Figure 5
From: MEP1A allele for meprin A metalloprotease is a susceptibility gene for inflammatory bowel disease
Greater colon injury and inflammation in meprin αKO compared with WT mice. (a) Colon shortening at day 7 for the mice treated with DSS. The average colon length for both WT and meprin αKO mice administered 3.5% DSS was shorter than that for their respective controls at day 7 (*P<0.02; #P<0.0001). The meprin αKO DSS group had shorter colons than WT DSS group (n=7 mice per group; **P<0.04). (b) Proximal colons from WT and meprin αKO mice were scored for injury. Representative histological sections from (i) WT control, (ii) meprin αKO control, (iii) WT DSS-treated, and (iv) meprin αKO DSS-treated colons are shown. Colon sections from both the control groups have normal appearance (i and ii). DSS-treated colon of WT mouse (iii) had crypt destruction (red arrow) along with leukocytic infiltration in the lamina propria as well as in the submucosa (black arrows). Greater damage is evident in the DSS-treated αKO section (iv) in which massive crypt destruction is seen in an area of ulceration (red arrow). Heavy leukocyte infiltration is evident in the lamina propria and submucosal regions (black arrows). (c) The injury scores of WT and meprin αKO DSS-treated groups were normalized to the corresponding control populations. Colons from meprin αKO mice show significantly greater damage than those from WT mice (n=7 mice per group; *P<0.04). (d) MPO activities of WT and meprin αKO colons from DSS-treated and -untreated animals were measured from days 1 to 5. The DSS-treated mice had increased MPO activity relative to their controls (n=6; *P<0.00002; #P<0.00005) and the colon MPO activity of DSS-treated meprin αKO mice was significantly greater than that of the DSS-treated WT mice on days 4 and 5 (**P<0.007). DSS, dextran sulfate sodium; MPO, myeloperoxidase; WT, wild type.
