Evidence for the role of mast cells in colon-bladder cross organ sensitization

Auton Neurosci. 2013 Jan;173(1-2):6-13. doi: 10.1016/j.autneu.2012.09.002. Epub 2012 Nov 24.

Abstract

This study examined the contribution of mast cells to colon-bladder cross organ sensitization induced by colon irritation with trinitrobenzene sulfonic acid (TNBS-CI). In urethane anesthetized rats 12 days after TNBS-CI, the voiding interval was reduced from 357 s to 201 s and urothelial permeability, measured indirectly by absorption of sodium fluorescein from the bladder lumen, increased six-fold. These effects were blocked by oral administration of ketotifen (10 mg/kg, for 5 days), a mast cell stabilizing agent. TNBS-CI in wild type mice produced a similar decrease in voiding interval (from 319 s to 209 s) and a 10-fold increase in urothelial permeability; however this did not occur in KitªWª/KitªW-vª mast cell deficient mice. Contractile responses of bladder strips elicited by Compound 48/80 (50 μg/ml), a mast cell activating agent, were significantly larger in strips from rats with TNBS-CI (145% increase in baseline tension) than in control rats (55% increase). The contractions of strips from rats with TNBS-CI were reduced 80-90% by pretreatment of strips with ketotifen (20 μM), whereas contractions of strips from control animals were not significantly changed. Bladder strips were pretreated with SLIGRL-NH2 (100 μM) to desensitize PAR-2, the receptor for mast cell tryptase. SLIGRL-NH2 pretreatment reduced by 60-80% the 48/80 induced contractions in strips from rats with TNBS-CI but did not alter the contractions in strips from control rats. These data indicate that bladder mast cells contribute to the bladder dysfunction following colon-bladder cross-sensitization.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Colitis / drug therapy
  • Colitis / immunology*
  • Colitis / metabolism
  • Colitis / physiopathology
  • Colon / drug effects
  • Colon / immunology*
  • Colon / innervation
  • Disease Models, Animal*
  • Female
  • Ketotifen / pharmacology
  • Ketotifen / therapeutic use
  • Mast Cells / drug effects
  • Mast Cells / immunology*
  • Mast Cells / metabolism
  • Membrane Transport Modulators / pharmacology
  • Mice
  • Mice, Knockout
  • Muscle Contraction / drug effects
  • Neurons, Afferent / drug effects
  • Neurons, Afferent / immunology*
  • Neurons, Afferent / metabolism
  • Oligopeptides / pharmacology
  • Permeability / drug effects
  • Proto-Oncogene Proteins c-kit / genetics
  • Proto-Oncogene Proteins c-kit / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Receptor, PAR-2 / agonists
  • Receptor, PAR-2 / metabolism
  • Trinitrobenzenesulfonic Acid
  • Urinary Bladder / immunology*
  • Urinary Bladder / innervation
  • Urinary Bladder / metabolism
  • Urinary Bladder / physiopathology
  • Urination Disorders / etiology
  • Urination Disorders / immunology*
  • Urination Disorders / metabolism
  • p-Methoxy-N-methylphenethylamine / pharmacology

Substances

  • Membrane Transport Modulators
  • Oligopeptides
  • Receptor, PAR-2
  • seryl-leucyl-isoleucyl-glycyl--arginyl-leucinamide
  • p-Methoxy-N-methylphenethylamine
  • Trinitrobenzenesulfonic Acid
  • Proto-Oncogene Proteins c-kit
  • Ketotifen