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Beatrice and Samuel A. Seaver Laboratory, Department of Medicine, Cornell University Medical College, New York, NY 10021
C3H/HeJ mice carry a mutant allele (Lpsd) of
a recently identified gene whose normal allele
(Lpsn) confers responsiveness to bacterial LPS
in C3H/HeN and most other mouse strains. Recently we reported a
differential display analysis of matched macrophage-derived cell lines
from C3H/HeJ and C3H/HeN mice under LPS-free conditions. Of the
12,000 transcripts evaluated, 4 were differentially expressed. One
transcript represented secretory leukocyte protease inhibitor. In this
study, we report another differentially expressed transcript, mouse
matrix metalloprotease-9 (MMP-9). Like secretory leukocyte protease
inhibitor, MMP-9 was expressed constitutively in the
Lpsd macrophage cell line and not in the
Lpsn cell line. Similarly, two additional
macrophage cell lines that respond readily to LPS by producing nitric
oxide and TNF expressed no MMP-9 under LPS-free conditions. However, in
all four cell lines, LPS induced MMP-9 or augmented its expression. In
primary macrophages, concentrations of LPS in the ng/ml range augmented
the expression of MMP-9 mRNA. Paradoxically, macrophages from
Lpsd mice expressed more MMP-9 transcripts than
macrophages from Lpsn mice. In contrast, the
induction of TNF in response to LPS was much more pronounced in
Lpsn macrophages. The present findings with
MMP-9 suggest that homozygosity at Lpsd does not
so much prevent a response to LPS as dysregulate it, resulting in the
suppression of some LPS signaling pathways and the preservation of
others.
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