scholarly journals Vaginal lactic acid elicits an anti-inflammatory response from human cervicovaginal epithelial cells and inhibits production of pro-inflammatory mediators associated with HIV acquisition

2017 ◽  
Vol 10 (6) ◽  
pp. 1480-1490 ◽  
Author(s):  
A C Hearps ◽  
D Tyssen ◽  
D Srbinovski ◽  
L Bayigga ◽  
D J D Diaz ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Inflammatory Mediators ◽  
Anti Inflammatory ◽  
Hiv Acquisition

Lactic Acid, a Vaginal Microbiota Metabolite, Elicits an Anti-inflammatory Response from Vaginal and Cervical Epithelial Cells

2014 ◽  
Vol 30 (S1) ◽  
pp. A238-A239 ◽  
Author(s):  
Anna Hearps ◽  
Raffi Gugasyan ◽  
Daniela Srbinovski ◽  
David Tyssen ◽  
Muriel Aldunate ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Vaginal Microbiota ◽  
Cervical Epithelial Cells ◽  
Anti Inflammatory

scholarly journals Inflammatory Response Elicited by Ureaplasma parvum colonization in human cervical epithelial, stromal, and immune cells

Reproduction ◽  
2021 ◽  
Author(s):  
Ourlad Alzeus Gaddi Tantengco ◽  
Talar Kechichian ◽  
Kathleen L Vincent ◽  
Richard B Pyles ◽  
Paul Mark B Medina ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Stromal Cells ◽  
Female Reproductive Tract ◽  
Ureaplasma Parvum ◽  
Cervical Epithelial Cells ◽  
Anti Inflammatory ◽  
The Impact

Ureaplasma parvum is a commensal bacterium in the female reproductive tract but has been associated with pregnancy complications such as preterm prelabor rupture of membranes and preterm birth (PTB). However, the pathologic effects of U. parvum in the cervix, that prevents ascending infections during pregnancy, are still poorly understood. To determine the impact of U. parvum on the cervix, ectocervical (ecto) and endocervical (endo) epithelial and stromal cells were incubated with U. parvum. Macrophages were also tested as a proxy for cervical macrophages to determine the antigenicity of U. parvum. The effects of U. parvum, including influence on cell cycle and cell death, antimicrobial peptide production, epithelial-to-mesenchymal transition (EMT), and inflammatory cytokine levels, were assessed. U. parvum colonized cervical epithelial and stromal cells 4 hours post-infection. Like uninfected control, U. parvum neither inhibited cell cycle progression and nor caused cell death in cervical epithelial and stromal cells. U. parvum increased the production of the antimicrobial peptides (AMPs) cathelicidin and human β-defensin 3 and exhibited weak signs of EMT evidenced by decreased cytokeratin 18 and increased vimentin expression in cervical epithelial cells. U. parvum induced a pro-inflammatory environment (cytokines) and increased MMP-9 in cervical epithelial cells but promoted pro- and anti-inflammatory responses in cervical stromal cells and macrophages. U. parvum may colonize the cervical epithelial layer, but induction of AMPs and anti-inflammatory response may protect the cervix and may prevent ascending infections that can cause PTB. These findings suggest that U. parvum is a weak inducer of inflammation in the cervix.

scholarly journals Platelet-Rich Fibrin Decreases the Inflammatory Response of Mesenchymal Cells

2021 ◽  
Vol 22 (21) ◽  
pp. 11333
Author(s):  
Zahra Kargarpour ◽  
Jila Nasirzade ◽  
Layla Panahipour ◽  
Richard J. Miron ◽  
Reinhard Gruber
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Mediators ◽  
Nuclear Translocation ◽  
Mesenchymal Cells ◽  
Pathological Process ◽  
Buffy Coat ◽  
Inflammatory Activity ◽  
Platelet Rich Fibrin ◽  
Enhanced Expression ◽  
Anti Inflammatory

Chronic inflammation is a pathological process where cells of the mesenchymal lineage become a major source of inflammatory mediators. Platelet-rich fibrin (PRF) has been shown to possess potent anti-inflammatory activity in macrophages, but its impact on mesenchymal cells has not been investigated. The aim of this study was, therefore, to expose mesenchymal cells to inflammatory cytokines together with lysates generated from liquid platelet-poor plasma (PPP), the cell-rich buffy coat layer (BC; concentrated-PRF or C-PRF), and the remaining red clot layer (RC), following centrifugation of blood. Heating PPP generates an albumin gel (Alb-gel) that when mixed back with C-PRF produces Alb-PRF. Membranes prepared from solid PRF were also subjected to lysis. We report here that lysates of PPP, BC, and PRF decreased the cytokine-induced expression of interleukin 6 (IL6) and nitric oxide synthase (iNOS) in the bone marrow-derived ST2 cells. Consistently, PPP, BC, and PRF greatly decreased the phosphorylation and nuclear translocation of p65 in ST2 cells. The inflammatory response caused by Pam3CSK4 was reduced accordingly. Moreover, PPP, BC, and PRF reduced the enhanced expression of inflammatory mediators IL6 and iNOS in 3T3-L1 pre-adipocyte mesenchymal cells, and iNOS and CCL5 in murine calvarial cells. Surprisingly, PRF lysates were not effective in reducing the inflammatory response of human gingival fibroblasts and HSC2 epithelial cells. The data from the present study suggest that both liquid PRF and solid PRF exert potent anti-inflammatory activity in murine mesenchymal cells.

scholarly journals Intestinal CD103+CD11b− dendritic cells restrain colitis via IFN-γ-induced anti-inflammatory response in epithelial cells

2015 ◽  
Vol 9 (2) ◽  
pp. 336-351 ◽  
Author(s):  
A R B M Muzaki ◽  
P Tetlak ◽  
J Sheng ◽  
S C Loh ◽  
Y A Setiagani ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Ifn Γ ◽  
Anti Inflammatory

scholarly journals Anti-Inflammatory and Anti-Oxidant Effect of Dimethyl Fumarate in Cystic Fibrosis Bronchial Epithelial Cells

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 2132
Author(s):  
Onofrio Laselva ◽  
Caterina Allegretta ◽  
Sante Di Gioia ◽  
Carlo Avolio ◽  
Massimo Conese
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Dimethyl Fumarate ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Inflammatory Status ◽  
Anti Oxidant ◽  
Anti Inflammatory ◽  
Oxidant Effect

Cystic Fibrosis (CF) is caused by mutations on the CF transmembrane conductance regulator (CFTR) gene and is associated with chronic infection and inflammation. Recently, it has been demonstrated that LPS-induced CFTR dysfunction in airway epithelial cells is due to an early oxidative stress. Dimethyl fumarate (DMF) is an approved anti-inflammatory and anti-oxidant drug for auto-immune and inflammatory diseases, but its role in the CF has never been investigated. In this study, we examined the effect of DMF on CF-related cytokines expression, ROS measurements and CFTR channel function. We found that DMF reduced the inflammatory response to LPS stimulation in both CF and non-CF bronchial epithelial cells, both as co-treatment and therapy, and restored LPS-mediated decrease of Trikafta™-mediated CFTR function in CF cells bearing the most common mutation, c.1521_1523delCTT (F508del). DMF also inhibited the inflammatory response induced by IL-1β/H2O2 and IL-1β/TNFα, mimicking the inflammatory status of CF patients. Finally, we also demonstrated that DMF exhibited an anti-oxidant effect on CF cells after different inflammatory stimulations. Since DMF is an approved drug, it could be further investigated as a novel anti-inflammatory molecule to ameliorate lung inflammation in CF and improve the CFTR modulators efficacy.

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