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HDL inhibit cytokine production in a mouse model of urate crystal-induced inflammation

Objectives: To evaluate whether high density lipoproteins (HDL) affect monosodium urate (MSU) crystal-induced inflammation in the murine air pouch model. Methods: MSU crystals were prepared by Denko’s method and sterilized by heating at 180°C for 2 h before each experiment. Human HDL were isolated f...

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Bibliographic Details
Published in:Reumatismo 2011-06, Vol.62 (4), p.266-272
Main Authors: Scanu, A., Oliviero, F., Luisetto, R., Sfriso, P., Dayer, J.M, Burger, D., Punzi, L.
Format: Article
Language:English
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Summary:Objectives: To evaluate whether high density lipoproteins (HDL) affect monosodium urate (MSU) crystal-induced inflammation in the murine air pouch model. Methods: MSU crystals were prepared by Denko’s method and sterilized by heating at 180°C for 2 h before each experiment. Human HDL were isolated from peripheral blood of healthy volunteers. MSU crystals (2 mg in 1 ml of PBS) were injected into subcutaneous air pouches in mice in the presence or absence of HDL (0.1 mg). Negative control pouches received 1 ml of PBS. To recover pouch fluid, the pouches were washed with 2 ml of PBS after the animals were sacrificed. The leukocyte count in the lavage fluids was obtained using a hemocytometer and differential leukocyte count was determined by May-Grünwald-Giemsa staining. IL-6, KC, CCL2 and TNF-α levels were measured in exudates by ELISA. Results: MSU crystals increased the number of leukocytes and the neutrophil migration, as well as the concentrations of IL-6, KC and CCL2 in pouch fluids, while the TNF-α levels were not detectable. The treatment with HDL led to a reduction in all inflammatory parameters: the leukocyte count decreased by 73%; the neutrophil density decreased by 35%; the IL-6, KC and CCL2 concentration decreased by 4-, 6- and 5-fold respectively. Conclusions: This study shows that HDL may limit the inflammatory process by inhibiting leukocyte recruitment and cytokine release. HDL are likely to represent a mechanism of control of crystal-induced inflammation.
ISSN:0048-7449
2240-2683
DOI:10.4081/reumatismo.2010.266