Interleukin-4 induces a switch of human intestinal mast cells from proinflammatory cells to Th2-type cells

Int Arch Allergy Immunol. 2001 Jan-Mar;124(1-3):151-4. doi: 10.1159/000053695.

Abstract

Background: During the last years, mast cells have been recognized as a potent cellular source of multiple cytokines. However, little is known about the regulation of cytokine production by mature human mast cells derived from mucosal sites.

Methods: Human mast cells were isolated from intestinal mucosa and cultured for 14 days in the presence of stem cell factor (SCF) alone or in combination with IL-4. Mast cells were then stimulated by IgE receptor cross-linking or bacterial infection and cytokine production was examined by RT-PCR and ELISA.

Results: We found that human intestinal mast cells produce proinflammatory cytokines such as TNF-alpha, IL-1beta and IL-6 without further stimulation. Stimulation of the cells with gram-negative bacteria (Escherichia coli and others) caused an upregulation of TNF-alpha expression. Following IgE receptor cross-linking, we found additional expression of the Th2 cytokines IL-3, IL-5 and IL-13. Interestingly, mRNA for IL-3, IL-5 and IL-13 was also expressed in unstimulated mast cells provided they were cultured in the presence of SCF and IL-4. Moreover, IL-4 rendered mast cells capable of releasing IL-5 in response to bacterial challenge.

Conclusion: In the presence of the mast cell survival factor SCF, mature human mast cells produce predominantly proinflammatory cytokines, whereas in the presence of SCF and IL-4, mast cells produce not only proinflammatory but also Th2 cytokines.

MeSH terms

  • Cells, Cultured
  • Cytokines / biosynthesis*
  • Cytokines / genetics
  • Gram-Negative Bacteria / immunology
  • Humans
  • Interleukin-4 / pharmacology*
  • Intestines / cytology*
  • Mast Cells / drug effects
  • Mast Cells / immunology*
  • RNA, Messenger / biosynthesis
  • Stem Cell Factor / pharmacology
  • Th2 Cells / immunology*
  • Transcriptional Activation

Substances

  • Cytokines
  • RNA, Messenger
  • Stem Cell Factor
  • Interleukin-4