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Lipopolysaccharide induces cell death in cultured porcine myenteric neurons.

In English

Författare

Summary, in English

Enteric bacteria execute, via lipopolysaccharide (LPS), a pathogenic role in intestinal inflammation. The effects of LPS on survival and neurotransmitter expression in cultured porcine myenteric neurons were investigated. Myenteric neurons were isolated and cultured for 6 days in medium, in LPS (100 ng/ml) with or without α-ketoglutarate or the nitric oxide synthase (NOS) inhibitor L-NAME, in α-ketoglutarate or in the NO donor SNAP. Neuronal survival and expression of vasoactive intestinal peptide (VIP) and NOS were evaluated by immunocytochemistry. Addition of LPS significantly decreased neuronal survival; only 40% survived, compared to controls run in parallel. The LPS-induced neurotoxic effect was not counteracted by the simultaneous presence of α-ketoglutarate or L-NAME. Either SNAP or α-ketoglutarate influenced neuronal survival. Culturing, particularly in the presence of LPS, markedly increased the proportion of VIP-immunoreactive neurons; NOS-immunoreactive neurons were unchanged. The reported LPS-induced neurotoxicity indicates loss of enteric neurons as a consequence of intestinal inflammation.

Avdelning/ar

Publiceringsår

2005

Språk

Engelska

Sidor

1661-1668

Publikation/Tidskrift/Serie

Digestive Diseases and Sciences

Volym

50

Issue

9

Dokumenttyp

Artikel i tidskrift

Förlag

Springer

Ämne

  • Gastroenterology and Hepatology

Nyckelord

  • Myenteric Plexus: cytology
  • Animals
  • Cell Culture Techniques
  • Cell Death
  • Cell Survival
  • Female
  • Immunohistochemistry
  • Inflammation
  • Intestinal Diseases: etiology
  • Intestinal Diseases: immunology
  • Intestinal Diseases: microbiology
  • Lipopolysaccharides: pharmacology
  • Male
  • Myenteric Plexus: pathology
  • Neurons: drug effects
  • Neurons: physiology
  • Neurotransmitters: biosynthesis
  • Research Support
  • Non-U.S. Gov't
  • Swine

Status

Published

Forskningsgrupp

  • Neurogastroenterology

ISBN/ISSN/Övrigt

  • ISSN: 1573-2568