Allergic diseases such as allergen-induced rhinitis represent an infla
mmatory reaction that is characterized by the chemotaxis and activatio
n of various cell populations. A high degree of cell-to-cell communica
tion is needed to orchestrate this inflammatory immune responses. A va
riety of cytokines an adhesion receptors seen to play an important rol
e in the allergic late phase reaction. Here we demonstrate that proinf
lammatory cytokines such as interleukin(IL)-1, IL-8 and TNF-alpha (tum
or necrosis factor-alpha) can be detected in nasal secretions and muco
sa by enzyme-linked immunosorbent assay and immunohistochemistry. The
increased expression of adhesion receptors in mucosa specimens of pati
ents with seasonal allergic rhinitis points to their role in regulatin
g the cellular migration and probably represents a key event in allerg
ic inflammation. We established an in vitro model using freshly taken
nasal mucosa to study the induction of adhesion receptors by proinflam
matory cytokines. E-selectin, an endothelial receptor, was strongly up
regulated by IL-1 beta, TNF-alpha and allergen. The induction due to a
llergen exposure of the mucosa was markedly inhibited by soluble cytok
ine receptors (sIL-1R, TNF-BP) or by a receptor antagonist (IL-1ra) an
d prednisolone, These findings indicate that proinflammatory cytokines
may be key factors for the upregulation of adhesion processes in huma
n nasal mucosa and the activation of various cell populations involved
in the allergic inflammation. They therefore represent a main target
for new therapeutic strategies.