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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: The NLRP3 inflammasome: an emerging therapeutic target for chronic pain

Fig. 1

Schematic picture showing NLRP3 inflammasome activation and expression in the sensory nerve system and its surrounding microenvironment during chronic pain. The inset box depicts NLRP3 inflammasome activation procedure. The first phase (priming) involves Toll-like receptors (TLRs) and cytokine receptor recognition of the PAMPs/ DAMPs or endogenous cytokines, which results in activation of nuclear factor kappa B (NF-κB) signaling in the nucleus and upregulation of the transcription levels of inactive NLRP3 and pro-IL-1β. The second phase (assembly) involves the assembly of NLRP3 with ASC into inflammasome complex, initiated by the stimulation of NLRP3 by a plethora of stimuli, and subsequent activation of pro-caspase-1 with autocatalytic activity. The active caspase-1 ultimately cleaves pro-IL-1β and pro-IL-18, leading to maturation and release of IL-1β and IL-18. The expression of NLRP3 inflammasome has been identified in the following types of cells related with the sensory nerve system and surrounding microenvironment during chronic pain: peripheral inflamed tissues (including macrophages, neutrophils, mast cells) [14, 18, 19]; peripheral nerves and DRG (including DRG neurons and infiltrated macrophages) [20, 21]; spinal cord dorsal horn (including neurons, astrocytes and microglia) [15, 22]; brain regions (including neurons and astrocytes in DRN and microglia in PFC [23, 24]. This figure was created with BioRender.com

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