Substance P and other neuropeptides do not induce mediator release in isolated human intestinal mast cells

S. C. Bischoff*, S. Schwengberg, A. Lorentz, M. P. Manns, H. Bektas, H. Sann, F. Levi-Schaffer, F. Shanahan, M. Schemann

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

72 Scopus citations


Neuropeptides such as substance P (SP) and related peptides are supposed to act as mast cell agonists, and thus as mediators of neuroimmune interactions. The data supporting this hypothesis were obtained mostly from rodent experiments. Here, we studied for the first time the effect of SP and other peptides on mediator release in human intestinal mast cells, either unpurified or enriched to 85-99% purity. We found that SP at 0.1-100 μmol L -1, or other peptides including neurokinin A and B, calcitonin gene-related peptide, vasoactive intestinal peptide and serotonin at 1 μmol L-1 do not induce release of mediators such as histamine, sulphidoleukotrienes, and tumour necrosis factor α. The peptides also failed to cause mediator release in mast cells isolated from inflamed tissue derived from Crohn's disease. Using reverse transcriptase-polymerase chain reaction, flow cytometry and immunohistochemistry, we could show that human intestinal mast cells do not express the tachykinin receptors NK-1, NK-2, or NK-3 under basal conditions. However, upon stimulation by immunoglobulin E (IgE) receptor-crosslinking, which induces an extensive mediator release reaction, a subpopulation of mast cells clearly expressed NK-1, the SP receptor. In conclusion, our data show that SP and other neuropeptides do not act as secretagogues in human intestinal mast cells that have not been pre-activated by IgE receptor-crosslinking.

Original languageAmerican English
Pages (from-to)185-193
Number of pages9
JournalNeurogastroenterology and Motility
Issue number2
StatePublished - Apr 2004


  • Leukotrienes
  • Mast cells
  • NK-1
  • Neuropeptides
  • Substance P
  • TNFα


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