L-selectin expression on polymorphonuclear leukocytes and monocytes in premature infants: reduced expression after dexamethasone treatment for bronchopulmonary dysplasia.

We examined the effect of dexamethasone on the expression of the adhesion molecule L-selectin on circulating polymorphonuclear leukocytes (PMLs) and monocytes from premature infants with bronchopulmonary dysplasia (BPD). Nineteen infants who received dexamethasone (Dex group) and 28 who did not receive dexamethasone (no Dex group) were studied. L-selectin expression, measured as mean fluorescence intensity, was lower on circulating PMLs (5.7 +/- 0.6 vs 10.6 +/- 0.7, p < 0.001) and monocytes (7.9 +/- 0.9 vs 12.5 +/- 0.9, p < 0.02) isolated from those who had received dexamethasone. Because L-selectin is important for the recruitment of PMLs to inflammatory foci in the lungs, we speculate that one of the mechanisms by which dexamethasone reduces inflammation in BPD is by impairing the ability of leukocytes to migrate into the BPD lesions.

The expression of adhesion molecules in cigarette smoke-induced airways obstruction.

Cigarette smoking produces peripheral airway inflammation in all smokers, and chronic airways obstruction in approximately 20% of heavy smokers. The present study was designed to test the hypothesis that airways obstruction is related to changes in the expression of adhesion molecules involved in the recruitment of cells to sites of inflammation in the lung. Freshly resected lungs from heavy smokers with airways obstruction (n = 10) and from heavy smokers with normal lung function (n = 10) were collected in the operating room, inflated with optimal cutting temperature (OCT) medium and frozen over liquid nitrogen. Six micrometres thick cryostat sections cut from random samples of this tissue were stained, using immunohistochemistry, with monoclonal antibodies to the adhesion molecules on leucocytes: L-selectin, very late activation antigen-4 (VLA-4), CD11a/CD18, CD11b/CD18, CD11c/CD18; and on endothelial and epithelial surfaces: E-selectin, P-selectin, vascular cell adhesion molecule (VCAM-1), intercellular adhesion molecule (ICAM)-1 and ICAM-2 using the alkaline phosphatase anti-alkaline phosphatase (APAAP) technique. The slides were coded and the expression of each molecule scored by three observers using a semiquantitative grading system. Two inducible adhesion molecules, E-selectin on endothelium and CD11b on leucocytes, were also evaluated using quantitative morphometric analysis. The results showed a distribution of adhesion molecules that was consistent with the inflammatory response in the airways and parenchyma of all subjects but failed to show any differences between those with or without airways obstruction. We conclude that development of airways obstruction in heavy smokers cannot be explained by differences in the expression of adhesion molecules known to be involved in the control of cell traffic in the lung.

[Ultrastructural observations on experimental shock lung]. / Observaciones ultraestructurales en el "pulmón de choque" experimental.

Intercellular junctions in the alveolar epithelium and in the capillary endothelium in the dogs after hemorrhagic shock (mean BP 40 mm Hg for 3 hours) and from control dogs were observed in the electron microscope using the freeze-fracture and etch technique. Following shock, tight junctions (zonulae occludentes) in the alveolar epithelium which were well developed with may strands in control animals showed alterations in substructure. Some desintegration and disappearance of junctional strands in "focal" regions were occasionally observed in the endothelium as well. The increased pulmonary capillary permeability observed physiologically after hemorrhagic shock may be explained by such alterations of endothelial zonulae occludentes.