Background: Allergic eye disease is common, but little is known about the u
nderlying disease mechanisms. Conjunctival allergen challenge causes sympto
ms similar to those of seasonal allergic conjunctivitis and is a useful mod
el to study.
Objective: We have used allergen challenge to investigate the course of the
ocular response, tear inflammatory mediators, tissue adhesion protein expr
ession, and cellular infiltration.
Methods: Eighteen atopic patients and 4 nonatopic control subjects were cha
llenged with extracted mixed grass or Dermatophagoides pteronyssinus in one
eye and control vehicle in the other. The clinical response was recorded,
and tears mere collected over a 6-hour period. Conjunctival biopsy specimen
s mere taken from the challenged eye at 6 or 24 hours.
Results: An early-phase response (maximal at 20 minutes) showed a significa
nt increase in tear histamine and tryptase levels, reducing to control leve
ls again by 40 minutes. At 6 hours, a late-phase response occurred with inc
reased symptoms, a second peak of tear histamine and eosinophil cationic pr
otein but not tryptase, upregulation of the adhesion molecules E-selectin a
nd intercellular adhesion molecule, and a cellular infiltrate of mast cells
, neutrophils, eosinophils, macrophages, and basophils, with T cells increa
sed only in bulbar biopsy specimens.
Conclusions: The early peaks of tear histamine plus tryptase indicate that
the mast cell is responsible for the early-phase response, but basophils ma
y be involved in the late-phase response. Both tear and biopsy findings und
erline the significance of the late-phase response as the transition betwee
n a type I response and clinical disease.