This review summarizes our current knowledge of nasal allergic inflamm
ation based on studies of cytokines, chemokines, and adhesion molecule
s in allergic rhinitis. The article also includes some aspects of vira
l rhinitis. Due to artificial or natural allergen exposure, an increas
e in the number of eosinophils and basophils, mast cells, IgE-positive
cells, macrophages, monocyte-like cells, Langerhans cells, and activa
ted T-cells can be observed within the mucosa and on the mucosal surfa
ce. Mediators are known to be released in response to allergens, but d
o not seem to be adequate to initiate the cell recruitment After antig
en challenge, the release of proinflammatory and regulatory cytokines
could be demonstrated and TH2-type cytokine mRNA upregulation in aller
gic mucosa has been shown. Proinflammatory cytokines initiate an adhes
ion cascade and activate T-cells that create an ''atopic'' cytokine en
vironment within the tissue, which also may be linked to the long-term
selective recruitment of eosinophils. However, the acute selective mi
gration of eosinophils after allergen challenge is not fully understoo
d nor is the role of chemokines in allergic and viral rhinitis. Allerg
ic rhinitis clearly represents an inflammatory reaction.