Selective induction of endothelial L-selectin ligand human lung inflammation

During inflammation, leukocyte emigration from the circulation can be direc ted by the endothelium, in part by the inducible endothelial adhesion ligan d for L-selectin. In this study, endothelial L-selectin ligand expression w as localized by immuno-histochemistry in human lung in several different ty pes of lung inflammation and in systemic inflammation. Endothelial L-select in ligand was not seen in normal lung or in acute pneumonia involving neutr ophil accumulation. However, the endothelial ligand was seen in most cases of chronic interstitial pneumonia with mononuclear cell accumulation (a mea n of 5.9% of microvessels positive). Regarding granulomatous conditions, in sarcoidosis the endothelial ligand was not identified, but in tuberculous infection some expression was seen in a minority of cases (mean 3.3% of mic rovessels positive). In contrast, consistent, typically extensive ligand in duction (mean 33.4% of microvessels positive) was present in bronchiectatic lung showing prominent lymphocytic accumulation and venules with thickened (high) endothelium, the latter being normally characteristic of lymphoid t issue in which L-selectin ligand is known to be constitutively expressed. L ung from subjects with systemic infection was negative for endothelial expr ession of the ligand. These studies show how in a defined extralymphoid tis sue induction of endothelial L-selectin ligand depended not only on the pre sence or absence of an inflammatory state, but also on the nature of the in flammation.