Gout has long been recognized as a disease of recurrent bouts of acute inflammation that undergo self-resolution. This inflammation is triggered by the body's response to monosodium urate (MSU) crystals. In this paper, we focus on recent studies that describe how interactions of MSU crystals with the components of the innate immune system trigger acute gouty inflammation as well as mechanisms that are involved in the resolution of this inflammation. Specifically, we describe how toll-like receptors mediate the uptake of MSU crystals involved in the initiation and resolution of gouty inflammation. We also describe recent findings on the role of apoptotic clearance in the resolution of gouty inflammation. In addition, how therapies used to treat gout act on the innate immune system to inhibit MSU crystal-induced inflammation and promote the resolution of inflammation is discussed.