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Electrophilic PPARγ Ligands Attenuate IL-1β and Silica-Induced Inflammatory Mediator Production in Human Lung Fibroblasts via a PPARγ-Independent Mechanism
Joint Authors
Phipps, Richard P.
Pollock, Stephen J.
Sime, Patricia J.
Ferguson, Heather E.
Jones, Carolyn
Sapinoro, Ramil E.
Gurell, Michael N.
Thatcher, Thomas H.
Hogan, Christopher M.
Source
Issue
Vol. 2011, Issue 2011 (31 Dec. 2011), pp.1-11, 11 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2011-06-16
Country of Publication
Egypt
No. of Pages
11
Main Subjects
Natural & Life Sciences (Multidisciplinary)
Biology
Abstract EN
Acute and chronic lung inflammation is associated with numerous important disease pathologies including asthma, chronic obstructive pulmonary disease and silicosis.
Lung fibroblasts are a novel and important target of anti-inflammatory therapy, as they orchestrate, respond to, and amplify inflammatory cascades and are the key cell in the pathogenesis of lung fibrosis.
Peroxisome proliferator-activated receptor gamma (PPARγ) ligands are small molecules that induce anti-inflammatory responses in a variety of tissues.
Here, we report for the first time that PPARγ ligands have potent anti-inflammatory effects on human lung fibroblasts.
2-cyano-3, 12-dioxoolean-1, 9-dien-28-oic acid (CDDO) and 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) inhibit production of the inflammatory mediators interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), COX-2, and prostaglandin (PG)E2 in primary human lung fibroblasts stimulated with either IL-1β or silica.
The anti-inflammatory properties of these molecules are not blocked by the PPARγ antagonist GW9662 and thus are largely PPARγ independent.
However, they are dependent on the presence of an electrophilic carbon.
CDDO and 15d-PGJ2, but not rosiglitazone, inhibited NF-κB activity.
These results demonstrate that CDDO and 15d-PGJ2 are potent attenuators of proinflammatory responses in lung fibroblasts and suggest that these molecules should be explored as the basis for novel, targeted anti-inflammatory therapies in the lung and other organs.
American Psychological Association (APA)
Hogan, Christopher M.& Thatcher, Thomas H.& Sapinoro, Ramil E.& Gurell, Michael N.& Ferguson, Heather E.& Pollock, Stephen J.…[et al.]. 2011. Electrophilic PPARγ Ligands Attenuate IL-1β and Silica-Induced Inflammatory Mediator Production in Human Lung Fibroblasts via a PPARγ-Independent Mechanism. PPAR Research،Vol. 2011, no. 2011, pp.1-11.
https://search.emarefa.net/detail/BIM-463069
Modern Language Association (MLA)
Hogan, Christopher M.…[et al.]. Electrophilic PPARγ Ligands Attenuate IL-1β and Silica-Induced Inflammatory Mediator Production in Human Lung Fibroblasts via a PPARγ-Independent Mechanism. PPAR Research No. 2011 (2011), pp.1-11.
https://search.emarefa.net/detail/BIM-463069
American Medical Association (AMA)
Hogan, Christopher M.& Thatcher, Thomas H.& Sapinoro, Ramil E.& Gurell, Michael N.& Ferguson, Heather E.& Pollock, Stephen J.…[et al.]. Electrophilic PPARγ Ligands Attenuate IL-1β and Silica-Induced Inflammatory Mediator Production in Human Lung Fibroblasts via a PPARγ-Independent Mechanism. PPAR Research. 2011. Vol. 2011, no. 2011, pp.1-11.
https://search.emarefa.net/detail/BIM-463069
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-463069