Interleukin-13 gene therapy reduces inflammation, vascularization, and bony destruction in rat adjuvant-induced arthritis.

Authors: Woods, JM  Amin, MA  Katschke KJ, JR  Volin, MV  Ruth, JH  Connors, MA  Woodruff, DC  Kurata, H  Arai, K  Haines GK, 3RD  Kumar, P  Koch, AE 
Citation: Woods JM, etal., Hum Gene Ther. 2002 Feb 10;13(3):381-93.
Pubmed: (View Article at PubMed) PMID:11860705
DOI: Full-text: DOI:10.1089/10430340252792512

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease characterized by synovial pannus formation, leukocyte infiltration, and angiogenesis. Adenoviral production of interleukin-13 (IL-13) reduces levels of proinflammatory mediators in an explant model of RA synovial tissue in vitro. To assess this approach in an animal model of arthritis, we compared intra-articular injections of an adenovirus producing rat IL-13 (AxCArIL-13), a control virus, and rat ankles receiving phosphate-buffered saline (PBS) in rat adjuvant-induced arthritis (AIA). We demonstrate that IL-13 levels are normally low in ankles throughout the course of rat AIA. We show that administration of AxCArIL-13 before arthritis onset significantly reduces ankle circumference, paw volume, bony destruction, the number of polymorphonuclear cells (PMNs), the quantity of blood vessels, and levels of monocyte chemoattractant protein (MCP)-1 in ankles. When administered as a treatment to inflamed ankles, AxCArIL-13 decreases articular index scores, paw volumes, bony destruction, vascularization, tumor necrosis factor-alpha (TNF-alpha) levels, and the quantity of monocytes, lymphocytes, and PMNs. Thus, increasing IL-13 levels significantly ameliorates the course of rat AIA, suggesting that similar strategies for the treatment of human RA are worthy of further study.


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Created: 2014-04-01
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.