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a
1250
1000
WT-Con
WT-DSS
b
750
*
**
*
KO-Con
b KO-DSS
#
#
**
500
*
#
#
*
*
*
250
0
3
4
5
# Days
**
b
#
1250
**
#
1000
#
WT-Con
WT-DSS
a KO-Con
a KO-DSS
*
*
750
*
500
*
#
*
#
*
#
250
0
3
4
# Days
5
Fig. 4.5 Active interleukin-18 (IL-18) in the serum of meprin-deficient and wild-type mice after
intestinal exposure to DSS. Intestinal bowel disease (IBD) was induced in mice by administering
3.5% DSS in the drinking water for 4 days and water on the fifth day. Controls ( Con ) were given
water all days. Serum was collected on days 3, 4, and 5, and the levels of active IL-18 were
measured by enzyme-linked immunosorbent assay. (a) WT and
KO mice had increased levels of
b
active IL-18 compared with their respective control groups ( n
¼
five/group; *, p
0.02, DSS
<
treated WT vs. control; #, p
KO mice treated
with DSS showed significantly lower levels of serum IL-18 compared with WT mice given DSS
treatment (**, p
0.0002, DSS-treated
KO vs. control). Meprin
<
b
b
KO mice showed significantly elevated levels of IL-18
compared with WT mice after the same DSS treatment ( n
0.05). (b) Meprin
<
a
0.0015). Both
DSS-treated groups showed significant elevation in their serum IL-18 levels compared with the
respective control populations (*, p
¼
seven/group; **, p
<
10 11 ,
0.0002, DSS-treated WT vs. control; #, p
5
<
<
DSS-treated
KO vs. control) (Banerjee and Bond 2008 )
a
homeostasis. Meprin
can cleave mature BNP at the N-terminal tail into a truncated
form which is then more readily degraded by neprilysin (Pankow et al. 2007 ).
Meprin-truncated BNP also has reduced renal bioactivity, although meprin-truncated
a
 
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