Abstract
Background: Anti-inflammatory targeting of IL-1β in people with previous MI is beneficial in terms of recurrent cardiovascular events. Mechanisms for modulation of IL-1β synthesis by macrophages is therefore also of potential value. The NLRP3 inflammasome complex plays a crucial role in IL-1β synthesis and is activated in a two-step process – “Signal 1” and “Signal 2”. This study investigated the possible role of mitochondrial and cytosolic superoxide and slow-release hydrogen sulfide generation in activation of the NLRP3 inflammasome in human THP-1 monocytes.
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