scholarly journals Nitro-fatty acids decrease type I interferons and monocyte chemoattractant protein 1 in ex vivo models of inflammatory arthritis

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
A. L. Hansen ◽  
L. S. J. Rahbek ◽  
A. S. Sørensen ◽  
M. P. Hundahl ◽  
S. Lomholt ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Synovial Fluid ◽  
Inflammatory Arthritis ◽  
Mononuclear Cells ◽  
Type I Interferon ◽  
Type I Interferons ◽  
Type I ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein

Abstract Background Inflammatory arthritis including rheumatoid arthritis (RA) and spondyloarthritis (SpA) is characterized by inflammation and destruction of the joints. Approximately one third of patients do not respond to first-line treatments. Nitro-fatty acids are bioactive lipids with anti-inflammatory properties and tissue-protective functions. The nitro-fatty acid 10-NO2-oleic acid (10-NO2-OA) is being tested in clinical trials for patients with fibrotic and inflammatory conditions. Here, we tested whether 10-NO2-OA could inhibit immune reactions involved in the inflammatory and joint destructive processes in inflammatory arthritis. Methods Synovial fluid and blood samples were obtained from 14 patients with active RA or SpA. The in vitro models consisted of synovial fluid mononuclear cells (SFMCs) cultured for 48 h, SFMCs cultured for 21 days, and fibroblast-like synovial cells (FLSs) co-cultured with peripheral blood mononuclear cells (PBMCs) for 48 h. Cells were treated with or without 10-NO2-OA or the tumor necrosis factor alpha (TNFα) inhibitor etanercept. Supernatants were analyzed for type I interferon, monocyte chemoattractant protein-1 (MCP-1), matrix metalloproteinase 3 (MMP3) and tartrate resistant acid phosphatase (TRAP). Results In SFMCs cultured for 48 h, 10-NO2-OA dose-dependently decreased the secretion of bioactive type I interferons and MCP-1 but not MMP3 (P = 0.032, P = 0.0001, and P = 0.58, respectively). Both MCP-1 and MMP3 were decreased by etanercept (P = 0.0031 and P = 0.026, respectively). In SFMCs cultured for 21 days, 10-NO2-OA significantly decreased the production of MCP-1 but not TRAP (P = 0.027 and P = 0.1523, respectively). Etanercept decreased the production of TRAP but not MCP-1 (P < 0.001 and P = 0.84, respectively). In co-cultures of FLSs and PBMCs, 10-NO2-OA decreased the production of MCP-1 (P < 0.0001). This decrease in MCP-1 production was not seen with etanercept treatment (P = 0.47). Conclusion 10-NO2-OA decreased the release of MCP-1 in three models of inflammatory arthritis. Of particular interest, 10-NO2-OA inhibited type I interferon, and 10-NO2-OA was more effective in reducing MCP-1 production in cultures dominated by FLSs compared with etanercept. Our results encourage clinical investigations of 10-NO2-OA in patients with inflammatory arthritis.

Monocyte Chemoattractant Protein 1 Expression in Synovial Fluid of Patients With Total Hip Arthroplasty

2011 ◽  
Vol 36 (5) ◽  
pp. 487-491 ◽  
Author(s):  
Monica Montesi ◽  
Alina Beraudi ◽  
Susanna Stea ◽  
Cristina Ancarani ◽  
Francesco Traina ◽  
...  
Keyword(s):  
Synovial Fluid ◽  
Total Hip Arthroplasty ◽  
Hip Arthroplasty ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Total Hip ◽  
Monocyte Chemoattractant Protein

Monocyte Chemoattractant Protein-1-Induced Protein in Age-Related Atrial Fibrillation and Its Association with Circulating Fibrosis Biomarkers

Cardiology ◽  
2019 ◽  
Vol 142 (4) ◽  
pp. 244-249 ◽  
Author(s):  
Gege Zhang ◽  
Asiyanmu Abuduoufu ◽  
Xianhui Zhou ◽  
Yaodong Li ◽  
Ling Zhang ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Correlation Analysis ◽  
The Elderly ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Type I ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Age Related

Background: Atrial fibrillation (AF), for which age is an independent risk factor, is the most common persistent arrhythmia. Monocyte chemoattractant protein-1-induced protein (MCPIP), a transcription factor that induces a series of inflammation and cell death procedures, has been indicated to cause cardiomyocyte death in ischemic cardiomyopathy. The objective of this research was to investigate the relationship between age-related AF and MCPIP. Methods: A total of 1,084 participants were included in this study, including 542 AF patients and 542 non-AF controls. Their medical histories were collected and analyzed. Moreover, blood samples were collected, and ELISA tests for expression of the inflammatory factor MCPIP and the fibrosis biomarkers pro-collagen type III N-terminal peptide (PIIINP) and type I collagen C-terminal telopeptide (ICTP) were conducted. Finally, a correlation analysis of these inflammatory factors and biomarkers was performed based on the ELISA results. Results: We compared the echocardiography results of AF patients and found that the left ventricular ejection fraction and left atrial appendage velocity decreased with age (p < 0.05). Moreover, ELISA analysis of these samples showed that the expression of MCPIP was the highest in elderly patients with AF (p < 0.05), and there was no significant difference in expression between adult AF patients and elderly controls (p > 0.05). Finally, the correlation analysis demonstrated that the expressions of MCPIP, PIIINP, and ICTP were positively correlated in the elderly AF patient group, the adult AF group, and the elderly control group (p < 0.05). Conclusion: MCPIP expression was higher in age-related AF than in the other patient groups and it was associated with AF-induced fibrosis.

scholarly journals The monocyte chemoattractant protein-1/CCR2 loop, inducible by TGF-β, increases podocyte motility and albumin permeability

2009 ◽  
Vol 297 (1) ◽  
pp. F85-F94 ◽  
Author(s):  
Eun Young Lee ◽  
Choon Hee Chung ◽  
Charbel C. Khoury ◽  
Tet Kin Yeo ◽  
Petr E. Pyagay ◽  
...  
Keyword(s):  
Transforming Growth Factor ◽  
Disease Process ◽  
Transforming Growth Factor Β ◽  
Cellular Migration ◽  
Type I ◽  
Kidney Cells ◽  
Monocyte Chemoattractant Protein 1 ◽  
Permeability Characteristics ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein

The role of monocyte chemoattractant protein-1 (MCP-1) in diabetic nephropathy is typically viewed through the lens of inflammation, but MCP-1 might exert noninflammatory effects on the kidney cells directly. Glomerular podocytes in culture, verified to express the marker nephrin, were exposed to diabetic mediators such as high glucose or angiotensin II and assayed for MCP-1. Only transforming growth factor-β (TGF-β) significantly increased MCP-1 production, which was prevented by SB431542 and LY294002, indicating that signaling proceeded through the TGF-β type I receptor kinase and the phosphatidylinositol 3-kinase pathway. The TGF-β-induced MCP-1 was found to activate the podocyte's cysteine-cysteine chemokine receptor 2 (CCR2) and, as a result, enhance the cellular motility, cause rearrangement of the actin cytoskeleton, and increase podocyte permeability to albumin in a Transwell assay. The preceding effects of TGF-β were replicated by treatment with recombinant MCP-1 and blocked by a neutralizing anti-MCP-1 antibody or a specific CCR2 inhibitor, RS102895. In conclusion, this is the first description that TGF-β signaling through PI3K induces the podocyte expression of MCP-1 that can then operate via CCR2 to increase cellular migration and alter albumin permeability characteristics. The pleiotropic effects of MCP-1 on the resident kidney cells such as the podocyte may exacerbate the disease process of diabetic albuminuria.

scholarly journals RANTES and Monocyte Chemoattractant Protein–1 (MCP-1) Play an Important Role in the Inflammatory Phase of Crescentic Nephritis, but Only MCP-1 Is Involved in Crescent Formation and Interstitial Fibrosis

1997 ◽  
Vol 185 (7) ◽  
pp. 1371-1380 ◽  
Author(s):  
Clare M. Lloyd ◽  
Andrew W. Minto ◽  
Martin E. Dorf ◽  
Amanda Proudfoot ◽  
Timothy N.C. Wells ◽  
...  
Keyword(s):  
Functional Role ◽  
Type I Collagen ◽  
Interstitial Fibrosis ◽  
Inflammatory Cells ◽  
Type I ◽  
Crescent Formation ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Inflammatory Phase

The involvement of chemokines in inflammation is well established, but their functional role in disease progression, and particularly in the development of fibrosis, is not yet understood. To investigate the functional role that the chemokines monocyte chemoattractant protein–1 (MCP-1) and RANTES play in inflammation and the progression to fibrosis during crescentic nephritis we have developed and characterized a murine model for this syndrome. Significant increases in T-lymphocytes and macrophages were observed within glomeruli and interstitium, paralleled by an induction of mRNA expression of MCP-1 and RANTES, early after disease initiation. Blocking the function of MCP-1 or RANTES resulted in significant decreases in proteinuria as well as in numbers of infiltrating leukocytes, indicating that both MCP-1 and RANTES (regulated upon activation in normal T cells expressed and secreted) play an important role in the inflammatory phase of crescentic nephritis. In addition, neutralization of MCP-1 resulted in a dramatic decrease in both glomerular crescent formation and deposition of type I collagen. These results highlight a novel role for MCP-1 in crescent formation and development of interstitial fibrosis, and indicate that in addition to recruiting inflammatory cells this chemokine is critically involved in irreversible tissue damage.

scholarly journals Glutamine May Repress the Weak LPS and Enhance the Strong Heat Shock Induction of Monocyte and Lymphocyte HSP72 Proteins but May Not Modulate the HSP72 mRNA in Patients with Sepsis or Trauma

2015 ◽  
Vol 2015 ◽  
pp. 1-15 ◽  
Author(s):  
Efrossini Briassouli ◽  
Marianna Tzanoudaki ◽  
Dimitris Goukos ◽  
Christina Routsi ◽  
Serafim Nanas ◽  
...  
Keyword(s):  
Heat Shock ◽  
Mononuclear Cells ◽  
Illness Severity ◽  
Healthy Individuals ◽  
Peripheral Blood Mononuclear ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Blood Mononuclear Cells ◽  
Heat Shock Induction

Objective. We assessed the lipopolysaccharide (LPS) or heat shock (HS) induction of heat shock protein-72 (HSP72) in peripheral blood mononuclear cells (PBMCs) of patients with severe sepsis (SS) or trauma-related systemic inflammatory response syndrome (SIRS), compared to healthy individuals (H); we also investigated any pre- or posttreatment modulating glutamine (Gln) effect.Methods. SS (11), SIRS (10), and H (19) PBMCs were incubated with 1 μg/mL LPS or 43°HS. Gln 10 mM was either added 1 h before or 1 h after induction or was not added at all. We measured monocyte (m), lymphocyte (l), mRNA HSP72, HSP72 polymorphisms, interleukins (ILs), monocyte chemoattractant protein-1 (MCP-1), and cortisol levels.Results. Baseline lHSP72 was higher in SSp<0.03, and mHSP72 in SIRSp<0.02, compared to H. Only HS induced l/mHSP72/mRNA HSP72; LPS induced IL-6, IL-8, IL-10, and MCP-1. Induced mRNA was related to l/mHSP72, and was related negatively to cytokines. Intracellular l/mHSP72/HSP72 mRNA was related to serum ILs, not being influenced by cortisol, illness severity, and HSP72 polymorphisms. Gln did not induce mRNA in any group but modified l/mHSP72 after LPS/HS induction unpredictably.Conclusions. HSP72 mRNA and l/mHSP72 are higher among critically ill patients, further induced by HS, not by LPS. HSP72 proteins and HSP72 mRNA are related to serum ILs and are negatively related to supernatant cytokines, not being influenced by HSP72 polymorphisms, cortisol, or illness severity. Gln may depress l/mHSP72 after LPS exposure and enhance them after HS induction, but it may not affect early induced HSP72 mRNA.

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