Up-regulation of L-selectin and E-selectin in hypersensitivity pneumonitis

Background: Selectins are adhesion molecules that contribute to leukocyte recruitment into the tissue after an injury,. Hypersensitivity pneumonitis (HP) is a lymphocytic alveolitis, and we hypothesized that the overexpression of selectins could play a role in this process. Patients and measurements: We studied 16 patients with HP and 7 healthy control subjects (HCs). Sera and BAL selectins and tumor necrosis factor-alpha were determined by enzyme-linked immunosorbent assay, and cellular lung localization was determined by immunohistochemistry. Additionally,, BAL L-selectin, and L-selectin-bearing T-lympbocytes analyzed by flow cytometry. were evaluated in HP patients and in exposed but as asymptomatic subjects (EAS). Setting: Tertian, referral center and immunohistochemistry laboratory. Results: Raised levels of E-selectin (mean [+/- SD], 178.9 +/- 30.5 vs 59.4 +/- 4.7 ng/mL, respectively; p < 0.001) and P-selectin (nican, 232.6 +/- 29.9 vs 67.6 +/- 14.2 ng/mL, respectively; p < 0.001) were detected in HP patient sera compared to control subjects, while L-selectin levels showed no differences between groups. Con-versely, HP patients displayed a significant increase in levels of L-selectin found in BAL fluid compared with both HCs an EAS (11.0 +/- 1.7 %,s 6.9 +/- 0.43 and 3.1 +/- 0.5 ng/mL, respectively; p < 0.05). The levels of E-selectin found in BAL fluid were similar in patients from both groups, and P-selectin was not detected. Percentage of CD3+CD62 L+ lymphocytes was lower in HP patients compared with EAS (2.33 +/- 0.8 vs 4.31 +/- 2.4, respectively; p = 0.05). By immunohistochemistry, L-selectin was detected in interstitial macrophages and polymorphonuclear cells, and E-selectin was detected in endothelial cells. Conclusion: These findings demonstrate that L-selectin and E-selectin are up-regulated during the development of HP, suggesting that they may, contribute to the increased traffic of lung inflammatory, cells.