Carrageenan-Induced Colonic Inflammation Is Reduced in Bcl10 Null Mice and Increased in IL-10-Deficient Mice
Figure 1
Histopathology of intestinal tissue in Bcl10 wild type and null mice following carrageenan exposure. (a), (b) Bcl10 WT, heterozygous, and null mice were sacrificed after ingestion of carrageenan (10 μg/mL) added in their water for 30 days. Histopathology of H&E sections of cecum demonstrated disruption of the mucosa in a WT mouse, with no similar findings in the Bcl10 null mice, consistent with reduced inflammation in the absence of Bcl10 [WT: wild type]. (c) Throughout the mouse intestine, the extent of inflammatory infiltrate, including granulocytes, lymphocytes, and plasma cells, was greater in the Bcl10 WT mice, than in the Bcl10 null mice. The histopathology was scored for 3 WT, 3 heterozygous, and 3 null mice, and the mean scores for leukocyte infiltration for each site are compared. The scores for the WT mice are higher at each site than for the null mice, although the differences are not statistically significant. The extent of inflammatory infiltrate was significantly greater in the small intestine than in the colon and rectum for each of the groups (). Cecal inflammation, including leukocyte infiltration and edema, was greater in the WT mice than in the heterozygous or null mice. (d) The mouse weights at the onset of the carrageenan exposure and at termination are presented and indicate no significant differences in weight and slight weight gain in all groups. (n for no CGN control=3; n for WT with CGN = 6; n for het with CGN = 3; n for null with CGN = 8) (WT: wild type; het: heterozygous; CGN: carrageenan).
