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The c-kit Ligand Stem Cell Factor and Anti-IgE Promote Expression of Monocyte Chemoattractant Protein-1 in Human Lung Mast Cells
Mehrdad Baghestanian,
Roland Hofbauer,
Hans P. Kiener,
Hans C. Bankl,
Friedrich Wimazal,
Martin Willheim,
Otto Scheiner,
Wolfgang Füreder,
Michael R. Müller,
Dorian Bevec,
Klaus Lechner, and
Peter Valent
From the Department of Internal Medicine I, the Division of Hematology and Hemostaseology, the Department of Anaesthesiology, the Department of Internal Medicine III, the Division of Rheumatology, the Department of General and Experimental Pathology, and the Department of Surgery II, University of Vienna, Austria; and Sandoz Research Institute, Vienna, Austria.
Recent data suggest that mast cells (MC) are involved in the regulation of leukocyte accumulation in inflammatory reactions. In this study, expression of leukocyte-chemotactic peptides (chemokines) in purified human lung MC (n = 16) and a human mast cell line, HMC-1, was analyzed. Northern blotting and reverse transcriptase-polymerase chain reaction (RT-PCR) showed baseline expression of monocyte chemoattractant protein (MCP)-1 mRNA in unstimulated MC. Exposure of MC to recombinant stem cell factor (rhSCF, 100 ng/mL) or anti-IgE (10 µg/mL) was followed by a substantial increase in expression of MCP-1 mRNA. Neither unstimulated nor stem cell factor (SCF )-stimulated lung MC expressed transcripts for interleukin-8 (IL-8), macrophage inflammatory protein-1 (MIP-1), MIP-1 , or RANTES by Northern blotting. The mast cell line HMC-1, which contains a mutated and intrinsically activated SCF-receptor, was found to express high levels of MCP-1 mRNA in a constitutive manner. Exposure of HMC-1 cells to rhSCF resulted in upregulation of MCP-1 mRNA expression, and de novo expression of MIP-1 mRNA. The SCF-induced upregulation of MCP-1 mRNA in lung MC and HMC-1 was accompanied by an increase in immunologically detectable MCP-1 in cell supernatants (sup) (lung MC [<98%], control medium, 1 hour: 159 ± 27 v SCF, 100 ng/mL, 1 hour: 398 ± 46 pg/mL/106 cells; HMC-1: control, 1 hour: 894 ± 116 v SCF, 1 hour: 1,536 ± 265 pg/mL/106). IgE-dependent activation was also followed by MCP-1 release from MC. MC-sup and HMC-1-sup induced chemotaxis in blood monocytes (Mo) (control: 100% ± 12% v 2-hour-MC-sup: 463% ± 38% v HMC-1-sup: 532% ± 12%), and a monoclonal antibody (MoAb) to MCP-1 (but not MoAb to IL-8) inhibited Mo-chemotaxis induced by MC-sup or HMC-1-sup (39% to 55% inhibition, P < .05). In summary, our study identifies MCP-1 as the predominant CC-chemokine produced and released in human lung MC. MCP-1 may be a crucial mediator in inflammatory reactions associated with MC activation and accumulation of MCP-1-responsive leukocytes.
Blood, Vol. 90 No. 11 (December 1), 1997:
pp. 4438-4449
© 1997 by The American Society of Hematology.
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