Am. J. Respir. Cell Mol. Biol., Vol 11, No. 3, 09 1994, 304-311.
Induction of intercellular adhesion molecule-1 by lipopolysaccharide in canine alveolar macrophages
J Grigg, GL Kukielka, KL Berens, WJ Dreyer, ML Entman and CW Smith
Speros P. Martel Laboratory, Department of Pediatrics, Methodist Hospital, Houston, Texas.
Previous studies have demonstrated that alveolar macrophages (AMphis)
adherent to plastic release interleukin-8 in response to lipopolysaccharide
(LPS). We sought to determine whether LPS could also alter surface adhesion
molecule expression and thus modulate additional AMphi adhesive
interactions. Canine AMphis obtained by bronchoalveolar lavage of excised
lung were adhered onto tissue culture plastic and exposed to LPS (0.01 to
100 ng/ml). Expression of beta 2 integrins and intercellular adhesion
molecule-1 (ICAM-1) was subsequently determined by flow cytometry, a cDNA
probe to canine ICAM-1 was used to quantify ICAM-1 mRNA, and changes in
adhesion molecule function were assessed by evaluating the extent of
homotypic aggregation. ICAM-1 and CD11a/CD18 were present on freshly
isolated AMphis. CD11b/CD18 and CD11c/CD18 were expressed at lower levels.
Nonadherent AMphis expressed a pattern of beta 2 integrin and ICAM-1
comparable to adherent cells. During short- term LPS stimulation (3 h),
adherent AMphis increased both the synthesis and expression of ICAM-1. CD18
expression was either decreased or remained unchanged with LPS stimulation.
LPS stimulation in vitro (> 0.01 ng/ml) enhanced the homotypic
aggregation of adherent AMphis. Aggregation was blocked by monoclonal
antibodies to ICAM-1 (CL18/6) and CD11a (R7.1) and CD18 (R15.7). Similar
kinetics were found for expression of ICAM-1 and homotypic aggregation,
suggesting that up- regulation of ICAM-1 is a major determinant of the
LPS-stimulated aggregation of AMphis.
