Possible implications of animal models for the assessment of visceral pain

Regmi, Bimal Raj; Shah, Manoj Kumar

doi:10.1002/ame2.12130

Cited by 16 publications

(16 citation statements)

References 87 publications

(143 reference statements)

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“…Giving that changes in inflammatory factors, including TNF‐α, IL‐1β, IL‐6, IL‐10, and iNOS, are a major characteristic of the sepsis model, 45 , 46 we measured the inflammatory cytokines after LPS treatment. We observed changes in inflammatory cytokines at different timepoints after LPS treatment ( S3 ).…”

Section: Resultsmentioning

confidence: 99%

TRDMT1 exhibited protective effects against LPS‐induced inflammation in rats through TLR4‐NF‐κB/MAPK‐TNF‐α pathway

Zhang

et al. 2022

Anim Models and Exp Med

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Background Inflammation is a complex physiological and pathological process. Although many types of inflammation are well characterized, their physiological functions are largely unknown. tRNA aspartic acid methyltransferase 1 (TRDMT1) has been implicated as a stress‐related protein, but its intrinsic biological role is unclear. Methods We constructed a Trdmt1 knockout rat and adopted the LPS‐induced sepsis model. Survival curve, histopathological examination, expression of inflammatory factors, and protein level of TLR4 pathway were analyzed. Results Trdmt1 deletion had no obvious impact on development and growth. Trdmt1 deletion slightly increased the mortality during aging. Our data showed that Trdmt1 strongly responded in LPS‐treated rats, and Trdmt1 knockout rats were vulnerable to LPS treatment with declined survival rate. We also observed more aggravated tissue damage and more cumulative functional cell degeneration in LPS‐treated knockout rats compared with control rats. Further studies showed upregulated TNF‐α level in liver, spleen, lung, and serum tissues, which may be explained by enhanced p65 and p38 phosphorylation. Conclusions Our data demonstrated that Trdmt1 plays a protective role in inflammation by regulating the TLR4‐NF‐κB/MAPK‐TNF‐α pathway. This work provides useful information to understand the TRDMT1 function in inflammation.

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Section: Resultsmentioning

confidence: 99%

TRDMT1 exhibited protective effects against LPS‐induced inflammation in rats through TLR4‐NF‐κB/MAPK‐TNF‐α pathway

Zhang

et al. 2022

Anim Models and Exp Med

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“…Another limitation of this study would be its translationality to humans [ 56 , 57 ]. Even though no animal model can mimic human visceral pain perfectly, visceral pain models have allowed the study of the pathophysiology of the disease, as well as the efficacy of potential analgesics [ 58 , 59 ]. Moreover, while interspecies differences have been described in BoNT sensitivity [ 60 ], protein engineering can produce BoNTs with improved affinity for human receptors to bypass these discrepancies [ 61 ].…”

Section: Discussionmentioning

confidence: 99%

The Isolated Mouse Jejunal Afferent Nerve Assay as a Tool to Assess the Effect of Botulinum Neurotoxins in Visceral Nociception

Retailleau

Martin

Lezmi

et al. 2022

Toxins

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For the past two decades, botulinum neurotoxin A (BoNT/A) has been described as a strong candidate in the treatment of pain. With the production of modified toxins and the potential new applications at the visceral level, there is a real need for tools allowing the assessment of these compounds. In this study, we evaluated the jejunal mesenteric afferent nerve assay to investigate BoNT/A effects on visceral nociception. This ex vivo model allowed the continuous recording of neuronal activity in response to various stimuli. BoNT/A was applied intraluminally during three successive distensions, and the jejunum was distended every 15 min for 3 h. Finally, samples were exposed to external capsaicin. BoNT/A intoxication was validated at the molecular level with the presence of cleaved synaptosomal-associated protein of 25 (SNAP25) in nerve terminals in the mucosa and musculosa layers 3 h after treatment. BoNT/A had a progressive inhibitory effect on multiunit discharge frequency induced by jejunal distension, with a significant decrease from 1 h after application without change in jejunal compliance. The capsaicin-induced discharge was also affected by the toxin. This assay allowed the description of an inhibitory effect of BoNT/A on afferent nerve activity in response to distension and capsaicin, suggesting BoNT/A could alleviate visceral nociception.

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“…Subsequent treatment with methyllycaconitine reversed the beneficial effects of PNU-282987. Varenicline, a non-selective agonist of α7 nAChRs, improved colonic motility and the cholinergic response in a rat IBS model [111]. Other α7-selective agonists including encenicline and AR-R17779 have shown anti-inflammatory effects in mouse models of colitis and postoperative ileus.…”

Section: Inflammatory Control In the Gut Involves The Vagus Nerve And α7 Nachrsmentioning

confidence: 99%

Nicotinic Acetylcholine Receptor Involvement in Inflammatory Bowel Disease and Interactions with Gut Microbiota

Ruzafa

Cedillo

Hone

2021

IJERPH

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The gut-brain axis describes a complex interplay between the central nervous system and organs of the gastrointestinal tract. Sensory neurons of dorsal root and nodose ganglia, neurons of the autonomic nervous system, and immune cells collect and relay information about the status of the gut to the brain. A critical component in this bi-directional communication system is the vagus nerve which is essential for coordinating the immune system’s response to the activities of commensal bacteria in the gut and to pathogenic strains and their toxins. Local control of gut function is provided by networks of neurons in the enteric nervous system also called the ‘gut-brain’. One element common to all of these gut-brain systems is the expression of nicotinic acetylcholine receptors. These ligand-gated ion channels serve myriad roles in the gut-brain axis including mediating fast synaptic transmission between autonomic pre- and postganglionic neurons, modulation of neurotransmitter release from peripheral sensory and enteric neurons, and modulation of cytokine release from immune cells. Here we review the role of nicotinic receptors in the gut-brain axis with a focus on the interplay of these receptors with the gut microbiome and their involvement in dysregulation of gut function and inflammatory bowel diseases.

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Possible implications of animal models for the assessment of visceral pain

Cited by 16 publications

References 87 publications

TRDMT1 exhibited protective effects against LPS‐induced inflammation in rats through TLR4‐NF‐κB/MAPK‐TNF‐α pathway

TRDMT1 exhibited protective effects against LPS‐induced inflammation in rats through TLR4‐NF‐κB/MAPK‐TNF‐α pathway

The Isolated Mouse Jejunal Afferent Nerve Assay as a Tool to Assess the Effect of Botulinum Neurotoxins in Visceral Nociception

Nicotinic Acetylcholine Receptor Involvement in Inflammatory Bowel Disease and Interactions with Gut Microbiota

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