During
inflammation, leukocyte emigration from the circulation can be directed by the endothelium, in part by the inducible endothelial adhesion
ligand for
L-selectin. In this study, endothelial
L-selectin ligand expression was localized by immunohistochemistry in human lung in several different types of
lung inflammation and in systemic
inflammation. Endothelial
L-selectin ligand was not seen in normal lung or in acute
pneumonia involving neutrophil accumulation. However, the endothelial
ligand was seen in most cases of chronic
interstitial pneumonia with mononuclear cell accumulation (a mean 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 microvessels positive). In contrast, consistent, typically extensive
ligand induction (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 tissue in which
L-selectin ligand is known to be constitutively expressed. Lung from subjects with systemic
infection was negative for endothelial expression of the
ligand. These studies show how in a defined extralymphoid tissue induction of endothelial
L-selectin ligand depended not only on the presence or absence of an inflammatory state, but also on the nature of the
inflammation.