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*
Department of Traumatology, University of Freiburg, Freiburg, Germany;
Department of Anesthesiology, University Hospital, Zurich, Switzerland; and
Department of Pathology, University of Michigan, Ann Arbor, MI 48109
Because of the important role of rat ICAM-1 in the development of
lung inflammatory injury, soluble recombinant rat ICAM-1 (sICAM-1) was
expressed in bacteria, and its biologic activities were evaluated.
Purified sICAM-1 did bind to rat alveolar macrophages in a
dose-dependent manner and induced production of TNF-
and the CXC
chemokine, macrophage inflammatory protein-2 (MIP-2). Alveolar
macrophages exhibited cytokine responses to both sICAM-1 and
immobilized sICAM-1, while rat PBMCs failed to demonstrate similar
responses. Exposure of alveolar macrophages to sICAM-1 resulted in
NF
B activation (which was blocked by the presence of the aldehyde
peptide inhibitor of 28S proteosome and by genistein, a tyrosine kinase
inhibitor). As expected, cross-linking of CD18 on macrophages with Ab
resulted in generation of TNF- and MIP-2. This response was also
inhibited in the presence of the proteosome inhibitor and by genistein.
Alveolar macrophages showed adherence to immobilized sICAM-1 in a
CD18-dependent manner. Finally, airway instillation of sICAM-1
intensified lung injury produced by intrapulmonary deposition of IgG
immune complexes in a manner associated with enhanced lung production
of TNF- and MIP-2 and increased neutrophil recruitment. Therefore,
through engagement of ß2 integrins, sICAM-1 enhances
alveolar macrophage production of MIP-2 and TNF-, the result of
which is intensified lung injury after intrapulmonary disposition of
immune complexes.
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