scholarly journals Is azithromycin associated with a reduction in acute placental inflammation in the setting of PPROM?

2022 ◽  
Vol 226 (1) ◽  
pp. S304-S305
Author(s):  
Irina R. Cassimatis ◽  
Jeffery A. Goldstein ◽  
Ashish Premkumar ◽  
Emily S. Miller
Keyword(s):  
Placental Inflammation

scholarly journals Paternal High Fat Diet and Exercise Differentially Regulate Placental Development and Inflammation in a Sex-Specific Manner in C57BL6/J Mice (P19-003-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Kate Larson ◽  
Amy Bundy ◽  
Travis Alvine ◽  
James Roemmich
Keyword(s):  
Skeletal Muscle ◽  
Agricultural Research ◽  
Wheel Running ◽  
Fetal Weight ◽  
High Fat ◽  
Placental Development ◽  
Funding Sources ◽  
Service Project ◽  
Diet And Exercise ◽  
Placental Inflammation

Abstract Objectives We have shown that increases in T2D risk in male offspring when the father consumes a high-fat (HF) diet can be normalized when the father also exercises during preconception, and that this protection may occur by epigenetic increases in insulin signaling within offspring skeletal muscle. In our current study, we investigated to determine how paternal HF diet and exercise conditions alter sperm miRNA, fetal weight and placental inflammation. Methods Three-week old male C57BL/6 mice were fed a normal-fat (NF) diet (16% fat) or a HF diet (45% fat) and assigned to either voluntary wheel running exercise or cage activity for 3 months prior to mating with NF diet fed dams. Sperm samples were collected to determine changes in miRNA that may account for the enhanced offspring skeletal muscle responses that helped normalize paternal HF-induced glucose intolerance. Placentae were collected to determine whether changes in sperm miRNA expression differed by amount of placental inflammation. Results Sperm expression of miRNA 193b increased with paternal HF and exercise. In F1 males, placental and fetal weight decreased with HF diet while, in F1 female, paternal HF and exercise had no effect on placental and fetal weights. Paternal HF diet decreased placental IL-6 and TNF-alpha mRNA expression in F1 females, while no effects were observed in F1 male placenta. Conclusions Taken together these data suggest that paternal HF diet has a greater impact on placental development of male fetuses while paternal exercise has greater impact on placental inflammation of female fetuses. For both female and male fetuses, these paternal influences are mediated via sperm miRNA 193b. miR-193b is involved in regulation of the cell cycle and adipogenesis but may have additional functions. Thus, the exact role of sperm miRNA 193b in sex-specific epigenetic transmission of paternal HF diet and exercise on placental and fetal development needs further evaluation. Funding Sources USDA Agricultural Research Service Project #3062-51000-052-00D.

scholarly journals Placental Inflammation and Fetal Hemodynamics in a Rat Model of Chorioamnionitis

2010 ◽  
Vol 68 (6) ◽  
pp. 513-518 ◽  
Author(s):  
Adegboyega A Abdulkadir ◽  
Tobita Kimimasa ◽  
Michael J Bell ◽  
Trevor A MacPherson ◽  
Bradley B Keller ◽  
...  
Keyword(s):  
Rat Model ◽  
Placental Inflammation

β-hydroxybutyrate suppresses NLRP3 inflammasome-mediated placental inflammation and lipopolysaccharide-induced fetal absorption

2021 ◽  
pp. 103433
Author(s):  
Yoshiki Hirata ◽  
Sayaka Shimazaki ◽  
Sae Suzuki ◽  
Yuka Henmi ◽  
Hiromu Komiyama ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Placental Inflammation

Maternal and Placental Inflammation and Oxidative stress in Women of Advanced Maternal Age

Placenta ◽  
2017 ◽  
Vol 57 ◽  
pp. 229 ◽  
Author(s):  
Samantha Lean ◽  
Katie Stephens ◽  
Alexander Heazell ◽  
Rebecca Jones
Keyword(s):  
Oxidative Stress ◽  
Maternal Age ◽  
Advanced Maternal Age ◽  
Placental Inflammation ◽  
And Oxidative Stress

scholarly journals Placental inflammation by HMGB1 activation of TLR4 at the syncytium

Placenta ◽  
2018 ◽  
Vol 72-73 ◽  
pp. 53-61 ◽  
Author(s):  
Line H. Tangerås ◽  
Gabriela B. Silva ◽  
Guro S. Stødle ◽  
Lobke M. Gierman ◽  
Bente Skei ◽  
...  
Keyword(s):  
Placental Inflammation

scholarly journals Placental Ras Regulates Inflammation Associated with Maternal Obesity

2018 ◽  
Vol 2018 ◽  
pp. 1-18 ◽  
Author(s):  
Stella Liong ◽  
Gillian Barker ◽  
Martha Lappas
Keyword(s):  
Protein Expression ◽  
Pregnant Women ◽  
Human Placenta ◽  
Maternal Obesity ◽  
Small Gtpase ◽  
Obese Women ◽  
Trophoblast Cells ◽  
Ras Protein ◽  
Placental Inflammation ◽  
Expression And Activity

Heightened placental inflammation and dysfunction are commonly associated in pregnant obese women compared to their pregnant lean counterparts. The small GTPase superfamily members known as the rat sarcoma viral oncogene homolog (Ras) proteins, in particular, the K-Ras and H-Ras isoforms, have been implicated to regulate inflammation. The aims were to determine the placental Ras expression and activity with maternal obesity and its role in regulating placental inflammation. Human placenta was obtained at term Caesarean section from lean and obese pregnant women to determine the effect of maternal obesity on Ras protein expression and activity. To determine the effect of Ras on inflammation induced by bacterial endotoxin LPS and proinflammatory cytokines TNF-α or IL-1β, the chemical inhibitor lonafarnib (total Ras inhibitor) and siRNA (siKRAS and siHRAS) were used. Total Ras protein expression together with combined K-Ras and H-Ras activity was significantly increased in the placenta of obese pregnant women and when stimulated with LPS, IL-1β, or TNF-α. Lonafarnib significantly suppressed LPS-, IL-1β-, or TNF-α-induced IL-6, IL-8, MCP-1, and GRO-α expression and secretion in placental tissue. Primary trophoblast cells transfected with siKRAS or siHRAS demonstrated only K-Ras silencing significantly decreased IL-1β-, TNF-α-, or LPS-induced IL-6, IL-8, and MCP-1 expression and secretion. Furthermore, siKRAS significantly reduced downstream ERK-1/2 activation induced by LPS. In trophoblast cells, ERK-1/2 signalling is required for IL-6, IL-8, MCP-1, and GRO-α secretion. These studies implicate a role for K-Ras in regulating inflammation in human placenta. Suppressing overactive placental K-Ras function may prevent adverse fetal outcomes complicated by maternal obesity.

scholarly journals Fetal death: an extreme manifestation of maternal anti-fetal rejection

2017 ◽  
Vol 45 (7) ◽  
Author(s):  
Kia Lannaman ◽  
Roberto Romero ◽  
Tinnakorn Chaiworapongsa ◽  
Yeon Mee Kim ◽  
Steven J. Korzeniewski ◽  
...  
Keyword(s):  
Cohort Study ◽  
Amniotic Fluid ◽  
Study Design ◽  
Fetal Death ◽  
Unknown Etiology ◽  
Amniotic Cavity ◽  
Inflammatory Lesions ◽  
Esi Ms ◽  
Chemokine Ligand ◽  
Placental Inflammation

AbstractObjective:The aim of this study was to determine the association between chronic placental inflammation and amniotic fluid (AF) markers of maternal anti-fetal rejection as well as the presence of microorganisms in the AF fluid of patients with fetal death.Study Design:This cohort study included 40 patients with fetal death whose placentas were examined for chronic inflammatory lesions and whose AF chemokine ligand (CXCL)10 and interleukin (IL)-6 concentrations were determined by immunoassays. AF was processed for bacteria, mycoplasmas and viruses using cultivation and molecular microbiologic techniques (i.e. PCR-ESI/MS).Results:(1) The most prevalent placental findings were maternal vascular underperfusion (63.2%, 24/38), followed by chronic inflammatory lesions (57.9%, 22/38); (2) chronic chorioamnionitis (18/38) was three times more frequent than villitis of unknown etiology (6/38); (3) an elevated AF CXCL10 concentration (above the 95Conclusion:In women with unexplained fetal death, there is an association between elevated AF CXCL10 and chronic placental inflammatory lesions. Therefore, we conclude that a subset of patients with fetal death may have endured a breakdown of maternal-fetal tolerance, which cannot be attributed to microorganisms in the amniotic cavity.

scholarly journals Transcriptomic analysis of equine chorioallantois reveals immune networks and molecular mechanisms involved in nocardioform placentitis

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Hossam El-Sheikh Ali ◽  
Shavahn C. Loux ◽  
Laura Kennedy ◽  
Kirsten E. Scoggin ◽  
Pouya Dini ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Glucose Transporter ◽  
Inflammasome Activation ◽  
Molecular Pathways ◽  
Toll Like Receptor ◽  
Inflammatory Signaling ◽  
Leukocytic Infiltration ◽  
Apoptosis Pathways ◽  
Placental Inflammation ◽  
First Time

AbstractNocardioform placentitis (NP) continues to result in episodic outbreaks of abortion and preterm birth in mares and remains a poorly understood disease. The objective of this study was to characterize the transcriptome of the chorioallantois (CA) of mares with NP. The CA were collected from mares with confirmed NP based upon histopathology, microbiological culture and PCR for Amycolatopsis spp. Samples were collected from the margin of the NP lesion (NPL, n = 4) and grossly normal region (NPN, n = 4). Additionally, CA samples were collected from normal postpartum mares (Control; CRL, n = 4). Transcriptome analysis identified 2892 differentially expressed genes (DEGs) in NPL vs. CRL and 2450 DEGs in NPL vs. NPN. Functional genomics analysis elucidated that inflammatory signaling, toll-like receptor signaling, inflammasome activation, chemotaxis, and apoptosis pathways are involved in NP. The increased leukocytic infiltration in NPL was associated with the upregulation of matrix metalloproteinase (MMP1, MMP3, and MMP8) and apoptosis-related genes, such as caspases (CASP3 and CASP7), which could explain placental separation associated with NP. Also, NP was associated with downregulation of several placenta-regulatory genes (ABCG2, GCM1, EPAS1, and NR3C1), angiogenesis-related genes (VEGFA, FLT1, KDR, and ANGPT2), and glucose transporter coding genes (GLUT1, GLUT10, and GLUT12), as well as upregulation of hypoxia-related genes (HIF1A and EGLN3), which could elucidate placental insufficiency accompanying NP. In conclusion, our findings revealed for the first time, the key regulators and mechanisms underlying placental inflammation, separation, and insufficiency during NP, which might lead to the development of efficacious therapies or diagnostic aids by targeting the key molecular pathways.

scholarly journals Obesity during pregnancy results in maternal intestinal inflammation, placental hypoxia, and alters fetal glucose metabolism at mid-gestation

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jessica G. Wallace ◽  
Christian J. Bellissimo ◽  
Erica Yeo ◽  
Yu Fei Xia ◽  
Jim J. Petrik ◽  
...  
Keyword(s):  
Structural Changes ◽  
Maternal Obesity ◽  
Intestinal Inflammation ◽  
Maternal Diet ◽  
Cell Number ◽  
Amino Acid Transporters ◽  
Metabolic Dysfunction ◽  
Transcript Levels ◽  
Increased Risk ◽  
Placental Inflammation

AbstractWe investigated whether diet-induced changes in the maternal intestinal microbiota were associated with changes in bacterial metabolites and their receptors, intestinal inflammation, and placental inflammation at mid-gestation (E14.5) in female mice fed a control (17% kcal fat, n = 7) or a high-fat diet (HFD 60% kcal fat, n = 9; ad libitum) before and during pregnancy. Maternal diet-induced obesity (mDIO) resulted in a reduction in maternal fecal short-chain fatty acid producing Lachnospiraceae, lower cecal butyrate, intestinal antimicrobial peptide levels, and intestinal SCFA receptor Ffar3, Ffar2 and Hcar2 transcript levels. mDIO increased maternal intestinal pro-inflammatory NFκB activity, colonic CD3+ T cell number, and placental inflammation. Maternal obesity was associated with placental hypoxia, increased angiogenesis, and increased transcript levels of glucose and amino acid transporters. Maternal and fetal markers of gluconeogenic capacity were decreased in pregnancies complicated by obesity. We show that mDIO impairs bacterial metabolite signaling pathways in the mother at mid-gestation, which was associated with significant structural changes in placental blood vessels, likely as a result of placental hypoxia. It is likely that maternal intestinal changes contribute to adverse maternal and placental adaptations that, via alterations in fetal hepatic glucose handling, may impart increased risk of metabolic dysfunction in offspring.

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