In recent years, a complex molecular network involving cytokines kinin
s and adhesion molecules has been demonstrated to operate in allergic
inflammation. In particular, the adhesion machinery plays a crucial ro
le for the recruitment and locomotion of the inflammatory cells and th
e Intercellular Adhesion Molecule 1 (ICAM-1) is a hallmark of the alle
rgic inflammatory process. The role and possible modulation of ICAM-1
can be investigated using both eye and nose experimental models. Conju
nctiva and nasal epithelium are easy to study either under natural all
ergen exposure or after specific/aspecific provocation tests; furtherm
ore the nasal/conjuctival challenge is well tolerated by the patients.
These experimental models have allowed us to investigate in vivo the
antiallergic properties of several compounds. Many of the new antihist
amines, but also deflazacort and local nasal immunotherapy, were demon
strated capable of reducing both inflammatory infiltration and ICAM-1
expression on epithelia. Because of the central role of adhesion molec
ules in allergic inflammation, their pharmacological modulation can be
regarded as a promising therapeutic approach.