Involvement of IL-10 in Peroxisome Proliferator-Activated Receptor γ-Mediated Anti-Inflammatory Response in Asthma

Kim, So Ri; Lee, Kyung Sun; Park, Hee Sun; Park, Seoung Ju; Min, Kyung Hoon; Jin, Sun; Lee, Yong Chul

doi:10.1124/mol.105.017160

Cited by 81 publications

(79 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We also found that IL-10 is required for the induction and effector function of regulatory cells in our model (38). Because activation of PPARc increases IL-10 production in mice (32,33) …”

Section: Adoptive Transfer Studiessupporting

confidence: 65%

Purified Eicosapentaenoic Acid Induces Prolonged Survival of Cardiac Allografts and Generates Regulatory T Cells

Iwami

Zhang

Aramaki

et al. 2009

American Journal of Transplantation

View full text Add to dashboard Cite

“…We also found that IL-10 is required for the induction and effector function of regulatory cells in our model (38). Because activation of PPARc increases IL-10 production in mice (32,33) …”

Section: Adoptive Transfer Studiessupporting

confidence: 65%

Purified Eicosapentaenoic Acid Induces Prolonged Survival of Cardiac Allografts and Generates Regulatory T Cells

Iwami

Zhang

Aramaki

et al. 2009

American Journal of Transplantation

View full text Add to dashboard Cite

“…In a recent study, pioglitazone also was shown to increase IL-10 levels in lung tissue of a murine model for asthma. 51 Taken together, these findings suggest that IL-10 could be one of the paracrine mechanisms leading to lower systemic MCP-1 levels in thiazolidinedione-treated mice.…”

Section: öHman Et Al Inflammatory Fat Increases Atherosclerosismentioning

confidence: 71%

Visceral Adipose Tissue Inflammation Accelerates Atherosclerosis in Apolipoprotein E–Deficient Mice

et al. 2008

View full text Add to dashboard Cite

Background-Fat inflammation may play an important role in comorbidities associated with obesity such as atherosclerosis. Methods and Results-To first establish feasibility of fat transplantation, epididymal fat pads were harvested from wild-type C57BL/6J mice and transplanted into leptin-deficient (Lep ob/ob ) mice. Fat transplantation produced physiological leptin levels and prevented obesity and infertility in Lep ob/ob mice. However, the transplanted fat depots were associated with chronically increased macrophage infiltration with characteristics identical to those observed in fat harvested from obese animals. The inflammation in transplanted adipose depots was regulated by the same factors that have been implicated in endogenous fat inflammation such as monocyte chemoattractant protein-1. To determine whether this inflamed adipose depot could affect vascular disease in mice, epididymal fat depots were transplanted into atherosclerosis-prone apolipoprotein E-deficient ApoE Ϫ/Ϫ mice. Plasma from ApoE Ϫ/Ϫ mice receiving fat transplants contained increased leptin, resistin, and monocyte chemoattractant protein-1 compared with plasma from sham-operated ApoE Ϫ/Ϫ mice. Furthermore, mice transplanted with visceral fat developed significantly more atherosclerosis compared with sham-operated animals, whereas transplants with subcutaneous fat did not affect atherosclerosis despite a similar degree of fat inflammation. Treatment of transplanted ApoE Ϫ/Ϫ mice with pioglitazone decreased macrophage content of the transplanted visceral fat pad and reduced plasma monocyte chemoattractant protein-1. Importantly, pioglitazone also reduced atherosclerosis triggered by inflammatory visceral fat but had no protective effect on atherosclerosis in the absence of the visceral fat transplantation. Conclusions-Our

show abstract

“…injection of 20 g of OVA (Sigma-Aldrich) emulsified in 1 mg of aluminum hydroxide (Pierce Chemical) in a total volume of 200 l, as described previously ( Fig. 1) (24,25). On days 21, 22, and 23 after the initial sensitization, the mice were challenged for 30 min with an aerosol of 3% (w/v) OVA in saline (or with saline as a control) using an ultrasonic nebulizer (NE-U12; Omron).…”

Section: Animals and Experimental Protocolmentioning

confidence: 99%

Peroxisome Proliferator-Activated Receptor γ Agonist Down-Regulates IL-17 Expression in a Murine Model of Allergic Airway Inflammation

Park

Lee

Kim

et al. 2009

The Journal of Immunology

Self Cite

View full text Add to dashboard Cite

Peroxisome proliferator-activated receptor γ (PPARγ) plays a critical role in the control of airway inflammation. Recently, IL-17 has been found to be implicated in many immune and inflammatory responses, including airway inflammation. However, no data are available concerning the effect of PPARγ on IL-17 production in airway inflammatory diseases. In this study, we used a mouse model of asthma to evaluate the effect of two PPARγ agonists, rosiglitazone or pioglitazone, on IL-17 expression in allergic airway disease. After OVA inhalation, mice developed the typical pathophysiological features of asthma, and the expression of IL-17 protein and mRNA in the lungs was increased. Administration of rosiglitazone or pioglitazone reduced the pathophysiological features of asthma and decreased the increased IL-17 protein and mRNA expression after OVA inhalation. In addition, the attenuating effect of PPARγ agonist on allergic airway inflammation and bronchial hyperresponsiveness is abrogated by coadministration of rIL-17. This study also showed that the inhibition of IL-17 activity with anti-IL-17 Ab remarkably reduced the increased numbers of inflammatory cells of the airways, airway hyperresponsiveness, and the increased levels of IL-4, IL-5, and IL-13 in bronchoalveolar lavage fluid and OVA-specific IgE in serum. In addition, we found that administration of rosiglitazone or pioglitazone decreased the increased NF-κB activity and that a NF-κB inhibitor, BAY 11-7085, substantially reduced the increased IL-17 protein levels in the lung tissues after OVA inhalation. These findings suggest that the therapeutic effect of PPARγ in asthma is partly mediated by regulation of IL-17 expression via NF-κB pathway.

show abstract

Involvement of IL-10 in Peroxisome Proliferator-Activated Receptor γ-Mediated Anti-Inflammatory Response in Asthma

Cited by 81 publications

References 36 publications

Purified Eicosapentaenoic Acid Induces Prolonged Survival of Cardiac Allografts and Generates Regulatory T Cells

Purified Eicosapentaenoic Acid Induces Prolonged Survival of Cardiac Allografts and Generates Regulatory T Cells

Visceral Adipose Tissue Inflammation Accelerates Atherosclerosis in Apolipoprotein E–Deficient Mice

Peroxisome Proliferator-Activated Receptor γ Agonist Down-Regulates IL-17 Expression in a Murine Model of Allergic Airway Inflammation

Contact Info

Product

Resources

About