Evidence that brain mast cells can modulate neuroinflammatory responses by tumour necrosis factor-alpha production

Neuroreport. 1998 Jan 5;9(1):95-8. doi: 10.1097/00001756-199801050-00019.

Abstract

Tumour necrosis factor-alpha (TNF-alpha) levels in mammalian brain increase during neuroinflammatory diseases. We used the competitive polymerase chain reaction (PCR) to quantify the amount of TNF-alpha in stimulated and unstimulated brain mast cells (BMC). A cDNA fragment shortened by a deletion of 56 bp was used as an internal TNF-alpha-specific standard. The immunological stimulus resulted in enhanced TNF-alpha mRNA expression and increased release of histamine and TNF-alpha. This is the first time that BMC showing functional FCepsilonRI-bound IgE receptors have been purified. Our results support the hypothesis that BMC mediators might induce an initial response in neuroinflammatory diseases.

MeSH terms

  • Animals
  • Binding, Competitive
  • Brain / cytology
  • Brain / metabolism
  • Brain / physiology*
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Histamine Release
  • Immunoglobulin E / immunology
  • Mast Cells / metabolism
  • Mast Cells / physiology*
  • Neuritis / metabolism
  • Neuritis / pathology
  • Neuritis / physiopathology*
  • Polymerase Chain Reaction / methods
  • Rats
  • Rats, Wistar
  • Transcription, Genetic
  • Tumor Necrosis Factor-alpha / biosynthesis*

Substances

  • Tumor Necrosis Factor-alpha
  • Immunoglobulin E