley & Nelson 2010), uterus, and cervix (Gonzalez et al 2007) and its expression is upregulated during gestation.…”

Section: Introductionmentioning

confidence: 99%

Impact of toll-like receptor 4 deficiency on the response to uterine ischemia/reperfusion in mice

Thaete

Jilling

et al. 2013

Reproduction

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Our objective was to determine the role of toll-like receptor 4 (TLR4) in uterine ischemia/reperfusion (I/R)-induced fetal growth restriction (FGR). Pregnant TLR4-deficient and wild-type mice were subjected to I/R or a sham procedure. Fetal and placental weights were recorded and tissues were collected. Pep-1 (inhibits low-molecular-weight hyaluronan (LMW-HA) binding to TLR4) was used to determine whether LMW-HA-TLR4 interaction has a role in FGR. TLR4-deficient mice exhibited significantly lower baseline fetal weights compared with wild-type mice (P!0.05), along with extensive placental calcification that was not present in wild-type mice. Following I/R, fetal and placental weights were significantly reduced in wild-type (P!0.05) but not in TLR4-deficient mice. However, I/R increased fetal loss (P!0.05) only in TLR4-deficient mice. Corresponding with the reduced fetal weights, uterine myeloperoxidase activity increased in wild-type mice (P!0.001), indicating an inflammatory response, which was absent in TLR4-deficient mice. TLR4 was shown to have a regulatory role for two anti-inflammatory cytokines: interferon-B1 decreased only in wild-type mice (P!0.01) and interleukin-10 increased only in TLR4-deficient mice (P!0.001), in response to I/R. Pep-1 completely prevented I/R-induced FGR (P!0.001), indicating a potential role for the endogenous TLR4 ligand LMW-HA in I/R-induced FGR. In conclusion, uterine I/R in pregnancy produces FGR that is dependent on TLR4 and endogenous ligand(s), including breakdown products of HA. In addition, TLR4 may play a role in preventing pregnancy loss after uterine I/R.

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Toll-like Receptors in Pregnancy Disorders and Placental Dysfunction

Cited by 70 publications

References 103 publications

Induction of avian β-defensins by CpG oligodeoxynucleotides and proinflammatory cytokines in hen vaginal cells in vitro

Induction of avian β-defensins by CpG oligodeoxynucleotides and proinflammatory cytokines in hen vaginal cells in vitro

Inflammatory pattern recognition receptors and their ligands: factors contributing to the pathogenesis of preeclampsia

Impact of toll-like receptor 4 deficiency on the response to uterine ischemia/reperfusion in mice

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