scholarly journals Inhibition of Wnt Signaling Pathways Impairs Chlamydia trachomatis Infection in Endometrial Epithelial Cells

2017 ◽  
Vol 7 ◽  
Author(s):  
Jennifer Kintner ◽  
Cheryl G. Moore ◽  
Judy D. Whittimore ◽  
Megan Butler ◽  
Jennifer V. Hall
Keyword(s):  
Chlamydia Trachomatis ◽  
Epithelial Cells ◽  
Wnt Signaling ◽  
Signaling Pathways ◽  
Chlamydia Trachomatis Infection ◽  
Endometrial Epithelial Cells

scholarly journals The multifaceted role of oestrogen in enhancing Chlamydia trachomatis infection in polarized human endometrial epithelial cells

2011 ◽  
Vol 13 (8) ◽  
pp. 1183-1199 ◽  
Author(s):  
Jennifer Vanover Hall ◽  
Maria Schell ◽  
Sophie Dessus-Babus ◽  
Cheryl G. Moore ◽  
Judy D. Whittimore ◽  
...  
Keyword(s):  
Chlamydia Trachomatis ◽  
Epithelial Cells ◽  
Chlamydia Trachomatis Infection ◽  
Endometrial Epithelial Cells

scholarly journals The proliferative effect of cortisol on bovine endometrial epithelial cells

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Junsheng Dong ◽  
Jun Li ◽  
Jianji Li ◽  
Luying Cui ◽  
Xia Meng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factors ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Signaling Pathways ◽  
Akt Signaling ◽  
Tissue Growth ◽  
Mrna Levels ◽  
Physiological Level ◽  
Endometrial Epithelial Cells

Abstract Background Bovine endometrial epithelial cells (BEECs) undergo regular regeneration after calving. Elevated cortisol concentrations have been reported in postpartum cattle due to various stresses. However, the effects of the physiological level of cortisol on proliferation in BEECs have not been reported. The aim of this study was to investigate whether cortisol can influence the proliferation properties of BEECs and to clarify the possible underlying mechanism. Methods BEECs were treated with different concentrations of cortisol (5, 15 and 30 ng/mL). The mRNA expression of various growth factors was detected by quantitative reverse transcription-polymerase chain reaction (qPCR), progression of the cell cycle in BEECs was measured using flow cytometric analysis, and the activation of the Wnt/β-catenin and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathways was detected with Western blot and immunofluorescence. Results Cortisol treatment resulted in upregulated mRNA levels of vascular endothelial growth factor (VEGF) and connective tissue growth factor (CTGF); however, it had no influence on transforming growth factor-beta1 (TGF-β1). Cortisol (15 ng/mL) accelerated the cell cycle transition from the G0/G1 to the S phase. Cortisol upregulated the expression of β-catenin, c-Myc, and cyclinD1 and promoted the phosphorylation of PI3K and AKT. Conclusions These results demonstrated that cortisol may promote proliferation in BEECs by increasing the expression of some growth factors and activating the Wnt/β-catenin and PI3K/AKT signaling pathways.

scholarly journals Activation of Lipid Metabolism Contributes to Interleukin-8 Production during Chlamydia trachomatis Infection of Cervical Epithelial Cells

2005 ◽  
Vol 73 (7) ◽  
pp. 4017-4024 ◽  
Author(s):  
Elaine Y. Fukuda ◽  
Sonya P. Lad ◽  
David P. Mikolon ◽  
Milena Iacobelli-Martinez ◽  
Erguang Li
Keyword(s):  
Lipid Metabolism ◽  
Chlamydia Trachomatis ◽  
Epithelial Cells ◽  
Mononuclear Cells ◽  
Interleukin 8 ◽  
Protein Activity ◽  
Peripheral Blood Mononuclear ◽  
Chemokine Production ◽  
Chlamydia Trachomatis Infection ◽  
Parasitic Pathogens

ABSTRACT Chlamydia trachomatis infection is the most common cause of bacterial sexually transmitted diseases. Infection of the urogenital tract by C. trachomatis causes chronic inflammation and related clinical complications. Unlike other invasive bacteria that induce a rapid cytokine/chemokine production, chlamydial infection induces delayed inflammatory response and proinflammatory chemokine production that is dependent on bacterial growth. We present data here to show that the lipid metabolism required for chlamydial growth contributes to Chlamydia-induced proinflammatory chemokine production. By gene microarray profiling, validated with biochemical studies, we found that C. trachomatis LGV2 selectively upregulated PTGS2 (COX2) and PTGER4 (EP4) in cervical epithelial HeLa 229 cells. COX2 is an enzyme that catalyzes the rate-limiting step of arachidonic acid conversion to prostaglandins, including prostaglandin E2 (PGE2) and other eicosanoids, whereas EP4 is a subtype of cell surface receptors for PGE2. We show that Chlamydia infection induced COX2 protein expression in both epithelial cells and peripheral blood mononuclear cells and promoted PGE2 release. Exogenous PGE2 was able to induce interleukin-8 release in HeLa 229 epithelial cells. Finally, we demonstrated that interleukin-8 induction by Chlamydia infection or PGE2 treatment was dependent on extracellular signal-regulated kinase/mitogen-activated protein activity. Together, these data demonstrate that the host lipid remodeling process required for chlamydial growth contributes to proinflammatory chemokine production. This study also highlights the importance of maintaining a balanced habitat for parasitic pathogens as obligate intracellular organisms.

Estrogen enhances attachment of Chlamydia trachomatis to human endometrial epithelial cells in vitro

1988 ◽  
Vol 159 (4) ◽  
pp. 1006-1014 ◽  
Author(s):  
Arthur S. Maslow ◽  
Carolyn H. Davis ◽  
John Choong ◽  
Priscilla B. Wyrick
Keyword(s):  
Chlamydia Trachomatis ◽  
Epithelial Cells ◽  
Endometrial Epithelial Cells

scholarly journals Chlamydia trachomatis Infection of Endocervical Epithelial Cells Enhances Early HIV Transmission Events

PLoS ONE ◽  
2016 ◽  
Vol 11 (1) ◽  
pp. e0146663 ◽  
Author(s):  
Lyndsey R. Buckner ◽  
Angela M. Amedee ◽  
Hannah L. Albritton ◽  
Pamela A. Kozlowski ◽  
Nedra Lacour ◽  
...  
Keyword(s):  
Chlamydia Trachomatis ◽  
Epithelial Cells ◽  
Hiv Transmission ◽  
Chlamydia Trachomatis Infection
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