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Departments of
* Microbiology and Immunology,
Pediatrics, and
Pathology, Dalhousie University, Halifax, Nova Scotia, Canada
Correspondence: Jean S. Marshall, Ph.D., Dept. of Pathology, Sir Charles Tupper Medical Building, Dalhousie University, Halifax, Nova Scotia B3H 4H7, Canada. E-mail Jean.Marshall{at}Dal.ca
Toll-like receptors (TLRs) are a family of pattern recognition
receptors that are critical for cellular responses to a variety of
bacterial, viral, and fungal products. Mast cells are important to host
survival in a number of models of bacterial infection and might act as
sentinel cells in host defense. We therefore examined the expression of
TLRs and associated molecules by murine bone marrow-derived mast cells
(BMMCs). BMMCs and the murine mast cell line MC/9 expressed mRNA for
TLR2, TLR4, and TLR6 but not TLR5 and for both adapter molecule MD-2
and signaling molecule MyD88 but lacked surface CD14. After activation
with the TLR2- and TLR4-dependent stimuli Staphylococcus
aureus-derived peptidoglycan and Escherichia
coli-derived lipopolysaccharide (LPS), respectively, mast cells
produced significant levels of interleukin-6 (IL-6) and tumor necrosis
factor 
(TNF-). To determine whether mast cells require TLR4 for
cellular responses to LPS, mast cells were derived from the bone marrow
cells of C3H/HeJ and C57Bl/10ScNCr mice containing a point mutation and
a null mutation, respectively, in TLR4. Using these models, we
demonstrated that the BMMC IL-6 and TNF- responses to LPS were
completely dependent on functional TLR4 with no significant LPS
response observed in its absence. These findings have important
implications for the mechanism of mast cell responses to pathogens and
their products and suggest that different TLR4-expressing cells might
have different thresholds for activation with LPS.
Key Words: LPS • bacteria • inflammation
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