Our in vivo data support that in the absence of Prg4 expression, the tissue microenvironment is shifted towards lack of resolution of acute gout inflammation, as indicated by higher neutrophil tissue accumulation and IL-1β levels, and that rhPRG4 promotes effective resolution by increasing the influx of anti-inflammatory NCMs and decreasing CXCL1 and neutrophil tissue accumulation. Here, IL1B is linked to gout.