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Department of Internal Medicine, Justus-Liebig-University, Giessen, Germany
Alveolar monocyte influx requires adherence and transmigration
through the vascular endothelium, extracellular matrix, and alveolar
epithelium. For investigating the monocyte migratory process across the
epithelial barrier, we employed both the A549 cell line and isolated
human alveolar epithelial cells. Under baseline conditions, spontaneous
bidirectional transepithelial monocyte migration was noted, which was
dose-dependently increased in the presence of the monocyte
chemoattractant protein-1. TNF-
stimulation of the alveolar
epithelium provoked the polarized apical secretion of monocyte
chemoattractant protein-1 and RANTES and up-regulation of ICAM-1
and VCAM-1 expression, accompanied by markedly enhanced transepithelial
monocyte traffic in the basal-to-apical direction. Multiple adhesive
interactions were noted to contribute to the enhanced monocyte traffic
across the TNF--stimulated alveolar epithelium: these included the
ß2 integrins CD11a, CD11b, CD11c/CD18, the
ß1 integrins very late Ag (VLA)-4, -5, and -6, and the
integrin-associated protein CD47 on monocytes, as well as ICAM-1,
VCAM-1, CD47, and matrix components on the epithelial side. In
contrast, spontaneous monocyte migration through unstimulated
epithelium depended predominantly on CD11b/CD18 and CD47, with some
additional contribution of VLA-4, -5, and -6. In summary, unlike
transendothelial monocyte traffic, for which ß1 and
ß2 integrins are alternative mechanisms, monocyte
migration across the alveolar epithelium largely depends on CD11b/CD18
and CD47 but required the additional engagement of the ß1
integrins for optimal migration. In response to inflammatory challenge,
the alveolar epithelium orchestrates enhanced monocyte traffic to the
apical side by polarized chemokine secretion and up-regulation of
ICAM-1 and VCAM-1.
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