scholarly journals Secretion of pro-inflammatory cytokines and chemokines and loss of regulatory signals by fibroblast-like synoviocytes in juvenile idiopathic arthritis

2017 ◽  
Vol 11 (5-6) ◽  
pp. 1600088 ◽  
Author(s):  
AnneMarie C. Brescia ◽  
Megan M. Simonds ◽  
Kathleen E. Sullivan ◽  
Carlos D. Rose
Author(s):  
Sanjukta Majumder et al.

IL-36 has been implicated in the pathogenesis of spondyloarthropathies (SpA) like psoriasis and inflammatory bowel disease. Enthesitis related arthritis (ERA) category of juvenile idiopathic arthritis is a form of juvenile SpA, however no data is available on the role of IL-36 in this disease. IL-36α, β, γ and IL-36R mRNA expression in blood and synovial fluid mononuclear cells and IL-36α, γ, IL-36Ra, IL-6 and IL-17 levels were measured in serum and synovial fluid (SF). IL-36γ production by fibroblast like synoviocytes (FLS) by pro-inflammatory cytokines and its effect on FLS was also studied.mRNA levels of IL-36α, IL-36γ and IL-36R were increased in PBMCs of ERA patients as compared to healthy controls however only IL-36γ was measurable in serum of one third of patients. In SFMCs, all 4 mRNA were detectable but were lower than RA patients. SF IL-36γ levels correlated with disease activity score (r=0.51, p< 0.0001), SF IL-6 (r=0.4,p= 0.0063) and IL-17 levels (r=0.57,p=0.0018). Pro-inflammatory cytokines increased expression of IL-36γ and IL-6 in FLS cultures. SFs from 5 ERA patients also increased expressions of IL-36γ and IL-6 in FLS which could be blocked by using IL-36Ra.This suggests that pro-inflammatory cytokines aid in upregulation of IL-36γ which in turn upregulates expression of IL-6. This might lead to a positive feedback loop of inflammation in ERA. Association of SF levels of IL-36γ with disease activity further supports this possibility. IL-36Ra based therapy may have a role in ERA.


Author(s):  
Anita Aminoshariae ◽  
Mohammed Bakkar ◽  
Tracey Bonfield ◽  
Santosh Ghosh ◽  
Thomas A Montagnese ◽  
...  

Objective: The aim of this study was to investigate the levels of Human Beta Defensin (hBD) 2 and 3, chemokine and cytokine expressions between teeth endodontically diagnosed with symptomatic irreversible pulpitis (SIP), asymptomatic irreversible pulpitis (ASIP) and normal pulps. We hypothesized that there would be a correlation between hBD’s and the immunoregulatory response. Design: Pulpal samples were collected with paper points. Six samples were obtained from normal teeth, 21 from SIP, 18 from ASIP. Levels of cytokines and betadefensins were measured by Luminex technology and ELISA, respectively. Data were statistically analyzed using Kruskal-Wallis, Wilcoxon Mann-Whitney test and Spearman correlation test. Differences were considered significant at p<0.05. Results: hBD-2 levels correlated with samples obtained from patients in the ASIP group, but not in the samples obtained from patients with SIP or the control group. HBD-3 concentrations associated with all of the cytokines and chemokines in both SIP and ASIP groups. However, in the normal group, hBD-3 correlated with only TNFα, IL-8, MCP-1, IL-1β, MIP-1a, RANTES, IL-17 in normal group. When comparing control levels of hBD-2 and hBD-3 with patients samples from either the ASIP or the SIP groups, hBD-2 and hBD-3 concentrations were highest in the ASIP group. Conclusions: The hBD-2 and-3 were highly associated with the levels of the chemokines and cytokines in ASIP group. HBD-3 concentrations correlate with the levels of the chemokines and the cytokines in the SIP and ASIP groups.


2008 ◽  
Vol 126 (3) ◽  
pp. 345-352 ◽  
Author(s):  
Jane E. Onken ◽  
Paula K. Greer ◽  
Brian Calingaert ◽  
Laura P. Hale

2020 ◽  
Author(s):  
Shashikant Ray ◽  
Keshav Rajarshi ◽  
Aroni Chatterjee

The world is currently facing one of its deadliest nightmares, the rise of a global pandemic called COVID-19. The disease is caused by a positive stranded RNA virus called SARS-CoV-2. The virus mainly targets the pulmonary epithelial cells as it’s initial site of infection by letting its surface spike protein interact and bind to the host ACE2 receptor. The internalization and gradual replication of the virus results in an exaggerated immune response triggering release of many pro-inflammatory cytokines and chemokines. This immune storm is responsible for multiple health hazards in the host ultimately leading to multiple organ failure. Mesenchymal stem cell therapy offers a promising approach towards mitigating the delirious effects of the infection in the COVID-19 patients. This therapy has shown to reduce the expression of pro-inflammatory cytokines as well as repair of damaged tissues in COVID-19 patients. This review has been organized to put forward all the positive aruments and implications in support of mesenchymal stem cell therapy as a necessary approach for treating COVID-19 patients.


2020 ◽  
Vol 14 (3) ◽  
pp. e0008101 ◽  
Author(s):  
Anuradha Rajamanickam ◽  
Saravanan Munisankar ◽  
Chandrakumar Dolla ◽  
Pradeep A. Menon ◽  
Kannan Thiruvengadam ◽  
...  

2019 ◽  
Vol 26 (3-4) ◽  
pp. 305-313 ◽  
Author(s):  
Oluwatobi T. Somade ◽  
Babajide O. Ajayi ◽  
Nurudeen O. Tajudeen ◽  
Eniola M. Atunlute ◽  
Adewale S. James ◽  
...  

2020 ◽  
Author(s):  
Xiao-Feng Li ◽  
Qing-Qing Xu ◽  
Man-Wen Yang ◽  
He Chen ◽  
Su-Qin Yin ◽  
...  

Abstract Background: Rheumatoid arthritis (RA) is characterized by a tumor-like expansion of the synovium and the subsequent destruction of adjacent articular cartilage and bone. Recent studies have shown that phosphatase and tension homolog deleted on chromosome 10 (PTEN) might contribute to the survival of fibroblast-like synoviocytes (FLS) and the production of pro-inflammatory cytokines in RA.Methods : The expression was determined in RA and adjuvant-induced arthritis (AIA) synovial tissues by immunohistochemistry. FLSs were treatment with bpv, PTEN-RNAi or over-expression plasmid in RA and AIA. FLSs migration was assessed. The ad-PTEN was also injected into the knee of AIA in vivo. Chromatin Immunoprecipitation (ChIP) and Methylation-special PCR (MSP) assay were used to study the expression of PTEN mRNA in DNA methylation.Results : Down-regulated level of PTEN expression was observed in RA and AIA. Inhibition PTEN expression by bpv or PTEN-RNAi could promote the expression of pro-inflammatory cytokines, chemokines and migration of FLS with TNF-α in RA and AIA. Consistently, over-expression of PTEN reduced their low-expression of pro-inflammatory cytokines, chemokines and migration. Intra-articular injection of ad-PTEN in AIA knees dramatically reduced inflammatory and paw swelling in vivo. The ChIP and MSP assay has clearly detected the DNA methylation of PTEN was increased in FLS with TNF-α. Moreover, intraperitoneally injected 5-Aza in AIA also suppressed the inflammatory and paws swelling in vivo.Conclusions: Our findings suggest that over-expression PTEN attenuates the formation of pro-inflammatory cytokines, chemokines and migration of FLS, and it may be regulated by DNA methylation in the pathogenesis of RA.


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