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
Patients and measurements: We studied 16
patients with HP and 7 healthy control subjects (HCs). Sera and BAL
selectins and tumor necrosis factor-α were determined by
enzyme-linked immunosorbent assay, and cellular lung localization was
determined by immunohistochemistry. Additionally, BAL L-selectin, and
L-selectin-bearing T-lymphocytes analyzed by flow cytometry were
evaluated in HP patients and in exposed but asymptomatic subjects
Setting: Tertiary referral center and
levels of E-selectin (mean [± SD], 178.9 ± 30.5 vs 59.4 ± 4.7
ng/mL, respectively; p < 0.001) and P-selectin (mean,
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.
Conversely, HP patients displayed a significant increase in levels of
L-selectin found in BAL fluid compared with both HCs and EAS
(11.0 ± 1.7 vs 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
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.