PP040. Expression of RANTES (CCL5) in maternal plasma, fetal plasma and placenta in pre-eclampsia and normotensive controls

Hentschke, Marta Ribeiro; Krauspenhar, Bruna; Guwzinski, A.; Caruso, Fernanda Borsatto; Silveira, Inês; Antonello, Ivan Carlos Ferreira; Gadonski, Giovani; Poli-de-Figueiredo, Carlos Eduardo; Costa, Bartira Ercí­lia Pinheiro da

doi:10.1016/j.preghy.2012.04.151

Cited by 11 publications

(5 citation statements)

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“…In a recent study, Salazar Garcia et al () described the occurrence of increased CCL3/MIP‐1α levels in women with PE. Moreover, increased CCL5/RANTES levels were also observed in both plasma and placental tissues of preeclamptic women compared to healthy pregnant ones (Hentschke et al, ), data which corroborate the upregulation of the RANTES gene expression in women with PE reported by Heikkilä et al (). Taking together, these findings suggest that a CCR5‐mediated inflammation during pregnancy could be involved in PE development.…”

Section: Introductionsupporting

confidence: 70%

Influence of NKG2C gene deletion and CCR5Δ32 in Pre‐eclampsia—Approaching the effect of innate immune gene variants in pregnancy

Kaminski

Ellwanger

Sandrim

et al. 2019

Int J Immunogenetics

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Pre‐eclampsia (PE) is a hypertensive disorder that affects an important number of pregnant women worldwide. The exact causes of PE remain poorly understood. However, inflammation and deregulation of innate immune cells, such as natural killer (NK) cells, contribute to PE pathogenesis. Besides, the mother's genetic background also impacts on PE susceptibility. Thus, genetic variants that potentially modify the behaviour of inflammatory cells may help us to understand the causes of PE. Variants of genes encoding NKG2C (expressed in NK cells) and C–C chemokine receptor type 5 (CCR5) (expressed mainly in leucocytes) are important targets in the study of gestational disorders. In this context, we evaluated the impact of both NKGC2 gene deletion and CCR5Δ32 gene variant on PE susceptibility in a population sample from central‐southeast Brazil composed by 369 women (156 with PE and 213 healthy pregnant women). No statistically significant association between the NKG2C gene deletion and susceptibility to PE was observed. However, taking into consideration the important role of NK cells in pregnancy, the influence of NKG2C gene deletion on PE pathogenesis should not be ruled out and deserves further studies in populations with different genetic/ethnic backgrounds. In addition, our results regarding CCR5Δ32 corroborate previous data from our group approaching a distinct cohort and reinforce CCR5Δ32 as a protective factor against PE development (p < 0.05).

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Section: Introductionsupporting

confidence: 70%

Influence of NKG2C gene deletion and CCR5Δ32 in Pre‐eclampsia—Approaching the effect of innate immune gene variants in pregnancy

Kaminski

Ellwanger

Sandrim

et al. 2019

Int J Immunogenetics

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“…We found significant increases in hippocampal RANTES (CCL5) levels, where water content was unchanged. There is evidence that both plasma and placental levels of RANTES are increased in preeclampsia patients (Hentschke et al, 2012). In addition to being increased in preeclampsia patients, RANTES is also increased in microvessels from Alzheimer’s disease patients; although in vitro studies showed a protective role of RANTES using neuronal cultures (Tripathy et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Postpartum increases in cerebral edema and inflammation in response to placental ischemia during pregnancy

Clayton

Shao

Paauw

et al. 2018

Brain, Behavior, and Immunity

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Reduced placental blood flow results in placental ischemia, an initiating event in the pathophysiology of preeclampsia, a hypertensive pregnancy disorder. While studies show increased mortality risk from Alzheimer's disease, stroke, and cerebrovascular complications in women with a history of preeclampsia, the underlying mechanisms are unknown. During pregnancy, placental ischemia, induced by reducing uterine perfusion pressure (RUPP), leads to cerebral edema and increased blood-brain barrier (BBB) permeability; however whether these complications persist after delivery is not known. Therefore, we tested the hypothesis that placental ischemia contributes to postpartum cerebral edema and neuroinflammation. On gestational day 14, time-pregnant Sprague Dawley rats underwent Sham (n = 10) or RUPP (n = 9) surgery and brain tissue collected 2 months post-delivery. Water content increased in posterior cortex but not hippocampus, striatum, or anterior cerebrum following RUPP. Using a rat cytokine multi-plex kit, posterior cortical IL-17, IL-1α, IL-1β, Leptin, and MIP2 increased while hippocampal IL-4, IL-12(p70) and RANTES increased and IL-18 decreased following RUPP. Western blot analysis showed no changes in astrocyte marker, Glial Fibrillary Acidic Protein (GFAP); however, the microglia marker, ionized calcium binding adaptor molecule (Iba1) tended to increase in hippocampus of RUPP-exposed rats. Immunofluorescence staining revealed reduced number of posterior cortical microglia but increased activated (Type 4) microglia in RUPP. Astrocyte number increased in both regions but area covered by astrocytes increased only in posterior cortex following RUPP. BBB-associated proteins, Claudin-1, Aquaporin-4, and zonular occludens-1 expression were unaltered; however, posterior cortical occludin decreased. These results suggest that 2 months postpartum, neuroinflammation, along with decreased occludin expression, may partly explain posterior cortical edema in rats with history of placental ischemia.

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“…Increased RANTES levels were associated with spontaneous PTB within 14 days after presentation with symptoms of preterm labor with [ 35 ]. In addition, RANTES was increased in the maternal plasma and placenta in preeclampsia patients [ 36 ]. In a murine LPS-induced PTB model, MCP-1 was determined in the maternal serum and uterus, in the myometrium and endometrium, indicating that MCP-1 potentially contributes to the pro-inflammatory immune response that leads to PTB [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

IL-10 Producing B Cells Protect against LPS-Induced Murine Preterm Birth by Promoting PD1- and ICOS-Expressing T Cells

Busse

Zenclussen

2022

Cells

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B cells and in particular IL-10-secreting B cells emerge as important players in immune balance during pregnancy. We have recently revealed that CD19-deficient (CD19−/−), B cell-specific IL-10-deficient (BIL-10−/−) and B cell-deficient µMT pregnant mice are highly susceptible to LPS-induced preterm birth (PTB). We aimed to analyze the ability of IL-10-secreting cells to protect from PTB and the underlying mechanisms. Wild type (WT), CD19−/−, BIL-10−/− and µMT mice were treated with LPS at gd16 and the cellular immune response was investigated 24 h later. LPS-treated BIL-10−/− dams showed a more pronounced PTB phenotype compared to WT, CD19−/− and µMT females, and increased inflammatory and reduced anti-inflammatory mediator concentrations in the peritoneal cavity and serum. CD19−/−, BIL-10−/− and µMT mice displayed altered immune cell population frequencies in the blood and uterus with lower numbers of IL-10-secreting B cells and T cells. BIL-10−/− mothers presented decreased frequencies of uterine CD4+CD25+Foxp3+ Treg cells. Co-stimulatory molecules are critical for feto-maternal tolerance and IL-10 secretion. We found dysregulated PD-1 expression in peripheral blood and ICOS expression in the uterus of CD19−/−, BIL-10−/− and µMT dams. Our data show that B cell-specific IL-10-signaling is essential for a balanced maternal immune response to an inflammatory stimulant that cannot be hampered without IL-10-secreting B cells.

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PP040. Expression of RANTES (CCL5) in maternal plasma, fetal plasma and placenta in pre-eclampsia and normotensive controls

Cited by 11 publications

References 0 publications

Influence of NKG2C gene deletion and CCR5Δ32 in Pre‐eclampsia—Approaching the effect of innate immune gene variants in pregnancy

Influence of NKG2C gene deletion and CCR5Δ32 in Pre‐eclampsia—Approaching the effect of innate immune gene variants in pregnancy

Postpartum increases in cerebral edema and inflammation in response to placental ischemia during pregnancy

IL-10 Producing B Cells Protect against LPS-Induced Murine Preterm Birth by Promoting PD1- and ICOS-Expressing T Cells

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