Skip to main content
. 2012 Apr;165(7):2100–2109. doi: 10.1111/j.1476-5381.2011.01772.x

Figure 2.

Figure 2

(A) When transepithelial exit from inflamed mucosae is inhibited by ‘anti-traffic’ drug treatment, leucocytes accumulate in mucosal tissues. In these cases, reduced cellularity in samples obtained from the lumen can be associated with aggravated mucosal tissue inflammation. This drug intervention effect also compromises immune defence at the mucosal surface. (B) It is suggested that drugs could be developed that speed up transepithelial exit of leucocytes and thus contribute to resolution of mucosal inflammation. It is currently unknown which molecular targets would be most suitable in this regard. (Several targets, integrin-dependent or -independent, are conceivably involved in the traffic through the tissue, across basement membranes, between epithelial cells and in release from the epithelial surface.) Spontaneous or drug-induced resolution of mucosal tissue inflammation is associated with a period of increased cellularity in the lumen of the involved hollow organ. During these periods, the occurrence of increased numbers of inflammatory cells in lumen samples is not a measure of inflammation but reflects inflammation resolution.