1092 - Food Antigen-Specific Sensitization of Nociceptive Nerves as an Underlying Mechanism of Visceral Pain in Ibs

Aguilera‐Lizarraga, Javier; Balemans, Dafne; Lopez, Cintya D. Lopez; Polanco, Josue O. Jaramillo; Florens, Morgane; Perna, Eluisa; Denadai‐Souza, Alexandre; Theofanous, Stavroula; Decraecker, Lisse; Jain, Piyush; Breynaert, Christine; Vanner, Stephen; Reed, David E.; Wouters, Mira M.; Boeckxstaens, Guy E.

doi:10.1016/s0016-5085(18)31107-7

Cited by 2 publications

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“…In an elegant study, Aguilera-Lizarraga and Florens demonstrated that the establishment of oral tolerance can be impaired due to stress or intestinal infection, two major triggers of FGID symptoms, without triggering a systemic allergic reaction. Their results showed that this impaired tolerance triggered a mast cell activation through local (but not systemic) IgE, leading to colonic hypersensitivity and hyperpermeability ( 196 , 197 ).…”

Section: Food-related Models Of Fgidmentioning

confidence: 99%

Animal Models for Functional Gastrointestinal Disorders

Accarie

Vanuytsel

2020

Front. Psychiatry

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Functional gastrointestinal disorders (FGID), such as functional dyspepsia (FD) and irritable bowel syndrome (IBS) are characterized by chronic abdominal symptoms in the absence of an organic, metabolic or systemic cause that readily explains these complaints. Their pathophysiology is still not fully elucidated and animal models have been of great value to improve the understanding of the complex biological mechanisms. Over the last decades, many animal models have been developed to further unravel FGID pathophysiology and test drug efficacy. In the first part of this review, we focus on stress-related models, starting with the different perinatal stress models, including the stress of the dam, followed by a discussion on neonatal stress such as the maternal separation model. We also describe the most commonly used stress models in adult animals which brought valuable insights on the brain-gut axis in stress-related disorders. In the second part, we focus more on models studying peripheral, i.e., gastrointestinal, mechanisms, either induced by an infection or another inflammatory trigger. In this section, we also introduce more recent models developed around food-related metabolic disorders or food hypersensitivity and allergy. Finally, we introduce models mimicking FGID as a secondary effect of medical interventions and spontaneous models sharing characteristics of GI and anxiety-related disorders. The latter are powerful models for brain-gut axis dysfunction and bring new insights about FGID and their comorbidities such as anxiety and depression.

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Section: Food-related Models Of Fgidmentioning

confidence: 99%

Animal Models for Functional Gastrointestinal Disorders

Accarie

Vanuytsel

2020

Front. Psychiatry

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Effect of resolvins on sensitisation of TRPV1 and visceral hypersensitivity in IBS

Perna

Aguilera‐Lizarraga

Florens

et al. 2020

Gut

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ObjectiveResolvins (RvD1, RvD2 and RvE1) are endogenous anti-inflammatory lipid mediators that display potent analgesic properties in somatic pain by modulating transient receptor potential vanilloid 1 (TRPV1) activation. To what extent these molecules could also have a beneficial effect on TRPV1 sensitisation and visceral hypersensitivity (VHS), mechanisms involved in IBS, remains unknown.DesignThe effect of RvD1, RvD2 and RvE1 on TRPV1 activation and sensitisation by histamine or IBS supernatants was assessed on murine dorsal root ganglion (DRG) neurons using live Ca2+ imaging. Based on the results obtained in vitro, we further studied the effect of RvD2 in vivo using a murine model of post-infectious IBS and a rat model of post-inflammatory VHS. Finally, we also tested the effect of RvD2 on submucosal neurons in rectal biopsies of patients with IBS.ResultsRvD1, RvD2 and RvE1 prevented histamine-induced TRPV1 sensitisation in DRG neurons at doses devoid of an analgesic effect. Of note, RvD2 also reversed TRPV1 sensitisation by histamine and IBS supernatant. This effect was blocked by the G protein receptor 18 (GPR18) antagonist O-1918 (3–30 µM) and by pertussis toxin. In addition, RvD2 reduced the capsaicin-induced Ca2+ response of rectal submucosal neurons of patients with IBS. Finally, treatment with RvD2 normalised pain responses to colorectal distention in both preclinical models of VHS.ConclusionsOur data suggest that RvD2 and GPR18 agonists may represent interesting novel compounds to be further evaluated as treatment for IBS.

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1092 - Food Antigen-Specific Sensitization of Nociceptive Nerves as an Underlying Mechanism of Visceral Pain in Ibs

Cited by 2 publications

References 0 publications

Animal Models for Functional Gastrointestinal Disorders

Animal Models for Functional Gastrointestinal Disorders

Effect of resolvins on sensitisation of TRPV1 and visceral hypersensitivity in IBS

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