Boosting Interleukin-10 Production: Therapeutic Effects and Mechanisms

2005 ◽  
Vol 5 (4) ◽  
pp. 465-475 ◽  
Author(s):  
Xiaoxia Zhou ◽  
Peter Schmidtke ◽  
Fred Zepp ◽  
Claudius U. Meyer
Keyword(s):  
Interleukin 10 ◽  
Therapeutic Effects

scholarly journals Ascidian Tunicate Extracts Attenuate Rheumatoid Arthritis in a Collagen-induced Murine Model

2014 ◽  
Vol 9 (6) ◽  
pp. 1934578X1400900
Author(s):  
Seong-Ho Hong ◽  
Jung-Taek Kwon ◽  
Jae-Ho Lee ◽  
Somin Lee ◽  
Ah Young Lee ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Interleukin 10 ◽  
Treated Group ◽  
Pcr Analysis ◽  
Prostaglandin E ◽  
Therapeutic Effects ◽  
Paw Edema ◽  
Mice Model ◽  
The Matrix ◽  
Inflammatory Proteins

Murine rheumatoid arthritis models are often used to investigate the potential therapeutic effects of candidate drugs. The present study has been conducted in order to investigate the therapeutic efficacy of ascidian tunicate extracts in a collagen-induced arthritis DBA1/J mice model. Four types of formulas, ascidian tunicate extracts (ATE), crude ascidian tunicate glycans (ATEC), ascidian tunicate extracts with licorice extracts (ATEL), and crude ascidian tunicate glycans with licorice extracts (ATECL) were orally administered into DBA/1J mice for 3 weeks and paw edema and thickness were evaluated. Changes in inflammatory proteins and cytokines levels were monitored in hind leg tissues by Western blot and quantitative PCR analysis. The oral administration of ascidian tunicate extracts alleviated paw edema and improved the histological hind leg cartilage status. The extracts also reduced the matrix metalloproteinase-9 (MMP-9) protein and prostaglandin E synthase (PGES) levels. In addition, the extracts-treated groups showed increased interleukin-10 (IL-10) levels compared with the non-treated group. These findings suggest that orally administered ascidian tunicate extracts might have potential therapeutic effects for the treatment of rheumatoid arthritis.

scholarly journals Involvement of Interleukin-10 in the Anti-Inflammatory Effect of Sanyinjiao (SP6) Acupuncture in a Mouse Model of Peritonitis

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Morgana Duarte da Silva ◽  
Giselle Guginski ◽  
Maria Fernanda de Paula Werner ◽  
Cristiane Hatsuko Baggio ◽  
Rodrigo Marcon ◽  
...  
Keyword(s):  
Vascular Permeability ◽  
Interleukin 10 ◽  
Sham Acupuncture ◽  
Therapeutic Effects ◽  
Plasma Extravasation ◽  
Sterile Saline ◽  
Cell Counts ◽  
Cytokine Levels ◽  
Anti Inflammatory ◽  
Inflammatory Effect

In this study, we determined the anti-inflammatory effect of manual acupuncture at the Sanyinjiao or Spleen 6 (SP6) point on carrageenan-induced peritonitis in mice and investigated mechanisms that may underlie this effect. In the first set of experiments, male Swiss mice were allocated into five groups: the control (sterile saline), dexamethasone (DEXA), invasive sham-acupuncture (non-acupoint), SP6 acupuncture and carrageenan-treated groups. Ten minutes after needle retention or 30 min after DEXA treatment, mice received an intraperitoneal injection of carrageenan (750 μg/mouse). After 4 h, total leukocyte and differential cell counts (neutrophils and mononuclear), myeloperoxidase (MPO) activity, vascular permeability and cytokine levels were evaluated. In another set of experiments, adrenalectomized (ADX) mice were used to study the involvement of the adrenal gland on the therapeutic effects of acupuncture. Mice were allocated into two groups: the ADX and sham-operated animals (Sham ADX) that were subdivided into four subgroups each: the control (sterile saline), DEXA, SP6 acupuncture and carrageenan-treated groups. The SP6 and DEXA treatments inhibited the inflammatory cell infiltration, vascular permeability and MPO activity in carrageenan-injected mice. In addition, the SP6 treatment also increased interleukin (IL)-10 levels. In contrast, when the animals were adrenalectomized, the SP6 treatment failed to reduce total leukocyte and the plasma extravasation. In conclusion, this study clearly demonstrates the anti-inflammatory effect of SP6 acupuncture in a model of carrageenan-induced peritonitis. Our results demonstrated that SP6 acupuncture depends of the adrenal glands and increased IL-10 levels to produce its anti-inflammatory action.

scholarly journals Effect of GCSB-5, a Herbal Formulation, on Monosodium Iodoacetate-Induced Osteoarthritis in Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Joon-Ki Kim ◽  
Sang-Won Park ◽  
Jung-Woo Kang ◽  
Yu-Jin Kim ◽  
Sung Youl Lee ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Protein Expression ◽  
Nuclear Factor Κb ◽  
Interleukin 10 ◽  
Cartilage Explants ◽  
Therapeutic Effects ◽  
Monosodium Iodoacetate ◽  
Factor Α

Therapeutic effects of GCSB-5 on osteoarthritis were measured by the amount of glycosaminoglycan in rabbit articular cartilage explantsin vitro, in experimental osteoarthritis induced by intra-articular injection of monoiodoacetate in ratsin vivo. GCSB-5 was orally administered for 28 days.In vitro, GCSB-5 inhibited proteoglycan degradation. GCSB-5 significantly suppressed the histological changes in monoiodoacetate-induced osteoarthritis. Matrix metalloproteinase (MMP) activity, as well as, the levels of serum tumor necrosis factor-α, cyclooxygenase-2, inducible nitric oxide synthase protein, and mRNA expressions were attenuated by GCSB-5, whereas the level of interleukin-10 was potentiated. By GCSB-5, the level of nuclear factor-κB p65 protein expression was significantly attenuated but, on the other hand, the level of inhibitor of κB-α protein expression was increased. These results indicate that GCSB-5 is a potential therapeutic agent for the protection of articular cartilage against progression of osteoarthritis through inhibition of MMPs activity, inflammatory mediators, and NF-κB activation.

scholarly journals Therapeutic Effects of Nitric Oxide Inhibition during Experimental Fecal Peritonitis: Role of Interleukin-10 and Monocyte Chemoattractant Protein 1

1998 ◽  
Vol 66 (2) ◽  
pp. 650-655 ◽  
Author(s):  
Cory M. Hogaboam ◽  
Matthew L. Steinhauser ◽  
Harold Schock ◽  
Nicholas Lukacs ◽  
Robert M. Strieter ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Interleukin 10 ◽  
Therapeutic Effects ◽  
Fecal Peritonitis ◽  
Monocyte Chemoattractant Protein 1 ◽  
Nitric Oxide Inhibition ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Oxide Inhibition

ABSTRACT This study demonstrates that the therapeutic effect of a nitric oxide inhibitor in a murine model of fecal peritonitis is mediated in part by increased levels of interleukin-10 (IL-10) and monocyte chemoattractant protein 1 (MCP-1). Female CD1 mice were subjected to cecal ligation and puncture (CLP) with a 21-gauge needle and, immediately following surgery, were injected intraperitoneally with saline,N G-nitro-l-arginine methyl ester (l-NAME; 8 mg/kg), orN G-nitro-d-arginine methyl ester (d-NAME; 8 mg/kg). At 96 h after surgery and drug treatment, 20% of mice that received d-NAME had survived whereas 60% of mice that received l-NAME were alive. To elucidate the effect of l-NAME treatment on chemokine and cytokine production during fecal peritonitis, the levels of macrophage inflammatory protein 2 (MIP-2), IL-10, and MCP-1 were measured in peritoneal washings from additional groups of mice 24 h after the CLP surgery. Peritoneal fluids froml-NAME-treated mice contained significantly higher levels of IL-10 and MCP-1 than did those from d-NAME-treated mice. To elucidate the effect of nitric oxide inhibition on potential cellular sources of IL-10 and MCP-1 in the CLP model, cultured alveolar and peritoneal macrophages were activated with bacterial lipopolysaccharide in the presence of l-NAME; these macrophages produced significantly more MCP-1 than did similarly activated macrophages in the presence of d-NAME. In the CLP surgery model, immunoneutralization of IL-10 alone or IL-10 and MCP-1 together with polyclonal antibodies prior to surgery significantly reduced the survival rates in l-NAME-treated groups compared with l-NAME-treated groups that received preimmune serum. Taken together, these data demonstrate that the inhibition of nitric oxide following experimental CLP fecal peritonitis is therapeutic, in part through the modulatory effect of this treatment on the synthesis of IL-10 and MCP-1.

scholarly journals Transplantation of bone marrow derived macrophages reduces markers of neuropathology in an APP/PS1 mouse model

2019 ◽  
Vol 8 (1) ◽  
Author(s):  
Luís Costa-Marques ◽  
Katrin Arnold ◽  
Marie-Christine Pardon ◽  
Christiane Leovsky ◽  
Samantha Swarbrick ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bone Marrow ◽  
Cell Therapy ◽  
Transgenic Mice ◽  
Amyloid Beta ◽  
Exploratory Study ◽  
Interleukin 10 ◽  
Mechanisms Of Action ◽  
Prostaglandin E ◽  
Therapeutic Effects

Abstract Background We investigated early hallmarks of putative therapeutic effects following systemic transplantation of bone marrow derived macrophages (BM-M) in APP/PS1 transgenic mice. Method BM-M were transplanted into the tail vein and the animals analysed 1 month later. Results BM-M transplantation promoted the reduction of the amyloid beta [37-42] plaque number and size in the cortex and hippocampus of the treated mice, but no change in the more heavily modified pyroglutamate amyloid beta E3 plaques. The number of phenotypically ‘small’ microglia increased in the hippocampus. Astrocyte size decreased overall, indicating a reduction of activated astrocytes. Gene expression of interleukin 6 and 10, interferon-gamma, and prostaglandin E receptor 2 was significantly lower in the hippocampus, while interleukin 10 expression was elevated in the cortex of the treated mice. Conclusions BM-M systemically transplanted, promote a decrease in neuroinflammation and a limited reversion of amyloid pathology. This exploratory study may support the potential of BM-M or microglia-like cell therapy and further illuminates the mechanisms of action associated with such transplants.

scholarly journals Anti-Gouty Arthritis and Antihyperuricemia Effects of Sunflower (Helianthus annuus) Head Extract in Gouty and Hyperuricemia Animal Models

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Lanzhou Li ◽  
Meiyu Teng ◽  
Yange Liu ◽  
Yidi Qu ◽  
Yuanzhu Zhang ◽  
...  
Keyword(s):  
Helianthus Annuus ◽  
Inflammatory Cytokines ◽  
Gouty Arthritis ◽  
Nitrogen Monoxide ◽  
Serum Levels ◽  
Joint Space ◽  
Interleukin 10 ◽  
Therapeutic Effects ◽  
Acute Gout ◽  
Monocyte Chemoattractant Protein 1

This study was performed to investigate the therapeutic effects and possible mechanisms of sunflower (Helianthus annuus) head extract (SHE) on gout. First, the components of sunflower head powder and SHE were analyzed systematically. SHE, especially SHEB (extracted with 20% ethanol and 80% double-distilled water), strongly suppressed the swelling of the ankles in rats with acute gout induced by monosodium urate (MSU) crystals and reduced the levels of uric acid and xanthine oxidase (XO) in mice with hyperuricemia induced by oteracil potassium and yeast extract powder. Hematoxylin and eosin staining indicated that SHEB reduced inflammation cells and increased the joint space in the ankle compared with the control rats with MSU-induced gout. In the rats with acute gout, among 13 detected inflammatory cytokines, SHEB significantly enhanced the serum levels of interleukin-10 and the monocyte chemoattractant protein 1α. In the mice with hyperuricemia, SHEB reduced the levels of glutathione peroxidase, superoxide dismutase, malondialdehyde, and nitrogen monoxide in liver tissues. The potential therapeutic effects of SHE on gout are probably due to the production of anti-inflammatory cytokines and the suppression of XO activity via the modulation of oxidative stress status.

scholarly journals Induction of antigen-specific regulatory T lymphocytes by human dendritic cells expressing the glucocorticoid-induced leucine zipper

Blood ◽  
2007 ◽  
Vol 110 (1) ◽  
pp. 211-219 ◽  
Author(s):  
Haifa Hamdi ◽  
Véronique Godot ◽  
Marie-Christine Maillot ◽  
Maria Victoria Prejean ◽  
Nicolas Cohen ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Lymphocytes ◽  
Antigen Presentation ◽  
Leucine Zipper ◽  
Ex Vivo ◽  
Antigen Presenting Cells ◽  
Interleukin 10 ◽  
Therapeutic Effects ◽  
Regulatory T Lymphocytes ◽  
Antigen Presenting

Dendritic cells (DCs) determine whether antigen presentation leads to immune activation or to tolerance. Tolerance-inducing DCs (also called regulatory DCs) act partly by generating regulatory T lymphocytes (Tregs). The mechanism used by DCs to switch toward regulatory DCs during their differentiation is unclear. We show here that human DCs treated in vitro with glucocorticoids produce the glucocorticoid-induced leucine zipper (GILZ). Antigen presentation by GILZ-expressing DCs generates CD25highFOXP3+CTLA-4/CD152+ and interleukin-10–producing Tregs inhibiting the response of CD4+ and CD8+ T lymphocytes. This inhibition is specific to the antigen presented, and only proliferating CD4+ T lymphocytes express the Treg markers. Interleukin-10 is required for Treg induction by GILZ-expressing DCs. It is also needed for the suppressive function of Tregs. Antigen-presenting cells from patients treated with glucocorticoids generate interleukin-10–secreting Tregs ex vivo. These antigen-presenting cells produce GILZ, which is needed for Treg induction. Therefore, GILZ is critical for commitment of DCs to differentiate into regulatory DCs and to the generation of antigen-specific Tregs. This mechanism may contribute to the therapeutic effects of glucocorticoids.

scholarly journals Hypoxia impairs mesenchymal stromal cell-induced macrophage M1 to M2 transition

TECHNOLOGY ◽  
2017 ◽  
Vol 05 (02) ◽  
pp. 81-86 ◽  
Author(s):  
Renea A. Faulknor ◽  
Melissa A. Olekson ◽  
Emmanuel C. Ekwueme ◽  
Paulina Krzyszczyk ◽  
Joseph W. Freeman ◽  
...  
Keyword(s):  
Wound Healing ◽  
Chronic Wounds ◽  
Interleukin 10 ◽  
M2 Macrophage ◽  
Therapeutic Effects ◽  
M1 Macrophages ◽  
Normal Wound Healing ◽  
Hypoxic Environment ◽  
Anti Inflammatory ◽  
M2 Phenotype

The transition of macrophages from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype is crucial for the progression of normal wound healing. Persistent M1 macrophages within the injury site may lead to an uncontrolled macrophage-mediated inflammatory response and ultimately a failure of the wound healing cascade, leading to chronic wounds. Mesenchymal stromal cells (MSCs) have been widely reported to promote M1 to M2 macrophage transition; however, it is unclear whether MSCs can drive this transition in the hypoxic environment typically observed in chronic wounds. Here we report on the effect of hypoxia (1% O[Formula: see text] on MSCs’ ability to transition macrophages from the M1 to the M2 phenotype. While hypoxia had no effect on MSC secretion, it inhibited MSC-induced M1 to M2 macrophage transition, and suppressed macrophage expression and production of the anti-inflammatory mediator interleukin-10 (IL-10). These results suggest that hypoxic environments may impede the therapeutic effects of MSCs.

scholarly journals Protective Potential of Ginseng and/or Coenzyme Q10 on Doxorubicin-induced Testicular and Hepatic Toxicity in Rats

2021 ◽  
Vol 9 (A) ◽  
pp. 993-1005
Author(s):  
Suzan Khodir ◽  
Aliaa Alafify ◽  
Essam Omar ◽  
Marwa Al-Gholam
Keyword(s):  
Gene Expression ◽  
Serum Cholesterol ◽  
Coenzyme Q10 ◽  
Interleukin 6 ◽  
Liver Enzymes ◽  
Serum Testosterone ◽  
Interleukin 10 ◽  
Therapeutic Effects ◽  
Hepatic Toxicity ◽  
Tnf Α

Introduction: Although doxorubicin (DOX) is a successful cancer chemotherapeutic, side effects limit the clinical utility of DOX-based therapy, including male infertility and hepatotoxicity. Objective: To evaluate the testicular and hepatoprotective effect of ginseng and/or coenzyme Q10 (CoQ10) in rats exposed to DOX and the possible underlying mechanisms. Materials and Methods:  Fifty adult male albino rats were divided into (10/group), control, DOX group, DOX/Gin group, DOX/CoQ10 group and DOX/Gin+CoQ10 group. Serum testosterone, serum liver enzymes, fasting serum cholesterol and triglyceride (TG), tissue malondialdehyde (MDA), tissue superoxide dismutase (SOD), serum tumor necrosis factor-alpha (TNF-α), serum interleukin 6, serum interleukin 10, nuclear factor E2‐related factor 2 (Nrf2) gene expression in liver and testis and organ indices were measured.  Histopathological and immunohistochemical assessments of apoptotic marker kaspase3 in testis and liver were also performed. Results DOX-induced toxicity is associated with a significant decrease in serum testosterone, testis and liver index values, testicular and hepatic SOD,  testicular and hepatic Nrf2 gene expression and serum interleukin 10. However, there was a significant increase in serum liver enzymes, serum cholesterol and TG, testicular and hepatic MDA, serum TNF-α and serum interleukin 6 when compared with the control group. The combination of ginseng and CoQ10 resulted in significant improvement of DOX-induced changes when compared with other treated groups. Conclusion: Ginseng and CoQ10 have valuable therapeutic effects on DOX-induced testicular and hepatic toxicity via up-regulation of Nrf2 gene expression, inhibition of apoptosis, anti-oxidant, anti-inflammatory and hypolipidemic effects.

Abstract 299: Natural Product Derivative Bio Promotes Recovery After Myocardial Infarction via Unique Modulation of the Cardiac Microenvironment

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Yong Sook Kim ◽  
Wan Seok Kang ◽  
Ju Hee Kang ◽  
Youngkeun Ahn
Keyword(s):  
Myocardial Infarction ◽  
Glycogen Synthase ◽  
Cardiac Fibroblasts ◽  
Serum Levels ◽  
Interleukin 10 ◽  
M2 Macrophage ◽  
Therapeutic Effects ◽  
Cardiomyocyte Proliferation ◽  
Related Factors ◽  
Anti Inflammatory

Rationale: Myocardial infarction (MI) induces cardiac remodeling, which is regulated by the cardiac microenvironment and results in scarring and loss of cardiac function. Targeting the microenvironment represents a novel therapeutic approach. Objective: To investigate the therapeutic effect of a natural compound derivative, BIO [(2’Z,3’E)-6-Bromoindirubin-3′-oxime], on cardiac microenvironment cells and remodeling post-MI. Methods and Results: Using a series of co-culture studies, BIO was shown to induce proliferation in cardiomyocytes and, conversely, inhibit proliferation in cardiac fibroblasts. In addition, BIO produced anti-fibrotic effects in the fibroblasts, such as reduced motility and expression changes in fibrosis-related factors. In macrophages, BIO inhibited the expression of pro-inflammatory inducible nitric oxide synthase. Interestingly, BIO modulated molecular crosstalk between cardiac fibroblasts and differentiating macrophages to increase expression of anti-inflammatory M2 macrophage markers. In the optically transparent zebrafish-based model of heart failure, BIO induced cardiomyocyte proliferation to recover survival rate. BIO is a known glycogen synthase kinase-3β inhibitor, but these effects could not be recapitulated using the classical inhibitor, lithium chloride; indicating novel, potential therapeutic effects of BIO on remodeling. We characterized these novel effects of BIO as differential modulation of p27 expression and potent induction of interleukin-10 in microenvironment cells. In rat MI model, BIO reduced fibrosis and improved cardiac performance. Histological analysis revealed a greater presence of anti-inflammatory M2 macrophages in the infarction zone. BIO treatment also reduced serum levels of pro-fibrotic interleukin-6. Conclusions: BIO differentially activates signaling pathways in cardiomyocytes, cardiac fibroblasts and cardiac macrophages to reduce fibrosis, increase cardiomyocyte proliferation and promote recovery post-MI.

Sign in / Sign up

Export Citation Format

Share Document