Regulation of chemokine production in response to pro-inflammatory cytokines in first trimester decidual cells

Huang, Su-Cheng; Schatz, Frederick; Masch, Rachel; Rahman, Mizanur; Buchwalder, Lynn; Niven‐Fairchild, Tracy; Tang, Caroline; Abrahams, Vikki M.; Krikun, Graciela; Lockwood, Charles J.

doi:10.1016/j.jri.2006.03.002

Cited by 75 publications

(78 citation statements)

References 52 publications

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“…In correspondence with these increases in the two immune cell populations an array of monocyte/macrophage-and dendritic cell-recruiting chemokines were observed to be significantly elevated in decidua from preeclamptic women extracts as measured by ELISA and specifically in decidual cells by immunohistochemical localization. 8,32 Subsequently, the second tier of our approach sought to determine by in vitro studies whether expression of these proteins is altered during incubation of first trimester leukocyte-free first trimester decidual cells with preeclampsia-associated proinflammatory cytokines, TNF-␣ and IL-1␤. These studies confirmed that TNF-␣ and IL-1␤ each markedly increased expression of monocyte/macrophage-and dendritic cell-recruiting chemokines in first trimester decidual cells, the major resident cell type encountered by invading extravillous cytotrophoblasts.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies from our laboratory reported parallel observations for IL-6 expression (ie, enhanced IL-6 levels were immunolocalized to decidual cells of preeclamptic versus control placental sections with inflammatory cytokines augmenting IL-6 mRNA and protein expression in cultured leukocyte-free first trimester decidual cells). 32,33 In several tissues, IL-6 mediates the transition from acute to chronic inflammation by reciprocally inhibiting neutrophil trafficking and promoting monocyte differentiation away from dendritic cells toward macrophages. 33 Taken together, previous reports from our laboratory indicate a crucial role for decidual cells in determining the macrophage and dendritic cell population of the decidua from preeclamptic women.…”

Section: Discussionmentioning

confidence: 99%

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The Implication of Aberrant GM-CSF Expression in Decidual Cells in the Pathogenesis of Preeclampsia

Huang

Zenclussen

Chen

et al. 2010

The American Journal of Pathology

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Preeclampsia is characterized by an exaggerated systemic inflammatory state as well as shallow placentation. In the decidual implantation site , preeclampsia is accompanied by an excessive number of both macrophages and dendritic cells as well as their recruiting chemokines, which have been implicated in the impairment of endovascular trophoblast invasion. Granulocyte-macrophage colony-stimulating factor is known to regulate the differentiation of both macrophages and dendritic cells, prompting both in vivo and in vitro evaluation of granulocyte-macrophage colony-stimulating factor expression in human decidua as well as in a mouse model of preeclampsia. This study revealed increased granulocyte-macrophage colony-stimulating factor expression levels in preeclamptic decidua. Moreover, both tumor necrosis factor-␣ and interleukin-1 ␤, cytokines that are implicated in the genesis of preeclampsia, markedly up-regulated granulocyte-macrophage colony-stimulating factor production in cultured first-trimester human decidual cells. The conditioned media of these cultures promoted the differentiation of both macrophages and dendritic cells from a monocyte precursor. Evaluation of a murine model of preeclampsia revealed that the decidua of affected animals displayed higher levels of immunoreactive granulocyte-macrophage colony-stimulating factor as well as increased numbers of both macrophages and dendritic cells when compared to control animals. Because granulocyte-macrophage colony-stimulating factor is a potent inducer of differentiation and activation of both macrophages and dendritic cells , these findings suggest that this factor plays a crucial role in the pathogenesis of preeclampsia. (Am J

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The Implication of Aberrant GM-CSF Expression in Decidual Cells in the Pathogenesis of Preeclampsia

Huang

Zenclussen

Chen

et al. 2010

The American Journal of Pathology

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“…Each cDNA sample was analyzed for the expression of IL-6, IL-1␤, CXCL3, and COX-2 using the POWER SYBER Green PCR master mix (Applied Biosystems, Foster City, CA). The forward and reverse oligonucleotide primers for IL-6 (5Ј-CCTGAGAAAGGAGA-CATGTAACAAGA, 5Ј-GGCAAGTCTCCTCATTGAATCC) (32), CXCL3 (5Ј-GTTTGACTATTTCTTACGAGGGTTC, 5Ј-ACCCATCATATTCCAATTAAATAATCAGG) (33), IL-1␣ (5Ј-TCAAGGAGAGCATGGTGGTAGTAG, 5Ј-TGGCTTA-AACTCAACCGTCTCTT), and COX-2 (5Ј-CATTCTTTGC-CCAGCACTTCAC, 5Ј-GACCAGGCACCAGACCAAAGAC) (34) were purchased from Sigma. PCR assays were performed using the 7300 Real Time PCR System (Applied Biosystems).…”

Section: Methodsmentioning

confidence: 99%

NF-κB-dependent Transcriptional Activation in Lung Carcinoma Cells by Farnesol Involves p65/RelA(Ser276) Phosphorylation via the MEK-MSK1 Signaling Pathway

Joo

Jetten

2008

Journal of Biological Chemistry

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In this study, we demonstrate that treatment of human lung adenocarcinoma H460 cells with farnesol induces the expression of a number of immune response and inflammatory genes, including IL-6, CXCL3, IL-1␣, and COX-2. This response was dependent on the activation of the NF-B signaling pathway. Isoprenoids are intermediates of the cholesterol/sterol biosynthetic pathway and are formed from mevalonate, which is synthesized from acetyl-CoA by the rate-limiting enzyme 3-hydroxy-3-methylglutaryl-CoA reductase, a major target for statins in the treatment of cardiovascular disease (1-3). Isoprenoids are important in the regulation of cell proliferation, apoptosis, and differentiation (4 -10).Farnesol and the related isoprenoids perillyl alcohol, geranylgeraniol, and geraniol have been reported to be effective in chemopreventative and -therapeutic strategies in several in vivo cancer models, including melanoma, colon, and pancreatic cancer (11)(12)(13)(14)(15)(16)(17)(18). In addition, these isoprenoids inhibit proliferation and induce cell death in a variety of neoplastic cell lines (5, 7, 10, 13, 15, 19 -21). The mechanisms by which these agents mediate their actions are not yet fully understood. In human pancreatic carcinoma cells, the antiproliferative response by these isoprenoids involves a p21-and p27-dependent mechanism (21). Farnesol has been reported to be able to weakly activate the farnesoid X-activated receptor (22) and inhibit phospholipase D (23), 3-hydroxy-3-methylglutaryl-CoA reductase activity (10), and the CDP-choline pathway (24). Study of farnesol-induced toxicity in yeast has indicated an important role for mitochondria and the PKC signaling pathway in the generation of reactive oxygen species (25).Recently, we reported that a large number of genes associated with the endoplasmic reticulum (ER) 2 stress response are rapidly induced by farnesol treatment, suggesting that farnesolinduced apoptosis is coupled to ER stress (26). Disturbance of ER homeostasis results in the activation of the unfolded protein response (27)(28)(29)(30). During this response, several prosurvival and proapoptotic signals are activated, and, depending on the extent of the ER stress, cells survive or undergo apoptosis. We demonstrated that farnesol induces activation of several MAPK pathways, including p38, MEK1/2-ERK1/2, and JNK1/2 (26) and provided evidence indicating that activation of MEK/ERK is an early and upstream event in farnesol-induced ER stress signaling cascade.In this study, we demonstrate that treatment of human lung adenocarcinoma H460 cells with farnesol induces the expression of a number of immune response and inflammatory-related genes, including COX-2 and several chemo/cytokines, and * This work was supported, in whole or in part, by the National Institutes of Health, NIEHS, Intramural Research Program. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely ...

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“…41,53 IL-6 has been shown to switch the differentiation away from dendritic cells to macrophages; 54 however, we found that treatment of first trimester decidual cells with proinflammatory cytokines markedly up-regulated the expression of several monocyte/macrophage chemoattracting and activating chemokines including CCL2, CCL5, CXCL2, CXCL3, and CXCL8. 51,55 These chemokines and IL-6 stimulate cells via different surface receptors suggesting that they synergize to contribute to the excess of macrophages described in the preeclamptic decidua. The results of in vitro studies suggest that macrophage-derived TNF-␣ inhibits cytotrophoblast invasion of the decidua by causing the cytotrophoblasts to undergo apoptosis 38 and/or by reciprocally inhibiting expression of urokinase typeplasminogen activator and enhancing expression of plasminogen activator-1, which then inactivates urokinase bound to its receptor at the leading edge of trophoblast invasion.…”

Section: 27mentioning

confidence: 99%

Preeclampsia-Related Inflammatory Cytokines Regulate Interleukin-6 Expression in Human Decidual Cells

Lockwood

Yen

Başar

et al. 2008

The American Journal of Pathology

140

100

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Preeclampsia, a common pregnancy disorder associated with an increase in systemic inflammation, is the leading cause of maternal and fetal morbidity and mortality throughout the world. It is associated with shallow extravillous trophoblast invasion of the decidua, leading to uteroplacental blood flow that is inadequate for the developing fetal-placental unit. In preeclamptic women, interleukin-6 (IL-6) levels in plasma, but not placenta, are elevated, prompting evaluation of the decidua as a potential source of this excess, circulating IL-6. The current study found significantly higher immunohistochemical staining for IL-6 in decidual cells from preeclamptic versus preterm, gestational age-matched control placentas. Proinflammatory cytokines associated with the genesis of preeclampsia (i.e., tumor necrosis factor-␣ and interleukin-1␤) enhanced IL-6 mRNA levels and increased secreted IL-6 levels in first trimester leukocytefree decidual cell incubations, as measured by real time quantitative RT-PCR , ELISA , and Western blotting. Therefore , decidual cell-derived IL-6 may contribute to excess circulating IL-6 levels that can promote both endothelial cell dysfunction (and subsequent vascular dysfunction) and the pathogenesis of preeclampsia whereas locally elevated IL-6 levels may contribute to an excess of decidual macrophages implicated in shallow extravillous trophoblast invasion of the decidua. Maternal-fetal interactions create a mild systemic inflammatory state exemplified by activation of both vascular endothelium and leukocytes that is most apparent in the third trimester of uncomplicated human pregnancies.

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Regulation of chemokine production in response to pro-inflammatory cytokines in first trimester decidual cells

Cited by 75 publications

References 52 publications

The Implication of Aberrant GM-CSF Expression in Decidual Cells in the Pathogenesis of Preeclampsia

The Implication of Aberrant GM-CSF Expression in Decidual Cells in the Pathogenesis of Preeclampsia

NF-κB-dependent Transcriptional Activation in Lung Carcinoma Cells by Farnesol Involves p65/RelA(Ser276) Phosphorylation via the MEK-MSK1 Signaling Pathway

Preeclampsia-Related Inflammatory Cytokines Regulate Interleukin-6 Expression in Human Decidual Cells

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