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*
Cardiovascular Research Group, Division of Clinical Sciences (Northern General Hospital), University of Sheffield, Sheffield, United Kingdom; and
Histopathology Department, Northern General Hospital, Sheffield, United Kingdom
Neutrophil migration to lung alveoli is a characteristic of lung
diseases and is thought to occur primarily via capillaries rather than
postcapillary venules. The role of adhesion molecules CD18 and CD29 on
this migration in a mouse model of lung inflammation has been
investigated. The number of neutrophils present in bronchoalveolar
lavage fluid was determined 4 h after intratracheal instillation
of LPS (0.1–1 µg) or murine recombinant KC (CXC chemokine, 0.03–0.3
µg). Both stimuli produced a dose-related increase in neutrophil
accumulation. Intravenous anti-mouse CD18 mAb, 2E6 (0.5 mg/mouse),
significantly (p < 0.001) attenuated LPS (0.3
µg)- but not KC (0.3 µg)-induced neutrophil accumulation. The
anti-mouse CD29 mAb, HM
1-1 (0.02 mg/mouse), significantly
(p < 0.05) inhibited both LPS (0.3 µg)- and KC
(0.3 µg)-induced neutrophil migration. A second mAb to CD18 (GAME-46)
and both F(ab')2 and Fab of HM1-1 produced similar
results to those above, while coadministration of mAbs did not result
in greater inhibition. Electron microscopy studies showed that CD29 was
involved in the movement of neutrophils from the interstitium into
alveoli. The effect of mAbs to CD49 (
integrin) subunits of CD29 was
also examined. mAbs to CD49e and CD49f inhibited both responses, while
anti-CD49b and CD49d significantly inhibited responses to KC only.
These data suggest that CD29 plays a critical role in neutrophil
migration in pulmonary inflammation and that CD49b and CD49d mediate
CD18-independent neutrophil accumulation.
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