Monosodium urate (MSU) crystals trigger acute inflammation through the TLR–NLRP3 two-signal model, where opsonization by plasma proteins enhances phagocytosis and NLRP3 inflammasome activation, resulting in IL-1β release and pyroptosis.

Uric acid crystals in the joint attract proteins from the blood that coat their surface, making them easier for immune cells to swallow. Once swallowed, the crystals break open the cell's internal sacs, causing a drop in potassium inside the cell and releasing harmful molecules. This, combined with a prior signal from the cell's surface receptors that read the crystals as dangerous, turns on a molecular machine that cuts inactive proteins into active inflammatory signals and bursts the cell open, spilling out more signals that cause swelling and pain.