Am. J. Respir. Cell Mol. Biol., Vol 11, No. 4, Oct 1994, 456-463.
Phenotypic and functional modulation of normal human alveolar macrophages by histamine
AM Vignola, P Chanez, P Paul-Lacoste, N Paul-Eugene, P Godard and J Bousquet
Clinique des Maladies Respiratoires, Hopital Arnaud de Villeneuve, Montpellier, France.
Alveolar macrophages (AM) play a regulatory role in asthma. AM from
asthmatics are activated, release increased amounts of cytokines, and
express higher levels of the low affinity receptor for IgE (Fc epsilon
RIIb/CD23b) and receptors for adhesion molecules. The bronchial
microenvironment may modulate the phenotypic and functional characteristics
of AM. On AM from normal subjects, the effects of histamine were studied on
the expression of adhesion molecules (LFA-1, ICAM-1) and CD23b as well as
on the release of fibronectin. The expression of LFA-1, ICAM-1, and CD23b
was examined by immunocytochemistry using the alkaline
phosphatase-anti-alkaline phosphatase technique. The expression of CD23b
mRNA was studied by in situ hybridization. The release of fibronectin was
measured by enzyme immunoassay. We found that histamine induced in a dose-
and time- dependent fashion a significant increase of AM expressing the
three membrane markers and a significant increase in the release of
fibronectin. The maximum effect of histamine was observed after an
incubation of 12 to 24 h and a dose of 1 microM. The histamine effects were
specific, since they were significantly inhibited by an H1- blocker,
pyrilamine, used at a concentration of 10 microM. The effect of an
H2-blocker (ranitidine, concentration of 10 microM) was inconstant.
Cycloheximide blocked the histamine effects, suggesting that it requires
protein synthesis for its action. This study provides an in vitro model of
cellular interaction between mast cells and AM, which might be relevant in
the airway inflammation in asthma.
