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C3a and C5a stimulate chemotaxis of human mast cells
K Hartmann, BM Henz, S Kruger-Krasagakes, J Kohl, R Burger, S Guhl, I Haase, U Lippert and T Zuberbier
Department of Dermatology, Virchow Clinics, Humboldt University of Berlin,
Germany.
The factors that control migration of mast cells to sites of inflammation
and tissue repair remain largely undefined. Whereas several recent studies
have described chemotactic factors that induce migration of murine mast
cells, only stem cell factor (SCF) is known to induce migration of human
mast cells. We report here that the anaphylatoxins C3a and C5a are
chemotactic factors for the human mast cell line HMC-1, human cord
blood-derived mast cells (CBMC) and cutaneous mast cells in vitro. The
presence of an extracellular matrix protein, laminin, was required for
chemotaxis in response to complement peptides. Migration of mast cells
towards C3a and C5a was dose- dependent, peaking at 1 microg/mL (100
nmol/L), and was inhibited by specific antibodies. Pretreatment with
pertussis toxin inhibited the anaphylatoxin-mediated migration of HMC-1
cells, indicating that Gi proteins are involved in complement-activated
signal transduction pathways in human mast cells. Both C3a and C5a also
induced a rapid and transient mobilization of intracellular free calcium
([Ca2+]i) in HMC-1 cells. Besides SCF, other chemotactic factors tested,
such as interleukin-3, nerve growth factor, transforming growth factor
beta, RANTES (regulated upon activation, normal Tcell expressed and
secreted), monocyte chemotactic protein-1 (MCP-1), MCP-2, MCP-3, macrophage
inflammatory protein-1alpha (MIP-1alpha), and MIP-1beta, failed to
stimulate migration of human mast cells. In summary, these findings
indicate that C3a and C5a serve as chemotaxins for human mast cells.
Anaphylatoxin-mediated recruitment of mast cells might play an important
role in hypersensitivity and inflammatory processes.
Volume 89,
Issue 8,
pp. 2863-2870,
04/15/1997
Copyright © 1997 by The American Society of Hematology
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