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*
Department of Pathology, Center for Blood Research and
Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115;
Massachusetts Institute of Technology, Cambridge, MA 02139; and
§
Department of Immunology, Duke University Medical Center, Durham, NC 27710
Although it is now appreciated that mast cell-mediated release of
TNF-
is critical for resolution of acute septic peritonitis,
questions remain as to how mast cells are activated upon peritoneal
bacterial infection. Clues to how this may occur have been derived from
earlier studies by Prodeus et al. in which complement proteins C3 and
C4 were shown to be required for survival following cecal ligation and
puncture (CLP), a model for acute septic peritonitis. To evaluate the
mechanism for mast cell activation in the CLP model, complement
receptor CD21/CD35-deficient mice (Cr2null) were examined
in the present study. Along with CD19-deficient (CD19null)
mice, these animals exhibit decreased survival following CLP compared
with wild-type littermates. Injection of IgM before CLP does not change
survival rates for Cr2null mice and only partially improves
survival of CD19null mice, implicating CD21/CD35 and CD19
in mast cell activation. Interestingly, early TNF- release is also
impaired in Cr2null and CD19null animals,
suggesting that these molecules directly affect mast cell activation.
Cr2null and CD19null mice demonstrate an
impairment in neutrophil recruitment and a corresponding increase in
bacterial load. Examination of peritoneal mast cells by flow cytometry
and confocal microscopy reveals the expression and colocalization of
CD21/CD35 and CD19. Taken together, these findings suggest that the
engagement of complement receptors CD21/CD35 along with CD19 on the
mast cell surface by C3 fragments may be necessary for the full
expression of mast cell activation in the CLP
model.
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