Relationship between mast cell degranulation and jejunal myoelectric alterations in intestinal anaphylaxis in rats

Fargeas, M. J.; Theodourou, Vassilia; Fioramonti, Jean; Buéno, Lionel

doi:10.1016/0016-5085(92)91795-6

Cited by 47 publications

(22 citation statements)

References 22 publications

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“…However, upon Ag challenge both fasted and postprandial intestinal and colonic motility are markedly altered with the initiation of aborally propagating spike complexes and increase in colonic myoelectric spike activity [117]. These changes were associated with an increase in plasma rat mast cell protease II levels and mediated by prostaglandins, leukotrienes and 5-HT [118,119]. Interestingly, when massive degranulation is provoked by chemical degranulators there is a profound inhibition of myoelectrical activity in both the colon and small intestine.…”

Section: Mast Cells and Intestinal Motilitymentioning

confidence: 95%

Pathogenesis of irritable bowel syndrome: The mast cell connection

Santos

Guilarte

Alonso

et al. 2005

Scandinavian Journal of Gastroenterology

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Section: Mast Cells and Intestinal Motilitymentioning

confidence: 95%

Pathogenesis of irritable bowel syndrome: The mast cell connection

Santos

Guilarte

Alonso

et al. 2005

Scandinavian Journal of Gastroenterology

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“…It is thought that mediators such as histamine, serotonin (5HT), prostaglandins or leukotrienes, which are released upon mast cell degranulation, are responsible for these gut disturbances. We showed re cently that a 5HT antagonist and a cyclo-oxygcnase inhib itor are able to reduce the motor alterations appearing upon antigen challenge in sensitized rats, whereas a hista mine antagonist fails to antagonize these effects [4]. How ever, it is not clearly understood if these agents act directly on intestinal smooth muscle cells or indirectly via neural pathways.…”

Section: Introductionmentioning

confidence: 98%

“…1). This activity was char acterized by the succession of propagated spike bursts oc curring at a frequency of 4-6 per min, as previously de scribed [4].…”

Section: Control Studiesmentioning

confidence: 99%

Involvement of Capsaicin-Sensitive Afferent Nerves in the Intestinal Motor Alterations Induced by Intestinal Anaphylaxis in Rats

Fargeas¹,

Fioramonti²,

Buéno³

1993

Int Arch Allergy Immunol

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Alteration of intestinal myoelectrical activity is a characteristic feature of food protein-induced intestinal anaphylaxis in the conscious rat. The motility changes induced by antigen challenge were appraised in egg-albumin-sensitized rats, chronically implanted with NiCr electrodes in the duodenojejunal wall. Intraduodenal infusion of egg albumin given to fasted sensitized rats triggered a disruption of the cyclic pattern of small intestinal motility lasting 79.1 ± 23.3 min. The duration of the challenge effect on intestinal myoelectrical activity was significantly reduced by systemic capsaicin pretreatment (125 mg/kg) but to a lesser extent by perivagal capsaicin. Substance P (SP) antagonists (SP 4-11 and CP 96.345) and atropine were also able to shorten the duration of the antigen-challenge-induced alteration of intestinal motility. It is concluded that SP and capsaicin-sensitive afferent nerve endings play an important role in the intestinal anaphylaxis-induced disturbances of intestinal motility.

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“…Mast cells produce histamine and serotonin, both of which can stimulate enteric smooth muscle contraction [20]. In other conditions mast cells are associated with impaired motility, often due to deleterious effects of mast cell proteases on the interstitial cells of Cajal [21] or on the enteric nervous system [2], [18], [22]–[24]. For example, using in vitro co-cultures of enteric nerves with peritoneal mast cells, it was shown that mast cells damage the nerves [25].…”

Section: Introductionmentioning

confidence: 99%

Mast Cells and Gastrointestinal Dysmotility in the Cystic Fibrosis Mouse

et al. 2009

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BackgroundCystic fibrosis (CF) has many effects on the gastrointestinal tract and a common problem in this disease is poor nutrition. In the CF mouse there is an innate immune response with a large influx of mast cells into the muscularis externa of the small intestine and gastrointestinal dysmotility. The aim of this study was to evaluate the potential role of mast cells in gastrointestinal dysmotility using the CF mouse (Cftrtm1UNC, Cftr knockout).MethodologyWild type (WT) and CF mice were treated for 3 weeks with mast cell stabilizing drugs (ketotifen, cromolyn, doxantrazole) or were treated acutely with a mast cell activator (compound 48/80). Gastrointestinal transit was measured using gavage of a fluorescent tracer.ResultsIn CF mice gastric emptying at 20 min post-gavage did not differ from WT, but was significantly less than in WT at 90 min post-gavage. Gastric emptying was significantly increased in WT mice by doxantrazole, but none of the mast cell stabilizers had any significant effect on gastric emptying in CF mice. Mast cell activation significantly enhanced gastric emptying in WT mice but not in CF mice. Small intestinal transit was significantly less in CF mice as compared to WT. Of the mast cell stabilizers, only doxantrazole significantly affected small intestinal transit in WT mice and none had any effect in CF mice. Mast cell activation resulted in a small but significant increase in small intestinal transit in CF mice but not WT mice.ConclusionsThe results indicate that mast cells are not involved in gastrointestinal dysmotility but their activation can stimulate small intestinal transit in cystic fibrosis.

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Relationship between mast cell degranulation and jejunal myoelectric alterations in intestinal anaphylaxis in rats

Cited by 47 publications

References 22 publications

Pathogenesis of irritable bowel syndrome: The mast cell connection

Pathogenesis of irritable bowel syndrome: The mast cell connection

Involvement of Capsaicin-Sensitive Afferent Nerves in the Intestinal Motor Alterations Induced by Intestinal Anaphylaxis in Rats

Mast Cells and Gastrointestinal Dysmotility in the Cystic Fibrosis Mouse

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