Figure 1 - uploaded by Oscar Rojas-Espinosa
Content may be subject to copyright.
Thickness of the rear paws of healthy (upper panel) and CIA (lower panel) DBA-1 mice measured 53 days after CII immunization. CIA mice subjected to treatment with dexamethasone presented pads similar to healthy pads, but the mice treated with ω3, ω6 and ω9 UFAs showed variable degrees of inflammation (see text).
Context in source publication
Context 1
... changes appeared by day 11, but the arthritis became overt by day 21 in the mice that received a booster on day 14. Representative images of the rear pads of a healthy mouse and a CII-immunized mouse are shown in Figure 1. Mice receiving diverse treatments showed inflammatory re- sponses that ranged between these two extremes. ...
Similar publications
Commencing with the breakdown of immune tolerance, multiple pathogenic factors, including synovial inflammation and harmful cytokines, are conjointly involved in the progression of rheumatoid arthritis. Intervening to mitigate some of these factors can bring a short-term therapeutic effect, but other unresolved factors will continue to aggravate th...
Objective
Using the traditional Chinese medicine theory of “Bi-zheng" caused by kidney deficiency, combined with modern medical science and technology, this study assessed the relationships among organ weight, cytokines, pathological manifestations, and traditional Chinese medicine kidney deficiency syndrome in rats with rheumatoid arthritis.
Meth...
Background
CTLA4Ig is a dimeric fusion protein of the extracellular domain of cytotoxic T-lymphocyte protein 4 (CTLA4) and an Fc (Ig) fragment of human IgG 1 that is approved for treating rheumatoid arthritis. However, CTLA4Ig may induce adverse effects. Developing a lesion-selective variant of CTLA4Ig may improve safety while maintaining the effic...
Objectives:
To investigate the effects of the oestradiol (ES) pulsed bone marrow-derived mesenchymal stem cells (BM-MSC) to treat adjuvant-induced arthritis in Wistar rats.
Materials and methods:
BM-MSCs were pulsed with ES (0, 10,100, and 1000 nM) for 24 hr. RA was induced by collagen and Freund's Complete Adjuvant into the base of the tail of...
Despite the remarkable advances in therapeutics for rheumatoid arthritis (RA), a large number of patients still lack effective countermeasures. Recently, the reprogramming of macrophages to an immunoregulatory phenotype has emerged as a promising therapeutic strategy for RA. Here, we report metabolically engineered exosomes that have been surface-m...
Citations
... Two weeks later, the mice received a similar, intraperitoneal injection of C-II in incomplete Freund's adjuvant. 23 Noninoculated DBA-1 mice were included as a control group. ...
... The dosages chosen were based on previous studies where significant anti-inflammatory effects were observed. 23,25 Following the initiation of treatment, the arthritis development was evaluated with a clinical score and by calculating an arthritis index as proposed by Sharma et al. 26 Clinical score was assessed by evaluating the inflammatory changes according to the scale: one inflamed finger/toe = 1 point; one knuckle = 1 point; one wrist = 5 points; and one ankle = 5 points (points per mouse = 60). The arthritis index (AI) was calculated from the pad thickness with the formula: AI = [(limb thickness on day X − limb thickness on day 0)/ limb thickness on day 0)] × 100. ...
... 46 Its beneficial effect in the CIA model has already been reported. 23,47 Finally, the histopathological findings correlated with the anti-inflammatory effects of DLE and ω-UFAs, as these substances significantly limited the disease signs, including inflammatory infiltrate, synovial hyperplasia, arthrosis, and bone and cartilage degeneration. ...
Rheumatoid arthritis is a disabling autoimmune disease with a high global prevalence. Treatment with disease‐modifying anti‐arthritic drugs (DIMARDs) has been routinely used with beneficial effects but with adverse long‐term consequences; novel targeted biologics and small‐molecule inhibitors are promising options. In this study, we investigated whether purified omega unsaturated fatty acids (ω‐UFAs) and dialysable leukocyte extracts (DLEs) prevented the development of arthritis in a model of collagen‐induced arthritis (CIA) in mice. We also investigated whether the transcription factor NF‐κB and the NLRP3 inflammasome were involved in the process and whether their activity was modulated by treatment. The development of arthritis was evaluated for 84 days following treatment with nothing, dexamethasone, DLEs, docosahexaenoic acid, arachidonic acid, and oleic acid. Progression of CIA was monitored by evaluating clinical manifestations, inflammatory changes, and histological alterations in the pads’ articular tissues. Both DLEs and ω‐UFAs led to an almost complete inhibition of the inflammatory histopathology of CIA and this was concomitant with the inhibition of NF‐kB and the inhibition of the activation of NLRP3. These data suggest that ω‐UFAs and DLEs might have NF‐κB as a common target and that they might be used as ancillary medicines in the treatment of arthritis.
... 36 Oleic acid exerts anti-arthritic effect by reducing inflammatory cell infiltration. 37 These reports imply that the inflammatory mediator inhibitory effect of DCEO may be, at least in part, due to the presence of these compounds. Further studies are needed to identify active constituents inside DCEO. ...
Background
Dingchuan tang (asthma-relieving decoction), a formula of nine herbs, has been used for treating respiratory inflammatory diseases for >400 years in the People’s Republic of China. However, the mechanisms underlying the anti-inflammatory action of dingchuan tang is not fully understood. This study aims to investigate the effects of Dingchuan tang essential oil (DCEO) on inflammatory mediators and the underlying mechanism of action.
Materials and methods
DCEO was extracted by steam distillation. Lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages were used as the cell model. Production of nitric oxide (NO) was determined by the Griess test. Protein secretion and mRNA levels of inflammatory mediators were measured by the enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. Protein levels were examined by Western blot. Nuclear localization of nuclear factor-kappa B (NF-κB) was detected using immunofluorescence analyses.
Results
DCEO significantly reduced LPS-triggered production of NO and prostaglandin E2 (PGE2) and decreased protein and mRNA levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). LPS induced upregulation of protein and mRNA levels of cytokines (interleukin-1β [IL-1β], interleukin-6 [IL-6], tumor necrosis factor-α [TNF-α]), and chemokines (monocyte chemoattractant protein-1 [MCP-1], chemokine [C-C motif] ligand 5 [CCL-5], and macrophage inflammatory protein [MIP]-1α) were suppressed by DCEO treatment. Phosphorylation and nuclear protein levels of transcription factors (activator protein-1 [AP-1], NF-κB, interferon regulatory factor 3 [IRF3]) were decreased by DCEO. Protein levels of phosphorylated IκB-α, IκB kinase α/β (IKKα/β), phosphatidylinositol 3-kinase (PI3K), protein kinase B (Akt), TGF β-activated kinase 1 (TAK1), TANK-binding kinase 1 (TBK1), extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (p38), and c-Jun N-terminal kinase (JNK) were lowered by DCEO. Moreover, degradation of interleukin-1 receptor-associated kinase 1 (IRAK1) and IRAK4 induced by LPS was inhibited by DCEO treatment.
Conclusion
Suppression of the interleukin-1 receptor-associated kinase (IRAK)/NF-κB, IRAK/AP-1 and TBK1/IRF3 pathways was associated with the inhibitory effects of DCEO on inflammatory mediators in LPS-stimulated RAW264.7 macrophages. This study provides a pharmacological justification for the use of dingchuan tang in managing inflammatory disorders.
Metabolic reprogramming of immune cells modulates their function and reduces the severity of autoimmune diseases. However, the long-term effects of the metabolically reprogrammed cells, specifically in the case of immune flare-ups, need to be examined. Herein, a re-induction rheumatoid arthritis (RA) mouse model was developed by injecting T-cells from RA mice into drug-treated mice to recapitulate the effects of T-cell-mediated inflammation and mimic immune flare-ups. Immune metabolic modulator paKG(PFK15 + bc2) microparticles (MPs) were shown to reduce clinical symptoms of RA in collagen-induced arthritis (CIA) mice. Upon re-induction, a significant delay in the reappearance of clinical symptoms in the paKG(PFK15 + bc2) microparticle treatment group was observed as compared to equal or higher doses of the clinically utilized U.S. Food and Drug Administration (FDA)-approved drug, Methotrexate (MTX). Furthermore, paKG(PFK15 + bc2) microparticle-treated mice were able to lower activated dendritic cells (DCs) and inflammatory T helper cell 1 (TH1) and increased activated, proliferating regulatory T-cells (Tregs) more effectively than MTX. The paKG(PFK15 + bc2) microparticles also led to a significant reduction in paw inflammation in mice as compared to MTX treatment. This study can pave the way for the development of flare-up mouse models and antigen-specific drug treatments.
It is estimated that 355 million people suffer from arthritis in the world. Rheumatoid arthritis (RA) is the most common type of autoimmune disease that primarily affects the joints. Humans obtain about 25–40% calories from dietary fats. This article summarizes the findings of recent studies regarding the effect of dietary fat on the risk and treatment of RA. The thorough literature review has clearly demonstrated that the effects of saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), n‐3 polyunsaturated fatty acids (PUFAs), and n‐6 polyunsaturated fatty acids (PUFAs) on RA are multifaceted. Research from both animal experiments and human clinical trials provide solid evidence that n‐3 PUFAs and MUFAs possess an anti‐inflammatory activity and have beneficial effects on RA. In contrast, SFAs may promote arthritis by enhancing inflammation and disturbing bone homeostasis. Amongst n‐6 PUFAs, gamma‐linolenic acid (GLA) and dihomo‐gamma‐linolenic acid (DGLA) are antiarthritic, whereas the effects of linoleic acid (LA) and arachidonic acid (ARA) on arthritic progression still remain elusive.
