Involvement of prostaglandins in an animal model of Shigella-related seizures

J Neuroimmunol. 2005 Nov;168(1-2):34-9. doi: 10.1016/j.jneuroim.2005.06.029.

Abstract

We investigated whether prostaglandins (PGs), proinflammatory mediators implicated in excitatory activity, are involved in Shigella-related seizures. Pretreatment with S. dysenteriae sonicate (2LD(50)) enhanced mice response to pentylenetetrazole-induced seizures, without increase of brain concentrations of PGE(2), PGD(2) or PGF(2alpha). Preinjection of NS-398, an inhibitor of cyclooxygenase-2, before treatment with Shigella sonicate, had no effect on seizures. The anticonvulsive PGD(2) increased after injection of 8 LD(50) of Shigella sonicate, which did not enhance seizures (32 pg/mg vs 26 pg/ml, p=0.0063). The findings indicate that PGs are not involved in the enhanced seizure response after exposure to Shigella. However, induction of PGD(2) may play an inhibitory role.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Chi-Square Distribution
  • Cyclooxygenase Inhibitors / pharmacology
  • Dinoprost / metabolism
  • Dinoprostone / metabolism
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Drug Interactions
  • Enzyme-Linked Immunosorbent Assay / methods
  • Lethal Dose 50
  • Male
  • Mice
  • Mice, Inbred ICR
  • Nitrobenzenes / pharmacology
  • Pentylenetetrazole
  • Prostaglandin D2 / metabolism
  • Prostaglandins / metabolism*
  • Seizures* / etiology
  • Seizures* / metabolism
  • Seizures* / microbiology
  • Shigella dysenteriae*
  • Sulfonamides / pharmacology

Substances

  • Cyclooxygenase Inhibitors
  • Nitrobenzenes
  • Prostaglandins
  • Sulfonamides
  • N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide
  • Dinoprost
  • Dinoprostone
  • Prostaglandin D2
  • Pentylenetetrazole