期刊連結：
http://www.gouthyperuricemia.comObjective: Gouty arthritis is an intense inflammatory arthritis induced by monosodium urate (MSU) crystals. Macrophages play critical roles in the development of gout. Previous studies suggest that the transforming growth factor-β (TGF-β) signaling can regulate the inflammation through direct effects on macrophage function through TGF-β inducible early gene 1 (TIEG1), which also increases pro-differentiation transcription factor PU.1 expression and control macrophage development. This study aims to investigate whether TIEG1 is involved in MSU crystals-induced gouty inflammation.
Methods: MSU suspensions were injected into the foot pads (1mg/40μl) or ankle joints (0.5mg/20μl) of TIEG1 knock-out (KO) mice and wild type (WT) controls to induce acute gouty arthritis. Paw edema or ankle swelling was measured with digital caliper at different time points after injection. In the peritoneal model, peritoneal cavity was injected with MSU (3mg/0.5ml) suspension, and then total peritoneal exudate cells harvested at 4 hours post-injection were counted and infiltrated macrophages and neutrophils were assessed by Fluorescence-Activated Cell Sorting.
Results: In the foot pad model of MSU-induced gouty arthritis, a paw swelling index was not significantly different in TIEG1 KO mice compared to WT controls. Consistent with the paw swelling model, ankle joint swelling index in TIEG1 KO mice was nearly the same as that from WT mice. Furthermore, there were not marked changes in total number of peritoneal exudate cells, infiltrated macrophages as well as neutrophil influx between KO and WT mice.
Conclusion: TIEG1 may not play a critical role in the development of gout.
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