Fig. 2

The potential role of gut microbiota in neuropathic pain. Gut microbiota-derived mediators participate in the modulation of neuropathic pain through three routes: a LPS and flagellin act on immune cells and macrophages through TLR, and lead to the release of pro-inflammatory mediators; b Different mediators alter nociceptor excitability via diverse receptors expressed on DRG neurons; c Metabolites regulate glial cells activity directly or through AHR. The red dotted line represents exacerbating pain and the green one represents alleviating pain. Abbreviations: DRG, dorsal root ganglion; TLR, Toll-like receptor; TRPA1, transient receptor potential cation channel, subfamily A, member 1; TRPV1, transient receptor potential cation channel, subfamily V, member 1; TRPV4, transient receptor potential cation channel, subfamily V, member 4; GABA, γ-aminobutyric acid; Glu, glutamate; AHR, aryl hydrocarbon receptor; LPS, lipopolysaccharide; PUFAs, polyunsaturated fatty acids; SCFAs, short-chain fatty acids; ECCs, enteroendocrine cells; SCI, spinal cord injury; PNI, peripheral nerve injury