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The role of P‐selectin in experimental colitis as determined by antibody immunoblockade and genetically deficient mice

We assessed the effects of genetic ablation of the P‐selectin gene in comparison with functional immunoblockade of P‐selectin on leukocyte recruitment and the course of disease in dextran sulfate sodium‐induced colitis in mice. Compared with control antibody‐treated wild‐type (WT) mice, WT mice treated with anti‐P‐selectin antibody and P‐selectin−/− mice had significantly decreased leukocyte rolling and adhesion in colonic venules and reduced clinical and pathological colitis scores. These reductions were more pronounced in anti‐P‐selectin‐treated than in P‐selectin−/− mice. In colonic endothelium, up‐regulation of ICAM‐1 was similar in WT and P‐selectin−/− mice, but VCAM‐1 up‐regulation was significantly higher in the latter group. Lung leukocyte infiltration and VCAM‐1 expression were increased only in P‐selectin−/− colitic mice. Mortality was observed only in P‐selectin−/− mice. Therefore, ablation of P‐selectin function ameliorates colitis, but this protection is attenuated in P‐selectin−/− mice, probably due to compensatory mechanisms that involve up‐regulation of other adhesion molecules such as VCAM‐1.