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 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.

Dexamethasone inhibits lung epithelial cell apoptosis induced by IFN-γ and Fas

1997 ◽  
Vol 273 (5) ◽  
pp. L921-L929 ◽  
Author(s):  
Long-Ping Wen ◽  
Kamyar Madani ◽  
Jimothy A. Fahrni ◽  
Steven R. Duncan ◽  
Glenn D. Rosen
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Cell Apoptosis ◽  
Inhibitor Of Apoptosis ◽  
Induced Expression ◽  
Lung Epithelial ◽  
Epithelial Cell Apoptosis ◽  
Ifn Γ ◽  
Induced Apoptosis

Lung epithelium plays a central role in modulation of the inflammatory response and in lung repair. Airway epithelial cells are targets in asthma, viral infection, acute lung injury, and fibrotic lung disease. Activated T lymphocytes release cytokines such as interferon-γ (IFN-γ) that can cooperate with apoptotic signaling pathways such as the Fas-APO-1 pathway to induce apoptosis of damaged epithelial cells. We report that IFN-γ alone and in combination with activation of the Fas pathway induced apoptosis in A549 lung epithelial cells. Interestingly, the corticosteroid dexamethasone was the most potent inhibitor of IFN-γ- and IFN-γ plus anti-Fas-induced apoptosis. IFN-γ induced expression of an effector of apoptosis, the cysteine protease interleukin-1β-converting enzyme, in A549 cells. Dexamethasone, in contrast, induced expression of an inhibitor of apoptosis, human inhibitor of apoptosis (hIAP-1), also known as cIAP2. We suggest that the inhibition of epithelial cell apoptosis by corticosteroids may be one mechanism by which they suppress the inflammatory response.

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.

scholarly journals Insulin-Attenuated Inflammatory Response of Dendritic Cells in Diabetes by Regulating RAGE-PKCβ1-IRS1-NF-κB Signal Pathway: A Study on the Anti-Inflammatory Mechanism of Insulin in Diabetes

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Liding Zhao ◽  
Ya Li ◽  
Qingbo Lv ◽  
Min Wang ◽  
Yi Luan ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Inflammatory Response ◽  
Neutralizing Antibody ◽  
Serine Phosphorylation ◽  
Dependent Manner ◽  
Diabetic Mice ◽  
Mice Model ◽  
Cytokines And Chemokines ◽  
Anti Inflammatory ◽  
Immune Maturation

Background. Diabetes is associated with chronic inflammation, and dendritic cells (DCs) have proinflammatory effect in diabetes. The anti-inflammatory effect of insulin on diabetes is not entirely clear. The study aims to examine insulin-induced effects on the inflammatory response in DCs. Methods. Twenty-one C57BL/6 mice were divided into 3 groups. Streptozotocin was injected into the diabetic mice model. The bone marrow-derived DCs (BMDCs) were obtained from C57BL/6 mice. CD83, CD86, and type II major histocompatibility complex (MHC-II) of BMDCs were measured by flow cytometry. The fluctuations in the RNA levels of cytokines and chemokines were analyzed by quantitative RT-PCR. The concentrations of IFN-γ and TNF-α were calculated using ELISA kits, and the proteins were detected using western blot. Results. In CD11c+ DCs derived from the spleens with hyperglycemia, the expression of CD83 and CD86 in diabetic mice was significantly upregulated, coupled with a higher secretion level of cytokines and chemokines, and increased phosphorylation of NF-κB and IκB. Insulin therapy was found to have a reversal effect on the inflammatory response and immune maturation in DCs. In AGEs-BSA-stimulated BMDCs, insulin repressed the immune maturation and downregulated the expression of RAGE, phospho-PKCβ1, and serine phospho-IRS1 in an adose-dependent manner. Such effects can be abolished by PMA, but not IR-neutralizing antibody. AGEs-BSA-induced BMDCs immune maturation was inhibited by the neutralizing antibody of RAGE, the PKCβ1 inhibitor, or the IRS1 siRNA. Conclusions. Insulin has the capability of attenuating the inflammatory response of DCs in diabetes, partly through the downregulation of RAGE expression followed by the inhibition of PKCβ1 phosphorylation and IRS1 serine phosphorylation, resulting in the inactivation of IR binding-independent NF-κB. This might partly explain the antiatherogenic effect of insulin on diabetes.

scholarly journals Nafamostat reduces systemic inflammation in TLR7-mediated virus-like illness

2021 ◽  
Author(s):  
Abi G. Yates ◽  
Caroline M. Weglinski ◽  
Yuxin Ying ◽  
Tatyana Strekalova ◽  
Daniel C. Anthony
Keyword(s):  
Virus Infection ◽  
Inflammatory Response ◽  
Forced Swim Test ◽  
Preference Test ◽  
Blood Analysis ◽  
Sickness Behaviour ◽  
Ssrna Virus ◽  
Ifn Γ ◽  
Anti Inflammatory ◽  
Sucrose Preference Test

Abstract Background: The serine protease inhibitor nafamostat has been proposed as a treatment for COVID-19, by inhibiting TMPRSS2-mediated viral cell entry. Nafamostat has been shown to have other, immunomodulatory effects, which may be beneficial for treatment, however animal models of ssRNA virus infection are lacking. In this study, we examined the potential of the dual TLR7/8 agonist R848 to mimic the host response to a ssRNA virus infection and the associated behavioural response. In addition, we evaluated the anti-inflammatory effects of nafamostat in this model. Methods: CD-1 mice received an intraperitoneal injection of R848 (200μg, prepared in DMSO, diluted 1:10 in saline) or diluted DMSO alone, and an intravenous injection of either nafamostat (100μL, 3mg/kg in saline) or saline. Sickness behaviour was determined by temperature, food intake, sucrose preference test, open field and forced swim test. Blood and fresh liver, lung and brain were collected 6 hours post-challenge to measure markers of peripheral and central inflammation by blood analysis and qPCR. Results: R848 induced a robust inflammatory response, as evidenced by increased expression of TNF, IFN-γ, CXCL1 and CXCL10 in the liver, lung and brain, as well as a sickness behaviour phenotype. Exogenous administration of nafamostat suppressed the hepatic inflammatory response, significantly reducing TNF and IFN-γ expression, but had no effect on lung or brain cytokine production. R848 administration depleted circulating leukocytes, which was restored by nafamostat treatment. Conclusions: Our data indicate that R848 administration provides a useful model of ssRNA virus infection, which induces inflammation in the periphery and CNS, and virus infection-like illness. In turn, we show that nafamostat has a systemic anti-inflammatory effect, in the presence of the TLR7/8 agonist. Therefore, the results indicate that nafamostat has anti-inflammatory actions, beyond its ability to inhibit TMPRSS2, that might potentiate its anti-viral actions in pathologies such as COVID-19.

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