Am. J. Respir. Cell Mol. Biol., Vol 17, No. 5, Nov 1997, 571-582.
Phenotyping and cytokine regulation of the BEAS-2B human bronchial epithelial cell: demonstration of inducible expression of the adhesion molecules VCAM-1 and ICAM-1
J Atsuta, SA Sterbinsky, J Plitt, LM Schwiebert, BS Bochner and RP Schleimer
Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224- 6801, USA.
Airway epithelium may actively participate in inflammatory responses, such
as occur in asthma. The presence and regulation of surface molecules on the
airway epithelium, however, is incompletely understood. We have determined
the phenotype of the human bronchial epithelial cell line BEAS-2B by flow
cytometry. We confirmed previous observations that human bronchial
epithelial cells constitutively express CD29, CD44, CD49a, CD49b, CD49c,
CD49d, CD49e, CD49f, CD51, CD54 (ICAM-1), CD61, and HLA class 1. BEAS-2B
cells were also found to constitutively express CD9, CD13, CD15, CD15s,
CD23, CD33, CD36, CD40, CD41b, CD42b, CD48, CD50, CD71, and CD102 (ICAM-2).
Culture of BEAS-2B cells with tumor necrosis factor (TNF)-alpha or
interleukin (IL)-1beta (1 ng/ml) was found to enhance intercellular
adhesion molecule-1 (ICAM- 1) expression (several fold) and induce de novo
CD106 [vascular cell adhesion molecule-1 (VCAM-1)] expression. TNF-alpha or
IL-1beta did not change the expression of CD9, CD13, CD16, CD23, CD29,
CD31, CD32, CD35, CD45, CD61, or CD64 in BEAS-2B cells. IL-4 (1 ng/ml) also
induced expression of VCAM-1 (1.5-fold) but not ICAM- expression while
interferon-gamma (1 ng/ml) enhanced only ICAM-1 expression (2-fold).
Maximal VCAM-1 expression was obtained with the combination of TNF- alpha
and IL-4 (8-fold). Using Northern blot hybridization analysis, ICAM-1 and
VCAM-1 mRNA was detected in BEAS-2B cells stimulated with cytokines. VCAM-1
on stimulated BEAS-2B was functionally active as determined by adhesion of
purified eosinophils and blockade with specific antibodies. Primary
isolates of bronchial epithelial cells produced detectable levels of VCAM-1
protein and mRNA as detected by enzyme-linked immunosorbent assay and
reverse transcription-polymerase chain reaction, respectively. These
results suggest that cytokine activation induces expression of ICAM-1 and
VCAM-1 on airway epithelium, an event which may influence leukocyte
infiltration and activation.
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Copyright © 1997 American Thoracic Society.
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