2020
DOI: 10.1016/j.bbadis.2019.165534
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Painful interactions: Microbial compounds and visceral pain

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Cited by 23 publications
(17 citation statements)
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“…We also found a higher abundance of Dialister in HNC patients who had voice/ speech difficulty than in patients without voice/speech difficulty ( Figure S1C). Pain could be directly or indirectly induced by microbial metabolites, neuroactive molecules, cell wall components, and proteins (van Thiel et al, 2020). Symptoms, such as voice/speech difficulty and pain, could hardly be triggered by one or two kinds of oral bacterial microbes.…”
Section: Discussionmentioning
confidence: 99%
“…We also found a higher abundance of Dialister in HNC patients who had voice/ speech difficulty than in patients without voice/speech difficulty ( Figure S1C). Pain could be directly or indirectly induced by microbial metabolites, neuroactive molecules, cell wall components, and proteins (van Thiel et al, 2020). Symptoms, such as voice/speech difficulty and pain, could hardly be triggered by one or two kinds of oral bacterial microbes.…”
Section: Discussionmentioning
confidence: 99%
“…Indeed, while GF mice show limited mucosal inflammation, visceral hypersensitivity due to altered pain processing in the brain is evident, which can be normalized by FMT with feces from conventional mice [ 143 , 144 , 145 ]. Gut microbe components, such as certain TLR ligands, formyl peptide receptor 1 agonists, and SCFAs, can directly enhance visceral pain sensitivity by stimulating primary nociceptive neurons in dorsal root ganglia (DRG) or indirectly by activating inflammatory immune response in the gut [ 146 , 147 ]. On the other hand, microbe-mediated kynurenic acid, serine proteases, and bile acids directly reduce pain by inactivating DRG neurons or indirectly by releasing opioid-like factors from mucosal immune cells [ 146 ].…”
Section: Microbiota-mediated Serotonergic Signaling In Ibs Pathologymentioning
confidence: 99%
“…Based on these findings, it is conceivable that gut dysbiosis and the consequent alterations in gut permeability may participate to the occurrence of vaginal dysbiosis and to the development of chronic submucosa vulvar inflammation in VVS patients [10]. Furthermore, findings that bacterial-derived factors may directly activate sensory neurons by acting on nociceptors [41,42], suggest that the presence of specific bacteria in contact with visceral organs may evoke vulvar pain in VVS women.…”
Section: Discussionmentioning
confidence: 98%