Visceral hyperalgesia and intestinal dysmotility in a mouse model of postinfective gut dysfunction

Berčík, Přemysl; Wang, Lu; Verdú, Elena F.; Mao, Yu; Blennerhassett, Patricia; Khan, Waliul I.; Kean, Iain; Tougas, Gervais; Collins, Stephen M.

doi:10.1053/j.gastro.2004.04.006

Cited by 200 publications

(188 citation statements)

References 35 publications

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“…Our findings are consistent with animal studies showing that transient enteric infection can lead to persistent gut dysmotility in nematode-infected mice [11]. Animal studies have demonstrated that inflammation-induced intestinal muscle hypercontractility persists even after resolution of the inflammation [12,27] and that increases in muscle contractility are associated with increases in intestinal 5-HT and infiltration of immunocytes [28].…”

Section: Colonic Motility Responses In Pi-ibssupporting

confidence: 92%

“…In one study, patients with PI-IBS showed higher scores for anxiety and depression compared with individuals who had no IBS symptoms 3 months following acute infection [7], whereas another study failed to identify anxiety or depression as an independent predictor of PI-IBS [10]. Third, a mild transient gut inflammation led to long-term change of visceral hypersensitivity in an animal model of PI-IBS [11]. In another animal study, persistent intestinal smooth muscle hypercontractility was present after resolution of chemically induced inflammation [12].…”

Section: Introductionmentioning

confidence: 99%

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670 Motility Response to Colonic Distention is Increased in Post-Infectious Irritable Bowel Syndrome (PI-IBS)

Kanazawa¹,

Palsson²,

Tilburg³

et al. 2010

Gastroenterology

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Background-Acute intestinal infection leads to persistent intestinal smooth muscle hypercontractility and pain hypersensitivity after resolution of the infection in animal models. We investigated whether post-infectious irritable bowel syndrome (PI-IBS) is associated with abnormalities in phasic contractions of the colon, smooth muscle tone and pain sensitivity compared to non-PI-IBS (NI-IBS) or healthy controls (HC).

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Section: Colonic Motility Responses In Pi-ibssupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

670 Motility Response to Colonic Distention is Increased in Post-Infectious Irritable Bowel Syndrome (PI-IBS)

Kanazawa¹,

Palsson²,

Tilburg³

et al. 2010

Gastroenterology

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“…We hypothesized that P2X 7 R activation would be implicated in the development of postinfectious visceral hypersensitivity and investigated this using an animal model of postinfectious gastrointestinal dysfunction, the Trichinella spiralis-infected mouse (22). Mice infected with T. spiralis develop a transient inflammatory response that resolves to leave a dysfunctional gut characterized by altered motor and sensory nerve function reminiscent of IBS (17,22,23).…”

mentioning

confidence: 99%

“…Mice infected with T. spiralis develop a transient inflammatory response that resolves to leave a dysfunctional gut characterized by altered motor and sensory nerve function reminiscent of IBS (17,22,23). In the current study, we used P2X 7 R 2/2 mice (21) to investigate the role of P2X 7 Rs and IL-1b release in establishing an inflammatory response to T. spiralis infection.…”

mentioning

confidence: 99%

P2X7 Receptor-Dependent Intestinal Afferent Hypersensitivity in a Mouse Model of Postinfectious Irritable Bowel Syndrome

Keating

Pelegrı́n²,

Martínez³

et al. 2011

The Journal of Immunology

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The ATP-gated P2X7 receptor (P2X7R) was shown to be an important mediator of inflammation and inflammatory pain through its regulation of IL-1β processing and release. Trichinella spiralis-infected mice develop a postinflammatory visceral hypersensitivity that is reminiscent of the clinical features associated with postinfectious irritable bowel syndrome. In this study, we used P2X7R knockout mice (P2X7R−/−) to investigate the role of P2X7R activation in the in vivo production of IL-1β and the development of postinflammatory visceral hypersensitivity in the T. spiralis-infected mouse. During acute nematode infection, IL-1β–containing cells and P2X7R expression were increased in the jejunum of wild-type (WT) mice. Peritoneal and serum IL-1β levels were also increased, which was indicative of elevated IL-1β release. However, in the P2X7R−/− animals, we found that infection had no effect upon intracellular, plasma, or peritoneal IL-1β levels. Conversely, infection augmented peritoneal TNF-α levels in both WT and P2X7R−/− animals. Infection was also associated with a P2X7R-dependent increase in extracellular peritoneal lactate dehydrogenase, and it triggered immunological changes in both strains. Jejunal afferent fiber mechanosensitivity was assessed in uninfected and postinfected WT and P2X7R−/− animals. Postinfected WT animals developed an augmented afferent fiber response to mechanical stimuli; however, this did not develop in postinfected P2X7R−/− animals. Therefore, our results demonstrated that P2X7Rs play a pivotal role in intestinal inflammation and are a trigger for the development of visceral hypersensitivity.

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“…23 Denervation hypersensitivity has also been reported 24 and these abnormalities of enteric nerves might lead to inco-ordinate contractions and high pressure producing diverticulosis, but this is highly speculative given the lack of good animal models of the condition. The associated muscular hypertrophy and altered enteric nerves 25 may result from remodelling after acute inflammation, which is known from many animal studies to be associated with muscular hypertrophy, abnormal motility, 26 visceral hypersensitivity and altered neurochemical coding. 27,28 Such changes may account for the common experience of the development of recurrent abdominal pain and disturbed bowel habit following acute diverticulitis 29 and the finding of visceral hypersensitivity in patients with symptomatic diverticular disease.…”

Section: Epidemiology and Pathogenesismentioning

confidence: 99%

Review article: the pathogenesis and management of acute colonic diverticulitis

Humes

Spiller

2014

Aliment Pharmacol Ther

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SummaryBackgroundAcute diverticulitis, defined as acute inflammation associated with a colonic diverticulum, is a common emergency presentation managed by both surgeons and physicians. There have been advances in both the medical and the surgical treatments offered to patients in recent years.AimTo review the current understanding of the aetiology and treatment of acute diverticulitis.MethodsA search of PubMed and Medline databases was performed to identify articles relevant to the aetiology, pathogenesis and management of acute diverticulitis.ResultsThere are 75 hospital admissions per year for acute diverticulitis per 100 000 of the population in the United States. Recent reports suggest a 26% increase in admissions over a 7‐year period. Factors predisposing to the development of acute diverticulitis include obesity, smoking, diet, lack of physical activity and medication use such as aspirin and nonsteroidal anti‐inflammatory drugs. The condition is associated with a low mortality of about 1% following medical therapy, rising to 4% in‐hospital mortality in those requiring surgery. There is limited evidence on the efficacy of individual antibiotic regimens, and antibiotic treatment may not be required in all patients. The rates of recurrence reported for patients with acute diverticulitis following medical management vary from 13% to 36%. The surgical management of those patients who fail medical treatment has moved towards a laparoscopic nonresectional approach; however, the evidence supporting this is limited.ConclusionsFurther high‐quality randomised controlled trials are required of both medical and surgical treatments in patients with acute diverticulitis, if management is to be evidence‐based.

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Visceral hyperalgesia and intestinal dysmotility in a mouse model of postinfective gut dysfunction

Cited by 200 publications

References 35 publications

670 Motility Response to Colonic Distention is Increased in Post-Infectious Irritable Bowel Syndrome (PI-IBS)

670 Motility Response to Colonic Distention is Increased in Post-Infectious Irritable Bowel Syndrome (PI-IBS)

P2X7 Receptor-Dependent Intestinal Afferent Hypersensitivity in a Mouse Model of Postinfectious Irritable Bowel Syndrome

Review article: the pathogenesis and management of acute colonic diverticulitis

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