IL-38 exerts anti-inflammatory and anti-fibrotic effects in thyroid-associated ophthalmopathy

2021 ◽  
Author(s):  
Lu Shi ◽  
Huijing Ye ◽  
Jun Huang ◽  
Yanbing Li ◽  
Xing Wang ◽  
...  
Keyword(s):  
Disease Activity ◽  
Protective Role ◽  
Enzyme Linked Immunosorbent Assay ◽  
Clinical Activity ◽  
Connective Tissues ◽  
Thyroid Associated Ophthalmopathy ◽  
Organ Specific ◽  
Anti Inflammatory ◽  
Star Molecules

Abstract Context Thyroid-associated ophthalmopathy (TAO) is an organ-specific autoimmune disease closely associated with Graves’ disease (GD). IL-38, a novel cytokine in the IL-1 superfamily, has been reported to be involved in the pathogenesis of various autoimmune diseases. Objectives To evaluate the relationship between IL-38 and TAO disease activity and its role in inflammation and fibrosis in TAO. Design/Setting/Participants Blood samples and orbital connective tissues were collected from TAO patients and controls. Orbital fibroblasts (OFs) were isolated from patients with TAO. Main Outcome Measures Enzyme-linked immunosorbent assay (ELISA), immunohistochemistry (IHC), flow cytometry, immunofluorescence, quantitative real-time PCR and western blot analysis were performed. Results Here, we demonstrated that IL-38 levels decreased in the circulation and orbital connective tissues of patients with TAO compared to the controls, and were negatively correlated with the clinical activity score (CAS). In vitro, potent anti-inflammatory and anti-fibrotic effects of IL-38 were observed. Furthermore, we revealed that IL-38 can counteract the phosphorylation of star molecules in multiple classical pathways. Conclusions IL-38 plays a protective role in TAO and is associated with its pathogenesis. Our data suggest that IL-38 may be a promising marker of TAO disease activity and a potential target for TAO therapy.

scholarly journals Artemisinin Ameliorates Osteoarthritis by Inhibiting the Wnt/β-Catenin Signaling Pathway

2018 ◽  
Vol 51 (6) ◽  
pp. 2575-2590 ◽  
Author(s):  
Gang Zhong ◽  
Ruiming Liang ◽  
Jun Yao ◽  
Jia Li ◽  
Tongmeng Jiang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Cruciate Ligament ◽  
Interleukin 1 ◽  
Cartilage Degradation ◽  
Chondrocyte Apoptosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cell Viability Assay ◽  
Necrosis Factor Alpha ◽  
Anti Inflammatory

Background/Aims: Current drug therapies for osteoarthritis (OA) are not practical because of the cytotoxicity and severe side-effects associated with most of them. Artemisinin (ART), an antimalarial agent, is well known for its safety and selectivity to kill injured cells. Based on its anti-inflammatory activity and role in the inhibition of OA-associated Wnt/β-catenin signaling pathway, which is crucial in the pathogenesis of OA, we hypothesized that ART might have an effect on OA. Methods: The chondro-protective and antiarthritic effects of ART on interleukin-1-beta (IL-1β)-induced and OA patient-derived chondrocytes were investigated in vitro using cell viability assay, glycosaminoglycan secretion, immunofluorescence, quantitative reverse transcription-polymerase chain reaction, and western blotting. We also used OA model rats constructed by anterior cruciate ligament transection and medial meniscus resection (ACLT+MMx) in the joints to investigate the effects of ART on OA by gross observation, morphological staining, immunohistochemistry, and enzyme-linked immunosorbent assay. Results: ART exhibited potent anti-inflammatory effects by inhibiting the expression of proinflammatory chemokines and cytokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor alpha, and matrix metallopeptidase-13. It also showed favorable chondro-protective effect as evidenced by enhanced cell proliferation and viability, increased glycosaminoglycan deposition, prevention of chondrocyte apoptosis, and degeneration of cartilage. Further, ART inhibited OA progression and cartilage degradation via the Wnt/β-catenin signaling pathway, suggesting that it might serve as a Wnt/β-catenin antagonist to reduce inflammation and prevent cartilage degradation. Conclusion: In conclusion, ART alleviates IL-1β-mediated inflammatory response and OA progression by regulating the Wnt/β-catenin signaling pathway. Thereby, it might be developed as a potential therapeutic agent for OA.

scholarly journals Antioxidant and Anti-Inflammatory Activities of Six Flavonoids from Smilax glabra Roxb

Molecules ◽  
2020 ◽  
Vol 25 (22) ◽  
pp. 5295
Author(s):  
Xinyu Zhao ◽  
Ruyi Chen ◽  
Yueyue Shi ◽  
Xiaoxi Zhang ◽  
Chongmei Tian ◽  
...  
Keyword(s):  
Antioxidant Activities ◽  
Radical Scavenging Activity ◽  
Radical Scavenging ◽  
Raw264.7 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Preparative Hplc ◽  
Antioxidant Power ◽  
Ferric Reducing Antioxidant Power ◽  
Anti Inflammatory

This study aimed to isolate, prepare and identify the main flavonoids from a standardized Smilax glabra flavonoids extract (SGF) using preparative HPLC, MS, 1H NMR and 13C NMR, determine the contents of these flavonoids using UPLC, then compare their pharmacological activities in vitro. We obtained six flavonoids from SGF: astilbin (18.10%), neoastilbin (11.04%), isoastilbin (5.03%), neoisoastilbin (4.09%), engeletin (2.58%) and (−)-epicatechin (1.77%). The antioxidant activity of six flavonoids were evaluated by determining the 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical and 2,2′-Azinobis (3-ethylbenzothiazoline-6-sulphonic acid) diammonium salt (ABTS+) radical scavenging activity and ferric reducing antioxidant power (FRAP). In addition, the anti-inflammatory activity of six flavonoids were evaluated by determining the production of cytokines (IL-1β, IL-6), nitric oxide (NO) using enzyme linked immunosorbent assay and the NF-κB p65 expression using Western blotting in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. The results showed that (−)-epicatechin, astilbin, neoastilbin, isoastilbin and neoisoastilbin had strong antioxidant activities, not only in DPPH and ABTS+ radicals scavenging capacities, but in FRAP system. Furthermore, all the six flavonoids could significantly inhibit the secretion of IL-1β, IL-6, NO (p < 0.01) and the protein expression of NF-κB p-p65 (p < 0.01) in LPS-stimulated RAW264.7 cells. This study preliminarily verified the antioxidant and anti-inflammatory activities of six flavonoids in S. glabra.

scholarly journals Inhibitory Effects of a Sargassum miyabei Yendo on Cutibacterium acnes-Induced Skin Inflammation

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2620
Author(s):  
Mi-Jin Yim ◽  
Jeong Min Lee ◽  
Hyun-Soo Kim ◽  
Grace Choi ◽  
Young-Mog Kim ◽  
...  
Keyword(s):  
Acne Vulgaris ◽  
Skin Lesions ◽  
Enzyme Linked Immunosorbent Assay ◽  
Hacat Cells ◽  
Chronic Inflammatory Condition ◽  
Cutibacterium Acnes ◽  
Anti Inflammatory ◽  
Sargassum Miyabei

Acne vulgaris is a chronic inflammatory condition of skin sebaceous follicles. To explore its effects on acne vulgaris, we investigated the antibacterial and anti-inflammatory activities of Sargassum miyabei Yendo (a brown alga) ethanolic extract (SMYEE) on Cutibacterium acnes (C. acnes)-stimulated inflammatory responses, both in vivo and in vitro. To induce inflammation in vivo, C. acnes was intradermally injected into the dorsal skin of mice, to which SMYEE was applied. The antimicrobial activity of SMYEE was evaluated by the determination of minimum inhibitory concentrations (MICs). To explore in vitro anti-inflammatory effects, HaCaT cells were stimulated with C. acnes after treatment with SMYEE. The levels of IL-8 and the underlying molecular effects in C. acnes-stimulated HaCaT cells were assessed by enzyme-linked immunosorbent assay, Western blotting, and an electrophoretic mobility shift assay. Mouse skin lesions improved after treatment with SMYEE (50 μg/mouse). Neutrophil infiltration was significantly reduced in SMYEE-treated compared to SMYEE-untreated skin lesions. SMYEE reversed the C. acnes-induced increase in IL-8 levels in HaCaT cells and suppressed dHL-60 cell migration. SMYEE also inhibited C. acnes-induced phosphorylation of the extracellular signal-regulated kinase and inhibited activator protein-1 signaling. SMYEE may be a useful treatment for C. acnes-induced acne vulgaris.

scholarly journals Inhibition of viral and bacterial trigger-stimulated prostaglandin E2 by a throat lozenge containing flurbiprofen: An in vitro study using a human respiratory epithelial cell line

2020 ◽  
Vol 8 ◽  
pp. 205031212096056
Author(s):  
Rob Lambkin-Williams ◽  
Alex Mann ◽  
Adrian Shephard
Keyword(s):  
Epithelial Cell ◽  
Sore Throat ◽  
A549 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Epithelial Cell Line ◽  
Prostaglandin E ◽  
Suitable Model ◽  
Tracheal Epithelial ◽  
Anti Inflammatory

Objectives: Symptoms of sore throat result from oropharyngeal inflammation, for which prostaglandin E2 is a key mediator. Flurbiprofen is a non-steroidal anti-inflammatory that provides sore throat relief. The preliminary objective of this study was to develop an in vitro model for assessing prostaglandin E2 stimulation by viral and bacterial triggers. The primary objective was to investigate the effect of diluted flurbiprofen-containing lozenges on prostaglandin E2 concentrations in stimulated cells. Methods: Prostaglandin E2 production was stimulated in three epithelial cell lines (A549, HEp2, and clonetics bronchial/tracheal epithelial) with influenza A virus (4.5 log10 tissue culture infectious dose50/mL), or bacterial lipopolysaccharide (10µ g/mL) and peptidoglycan (3µ g/mL) and incubated overnight. Prostaglandin E2 levels were assessed by enzyme-linked immunosorbent assay up to 24 h after stimulation. The effect of flurbiprofen 8.75 mg lozenges (diluted to 0.44 mg/mL) on PGE2 production in stimulated cells was assessed in parallel; prior to viral/LPS/PEP stimulation of cells, 300 μL of test product or control was added and incubated for 30 s, 2 and 5 min (and 10 min for bacterial trigger). Prostaglandin E2 levels were measured following stimulation. Results: Viral and lipopolysaccharide/peptidoglycan infection did not consistently stimulate HEp2 cells and bronchial/tracheal epithelial cells to produce prostaglandin E2. Influenza virus, and lipopolysaccharide/peptidoglycan stimulated high prostaglandin E2 concentrations in A549: mean prostaglandin E2 concentration 106.48 pg/mL with viral stimulation vs 33.82 pg/mL for uninfected cells; 83.84 pg/mL with lipopolysaccharide/peptidoglycan vs 71.96 pg/mL for uninfected cells. Flurbiprofen produced significant reductions in virus-stimulated prostaglandin E2 vs stimulated untreated cells at 2 min (p = 0.03). Flurbiprofen produced significant reductions in lipopolysaccharide/peptidoglycan-stimulated prostaglandin E2 concentrations from 30 s (p = 0.02), and at 2, 5 and 10 min (all p < 0.005) vs stimulated untreated cells. Conclusions: A549 cells provide a suitable model for assessment of prostaglandin E2 stimulation by viral and bacterial triggers. Diluted flurbiprofen-containing lozenges demonstrated rapid anti-inflammatory activity in viral- and lipopolysaccharide/peptidoglycan-stimulated A549 cells.

scholarly journals Protective Role of C3aR (C3a Anaphylatoxin Receptor) Against Atherosclerosis in Atherosclerosis-Prone Mice

2020 ◽  
Vol 40 (9) ◽  
pp. 2070-2083
Author(s):  
Lin-Lin Wei ◽  
Ning Ma ◽  
Kun-Yi Wu ◽  
Jia-Xing Wang ◽  
Teng-Yue Diao ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Macrophage Polarization ◽  
Protective Role ◽  
Plaque Burden ◽  
Aortic Tissue ◽  
M2 Macrophage ◽  
Proinflammatory Mediators ◽  
Anti Inflammatory

Objective: Emerging evidence suggests that C3aR (C3a anaphylatoxin receptor) signaling has protective roles in various inflammatory-related diseases. However, its role in atherosclerosis has been unknown. The purpose of the study was to investigate the possible protective role of C3aR in aortic atherosclerosis and explore molecular and cellular mechanisms involved in the protection. Approach and Results: C3ar −/− /Apoe −/− mice were generated by cross-breeding of atherosclerosis-prone Apoe −/− mice and C3ar −/− mice. C3ar −/− /Apoe −/− mice and Apoe −/− mice (as a control) underwent high-fat diet for 16 weeks were assessed for (1) atherosclerotic plaque burden, (2) aortic tissue inflammation, (3) recruitment of CD11b + leukocytes into atherosclerotic lesions, and (4) systemic inflammatory responses. Compared with Apoe −/− mice, C3ar −/− /Apoe −/− mice developed more severe atherosclerosis. In addition, C3ar −/− /Apoe −/− mice have increased local production of proinflammatory mediators (eg, CCL2 [chemokine (C-C motif) ligand 2], TNF [tumor necrosis factor]-α) and infiltration of monocyte/macrophage in aortic tissue, and their lesional macrophages displayed an M1-like phenotype. Local pathological changes were associated with enhanced systemic inflammatory responses (ie, elevated plasma levels of CCL2 and TNF-α, increased circulating inflammatory cells). In vitro analyses using peritoneal macrophages showed that C3a stimulation resulted in upregulation of M2-associated signaling and molecules, but suppression of M1-associated signaling and molecules, supporting the roles of C3a/C3aR axis in mediating anti-inflammatory response and promoting M2 macrophage polarization. Conclusions: Our findings demonstrate a protective role for C3aR in the development of atherosclerosis and suggest that C3aR confers the protection through C3a/C3aR axis–mediated negative regulation of proinflammatory responses and modulation of macrophage toward the anti-inflammatory phenotype.

Aspirin Blocks Orthodontic Relapse via Inhibition of CD4+ T Lymphocytes

2017 ◽  
Vol 96 (5) ◽  
pp. 586-594 ◽  
Author(s):  
Y. Liu ◽  
T. Zhang ◽  
C. Zhang ◽  
S.S. Jin ◽  
R.L. Yang ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Relapse Rate ◽  
Immune Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Th1 Cells ◽  
Tnf Α ◽  
Inflammatory Drugs ◽  
Ifn Γ ◽  
Anti Inflammatory

Immunologic response plays an important role in orthodontic tooth movement (OTM) and relapse. Nonsteroidal anti-inflammatory drugs, such as aspirin, affect immune cells and clinical orthodontic treatment. However, the mechanisms by which nonsteroidal anti-inflammatory drugs regulate immune cells to affect orthodontic relapse are unclear. In this study, male Sprague-Dawley rats were grouped as relapse and relapse + aspirin for 10 d after 14 d of OTM. Silicone impressions of the rats’ maxillary dentitions were obtained to record the distance of OTM at the indicated time point. CD4+ T lymphocytes in spleen were examined by flow cytometry. Serum levels of type 1 T-helper (Th1) cell–associated cytokines tumor necrosis factor α (TNF-α), and interferon γ (IFN-γ) were determined through enzyme-linked immunosorbent assay. The effects of aspirin on CD4+ T and Th1 cells were also analyzed in vitro. Aspirin treatment significantly reduced the relapse rate. More interestingly, injection of CD25 neutralizing antibody basiliximab or TNF-α inhibitor etanercept can significantly reduce the relapse rate as well. Correspondingly, aspirin treatment significantly accelerated the decrease of orthodontic force–induced secretion of TNF-α and IFN-γ in serum and the expression of TNF-α and IFN-γ in periodontal ligament during relapse. Furthermore, aspirin treatment in vitro significantly repressed the differentiation of CD4+ T and Th1 cells. Overall, results indicated that aspirin treatment can block orthodontic relapse by regulating Th1 cells.

scholarly journals Hordenine Protects Against Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting Inflammation

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiyue Zhang ◽  
Li Du ◽  
Jinrong Zhang ◽  
Chunyan Li ◽  
Jie Zhang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Protein Kinase ◽  
Lung Injury ◽  
Biological Activities ◽  
Mitogen Activated Protein Kinase ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Anti Inflammatory

Acute lung injury (ALI) is a respiratory disease that leads to death in severe cases. Hordenine (Hor), a barley-derived natural product, has various biological activities, including anti-inflammatory, and anti-oxidation activities. We investigated the effect of Hor on lipopolysaccharide-induced ALI and its potential mechanism. The anti-inflammatory effects of Hor were detected using in vivo and in vitro models by enzyme-linked immunosorbent assay, real-time polymerase chain reaction, western blotting, and molecular docking simulations. Hor inhibited increases in the levels of inflammatory factors both in vivo and in vitro, and its anti-inflammatory effect inhibited activation of protein kinase B, nuclear factor-κB, and mitogen-activated protein kinase signaling. Hor alleviated lipopolysaccharide-induced ALI by inhibiting inflammatory cytokine increases in vivo and in vitro and shows potential for preventing inflammatory disease.

scholarly journals Anti-periodontal Pathogen and Anti-inflammatory Activities of Oxyresveratrol

2013 ◽  
Vol 8 (5) ◽  
pp. 1934578X1300800 ◽  
Author(s):  
Waranyoo Phoolcharoen ◽  
Sireerat Sooampon ◽  
Boonchoo Sritularak ◽  
Kittisak Likhitwitayawuid ◽  
Jintakorn Kuvatanasuchati ◽  
...  
Keyword(s):  
Antibacterial Activity ◽  
Pathogenic Bacteria ◽  
Biological Activities ◽  
Mrna Level ◽  
Periodontal Pathogen ◽  
Enzyme Linked Immunosorbent Assay ◽  
Minimal Bactericidal Concentration ◽  
Potential Candidate ◽  
Anti Inflammatory

Oxyresveratrol, a compound in the heartwood of Artocarpus lakoocha Roxb and other medicinal plants, has been shown to have various biological activities. However, these have not been studied in periodontal research. In this study, we investigated whether oxyresveratrol has antibacterial activity against the predominant perio-pathogenic bacteria Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans. Moreover, the anti-inflammatory properties of oxyresveratrol were studied in LPS-stimulated human periodontal ligament (hPDL) cells. The antibacterial activity of oxyresveratrol on P. gingivalis and A. actinomycetemcomitans was initially evaluated using a disc diffusion test. The anti-bacterial strength of oxyresveratrol was then assessed in vitro by determining the minimal inhibitory concentration (MIC) and the minimal bactericidal concentration (MBC). Furthermore, the effects of oxyresveratrol on the LPS-induced production of inflammatory mediators were measured in hPDL cells. The levels of cytokine mRNA and protein expression were determined using reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Our results showed that oxyresveratrol exhibited antibacterial activities against P. gingivalis with MIC and MBC values of 0.07 mg/mL and 0.16 mg/mL, respectively. The MIC and MBC values against A. actinomycetemcomitans were 0.08 mg/mL and 0.16 mg/mL, respectively. When examining inflammatory stimulation, LPS treatment strongly induced the expression of pro-inflammatory cytokines in hPDL cells. However, pre-treatment with oxyresveratrol significantly inhibited the expression of IL-6 and IL-8 at both the mRNA and protein levels. The IL-1β mRNA level was suppressed by oxyresveratrol, but the level of secreted IL-1β protein was not detectable using ELISA. The results of the present study indicate that oxyresveratrol is a potential candidate for use as an anti-periodontitis agent because of its anti-bacterial activity against the main oral pathogens related to periodontal disease and its anti-inflammatory activity in LPS-stimulated hPDL cells.

scholarly journals Anti-Inflammatory Effect of Cherry Extract Loaded in Polymeric Nanoparticles: Relevance of Particle Internalization in Endothelial Cells

Pharmaceutics ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 500 ◽  
Author(s):  
Denise Beconcini ◽  
Francesca Felice ◽  
Ylenia Zambito ◽  
Angela Fabiano ◽  
Anna Maria Piras ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Prunus Avium ◽  
Umbilical Vein ◽  
Water Soluble ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tetrazolium Salt ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Inflammatory Effect

This study aimed at evaluating the anti-inflammatory effect of natural cherry extract (CE), either free or encapsulated in nanoparticles (NPs) based on chitosan derivatives (Ch-der) or poly(lactic-co-glycolic acid) (PLGA), on human umbilical vein endothelial cells (HUVEC). CE from Prunus avium L. was characterized for total polyphenols, flavonoids, and anthocyanins content. CE and CE-loaded NP cytotoxicity and protective effect on lipopolysaccharide (LPS)-stressed HUVEC were tested by water-soluble tetrazolium salt (WST-1) assay. Pro- and anti-inflammatory cytokines (TNF-α, IL-6, IL-10, and PGE2) released by HUVEC were quantified by enzyme-linked immunosorbent assay (ELISA). All NP types were internalized into HUVEC after 2 h incubation and promoted the anti-inflammatory effect of free CE at the concentration of 2 µg gallic acid equivalents (GAE)/mL. CE-loaded Ch-der NPs showed the highest in vitro uptake and anti-inflammatory activity, blunting the secretion of IL-6, TNF-α, and PGE2 cytokines. Moreover, all NPs reduced the production of nitric oxide and NLRP3 inflammasome, and had a stronger anti-inflammatory effect than the major corticosteroid dexamethasone. In particular, the results demonstrate that natural CE protects endothelial cells from inflammatory stress when encapsulated in NPs based on quaternary ammonium chitosan. The CE beneficial effects were directly related with in vitro internalization of CE-loaded NPs.

scholarly journals Crotalus durissus terrificusVenom Interferes With Morphological, Functional, and Biochemical Changes in Murine Macrophage

2005 ◽  
Vol 2005 (6) ◽  
pp. 349-359 ◽  
Author(s):  
Anselmo Hernández Cruz ◽  
Ronaldo Z. Mendonça ◽  
Vera L. Petricevich
Keyword(s):  
Functional Status ◽  
Peritoneal Macrophages ◽  
Phagocytic Index ◽  
Enzyme Linked Immunosorbent Assay ◽  
Phenol Red ◽  
Vacuole Formation ◽  
Inflammatory Status ◽  
Anti Inflammatory ◽  
Crotalus Durissus

Crotalus durissus terrificusvenom (Cdt) is toxic for a variety of eukaryotic cells, especially at high concentrations. However its effects on host immune cells are not well known. The purpose of this study was to determine the effect of Cdt on functional status and the mediators production in peritoneal macrophages. The effects of Cdt were analyzed in vitro and were detected using functional status of macrophages as determined by the H2O2release, spreading percentage, phagocytic index, vacuole formation, and mediators production. Several functional bioassays were employed: cytotoxicity was determined by taking the lyses percentage and the presence of hydrogen peroxide (H2O2) in macrophages, using the horseradish peroxidase-dependent oxidation of phenol red and nitric oxide (NO) in the supernatants of macrophages by the Griess reaction. The tumor necrosis factor (TNF) activity was detected by measuring its cytotoxic activity on L929 cells, and the production the level of other cytokines was assayed using enzyme-linked immunosorbent assay. In vitro studies revealed that Cdt produced (a) a discrete increase in the release of H2O2and vacuole formation; (b) a decrease in spreading percentage and in the phagocytic index; and (c) an increment in the mediators production. More pronounced increments of IL-6 and TNF were observed after 24 and 48 hours, respectively. Maximum levels of IFN-γand NO were observed after 96 hours. Interestingly, levels of all mediators presented a discreet decrease, as the amount of Cdt was increased. In contrast, the IL-10 levels observed for all doses studied here did not alter. The IL-6/IL-10 ratio may possibly reflect the balance of pro- and anti-inflammatory cytokines in macrophages, which may be manifested in the inflammatory status during the envenoming processes. Taken together, these data indicate that Cdt have a differential effect on macrophage activation and that this venom is a potent inhibitor of anti-inflammatory response.

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