Extended report
Interleukin 13 blocks the release of collagen from bovine nasal
cartilage treated with proinflammatory cytokines
C S Cleaver, A D Rowan, T E Cawston
Department of
Rheumatology, School of Clinical and Medical Sciences, 4th Floor
Catherine Cookson Building, The Medical School, Framlington Place,
University of Newcastle-upon-Tyne, Newcastle-upon-Tyne NE2 4HH, UK
Correspondence to: Dr Cleaver C.S.Cleaver{at}ncl.ac.uk
Accepted for publication 28 June 2000
OBJECTIVE
To
investigate whether interleukin 13 (IL13) could act in a
chondroprotective manner and protect cartilage stimulated to resorb with a combination of IL1
and oncostatin M (OSM), in a similar way
to the anti-inflammatory cytokine, IL4.
METHODSIL13 was added
to explant cultures of bovine nasal cartilage stimulated to resorb with
IL1 and OSM, and the release of collagen and proteoglycan
determined. Collagenolytic and tissue inhibitors of metalloproteinase
(TIMP) activities were determined by bioassay. Northern blot analyses
were performed to determine the effects of IL13 on the induction of
matrix metalloproteinase-1 (MMP-1), MMP-3, MMP-13, and TIMP-1 gene expression.
RESULTSIL13 can
prevent the release of collagen from bovine nasal cartilage in a dose
dependent manner. This was accompanied by a concomitant decrease in
measurable collagenolytic activity in the culture supernates and an
increase in TIMP activity. Northern blot analysis showed that IL13 down
regulated MMP-3 and MMP-13 levels but up regulated MMP-1 and TIMP-1
gene expression in bovine nasal chondrocytes at 24 hours.
CONCLUSIONThis study
showed for the first time that IL13 can block collagen release from
resorbing cartilage in a similar manner to IL4. This is accompanied by
a reduction in detectable collagenolytic activity, a decrease in MMP-3
and MMP-13 mRNA levels, and an up regulation of TIMP-1 expression.
© 2001 by Annals of the Rheumatic Diseases
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