Mechanisms Underlying the Maintenance of Muscle Hypercontractility in a Model of Postinfective Gut Dysfunction

Akiho, Hirotada; Deng, Yikang; Blennerhassett, Patricia; Kanbayashi, Hiroshi; Collins, Stephen M.

doi:10.1053/j.gastro.2005.03.049

Cited by 129 publications

(120 citation statements)

References 47 publications

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“…It has been reported that a greater number of EC cells is associated with visceral hypersensitivity in patients with IBS [40]. Experimental studies in animals support the findings that PI-IBS shows colonic hypercontractility during noxious stimulation of the gut [12,27], and our study confirms this in human IBS patients. Further prospective observations of the relationships between such a physiological exacerbation and changes in mucosal immunocyte infiltration [13,14], epithelial permeability [15] and composition of gut microbiome [41,42] are needed to confirm the hypothesis that the exaggerated motility responses to distention are mediated by persisting immune activation.…”

Section: Study Limitationssupporting

confidence: 89%

“…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]. Several reports on histologic and immunohistochemical analyses in the intestinal mucosa [7,14,29] suggest that subtle morphologic changes involving lymphocytes, mast cells, enterochromaffin (EC) cells which contain serotonin, and enteric nerves may be associated with IBS symptoms.…”

Section: Colonic Motility Responses In Pi-ibsmentioning

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: Study Limitationssupporting

confidence: 89%

Section: Colonic Motility Responses In Pi-ibsmentioning

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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“…The increase in EC concentrations associated with PI-IBS may contribute to gastrointestinal symptoms through serotonin-mediated mechanisms (1,6) . As EC are the primary source of intestinal serotonin -a Recurrent abdominal pain or discomfort* at least 3 days/month in the last 3 months associated with two or more of the following: 1. improvement with defecation 2. onset associated with a change in frequency of stool 3. onset associated with a change in form (appearance) of stool…”

Section: Introductionmentioning

confidence: 99%

“…The maintenance of hypercontractility results from Th2 cytokine-induced expression of transforming growth factor (TGF-beta1) and the subsequent upregulation of cyclooxygenase 2 (COX-2) and prostaglandin E 2 (PGE-2) at the level of the smooth muscle (1) . The same studies also support that COX-2 inhibitors attenuated TGF-beta1-induced muscle hypercontractility (1) .…”

Section: Introductionmentioning

confidence: 99%

Treatment of postinfectious irritable bowel syndrome and noninfective irritable bowel syndrome with mesalazine

Boiocchi

Almeida

Leite

et al. 2011

Arq. Gastroenterol.

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-Context -Recent studies support the hypothesis that postinfectious irritable bowel syndrome and some irritable bowel syndrome patients display persistent signs of minor mucosal inflammation. Mesalazine has intestinal anti-inflammatory properties including cyclooxygenase and prostaglandin inhibition. The effects of mesalazine on postinfectious irritable bowel syndrome and noninfective irritable bowel syndrome patients are still unknown. Objective -To observe the effects of mesalazine on postinfectious irritable bowel syndrome and noninfective irritable bowel syndrome with diarrhea patients. Methods -Based on Rome III criteria, 61 irritable bowel syndrome with diarrhea patients (18 years old or more) were included in the evaluation. Patients were divided into two groups: postinfectious irritable bowel syndrome group, with 18 patients medicated with mesalazine 800 mg 3 times a day for 30 days; noninfective irritable bowel syndrome group, with 43 patients medicated with mesalazine 800 mg 3 times a day for 30 days. Symptom evaluations at baseline and after treatment were performed by means of a four-point Likert scale including stool frequency, stool form and consistency (Bristol Stool Scale), abdominal pain and distension (maximum score: 16; minimum score: 4).

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“…These differences in contractile responses may be due to differences in cytokine profiles. Reports from the Collins group (Akiho et al, 2002;Akiho et al, 2005a;Akiho et al, 2005b) have suggested that nematode-induced hypercontractility is mediated by an increase in prostaglandin E2 (PGE2) levels after induction of the expression of Th2 cytokines such as interleukin (IL)-4 and IL-13.On the other hand, reports suggest that TNBS-induced gut inflammation is mediated mainly by Th1 cytokines such as IL-1β, tumor necrosis factor-α (TNF-α) and IL-12 (Neurath et al, 1995; Kinoshita et al, 2006; Kiyosue et al, 2006;Ohama et al, 2007b). In this review, we focused on the molecular mechanisms that are responsible for the decreased motility of the inflamed intestine.…”

mentioning

confidence: 99%

Mechanism of abnormal intestinal motility in inflammatory bowel disease: how smooth muscle contraction is reduced?

Ohama

Hori

Ozaki

2007

J Smooth Muscle Res

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Intestinal inflammation alters the contractile activity of intestinal smooth muscle. Motility disorders of the gastrointestinal tract are clinically important symptoms, because they are often associated with severe interstitial inflammation. In addition, the motility disorders secondarily induce abnormal growth of the intestinal flora, and the resulting disturbance of this flora aggravates the pathogenesis of mucosal inflammation. This in turn aggravates the intestinal dysmotility; i.e., it is an inflammatory spiral. Therefore, it is important to elucidate the mechanisms involved in the changes in motor function which occur in intestinal inflammation. Recent studies have revealed several molecular mechanisms responsible for the decreased motility which occurs in an inflamed gastrointestinal tract. In the present review, we discuss the functional failure of smooth muscle cells, including changes in the activity of muscarinic receptors, ion channels and the endogenous myosin phosphatase inhibitor CPI-17.Key words: intestinal inflammation, smooth muscle, contraction, CPI-17 Motility disorders in intestinal inflammationMotility disorders of the gastrointestinal tract are extremely important clinically because they can lead to systemic disease. In humans and in animal models, intestinal inflammation results in the disturbance of motility, which may reflect changes in smooth muscle function and/or the enteric nervous system (Vermillion et al., 1993;Vrees et al., 2002). Both increased and decreased smooth muscle contractility has been observed in intestinal inflammation. In a model of nematode infection-induced gut inflammation, such as Trichinella spiralis infectioninduced gut inflammation, smooth muscle contractility is increased (Vermillion and Collins, 1988;Blennerhassett et al., 1992). On the other hand, smooth muscle contractility is decreased T. OHAMA et al. 44 in the intestinal inflammation induced by trinitrobenzene sulphonic acid (TNBS), surgical manipulation, experimental obstruction, hemorrhagic shock, or peritonitis (Kalff et al., 1998;Moreels et al., 2001; Koyluoglu et al., 2002;Hierholzer et al., 2004; Kinoshita et al., 2006; Kiyosue et al., 2006;Won et al., 2006; Kinoshita et al., 2007;Ohama et al., 2007b). These differences in contractile responses may be due to differences in cytokine profiles. Reports from the Collins group (Akiho et al., 2002;Akiho et al., 2005a;Akiho et al., 2005b) have suggested that nematode-induced hypercontractility is mediated by an increase in prostaglandin E2 (PGE2) levels after induction of the expression of Th2 cytokines such as interleukin (IL)-4 and IL-13.On the other hand, reports suggest that TNBS-induced gut inflammation is mediated mainly by Th1 cytokines such as IL-1β, tumor necrosis factor-α (TNF-α) and IL-12 (Neurath et al., 1995; Kinoshita et al., 2006; Kiyosue et al., 2006;Ohama et al., 2007b). In this review, we focused on the molecular mechanisms that are responsible for the decreased motility of the inflamed intestine. Nematode-induced hyper-co...

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Mechanisms Underlying the Maintenance of Muscle Hypercontractility in a Model of Postinfective Gut Dysfunction

Cited by 129 publications

References 47 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)

Treatment of postinfectious irritable bowel syndrome and noninfective irritable bowel syndrome with mesalazine

Mechanism of abnormal intestinal motility in inflammatory bowel disease: how smooth muscle contraction is reduced?

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