Df. Anderson et al., SEASONAL ALLERGIC CONJUNCTIVITIS IS ACCOMPANIED BY INCREASED MAST-CELL NUMBERS IN THE ABSENCE OF LEUKOCYTE INFILTRATION, Clinical and experimental allergy, 27(9), 1997, pp. 1060-1066
Background Seasonal allergic conjunctivitis (SAG) is the most common a
llergic disease to affect the eye, occurring alone or in association w
ith allergic rhinitis. Infiltration with mast cells and eosinophils is
characteristic of the chronic forms of allergic conjunctivitis such a
s vernal and atopic keratoconjunctivitis, and these cell types also co
ntribute significantly to allergic inflammation in the skin. indirect
evidence fur a similar pattern of cellular events in SAC comes from st
udies which demonstrate raised eosinophil and neutrophil numbers in co
njunctival scrapings and elevated levels of mast cell tryptase in tear
s following allergen challenge. Objective To directly characterize the
inflammatory cell infiltrate in SAC and to determine its clinical rel
evance. Methods We employed specific immunohistochemical staining to c
ount mast cells, eosinophils and neutrophils in the conjunctival epith
elium and lamina propria of eight atopic patients with SAC in, and 12
SAC patients out of the hay fever season. Sixteen patients with no his
tory of ocular allergy were used as control subjects. Results Mast cel
ls were absent from normal epithelium. During the pollen season median
mast cell numbers in the lamina propria were found to be increased by
61% in patients with SAC compared with normals (P = 0.012). Eosinophi
ls were found in the lamina propria in less than half of the symptomat
ic patients with SAC and in only three patients were eosinophils prese
nt in the epithelium. The neutrophil numbers in the lamina propria of
patients with SAC tended to be higher than normals but these changes d
id not reach statistical significance. Conclusion These data based on
the direct assessment of conjunctival tissue provide evidence that sym
ptoms occur in SAC in the absence of detectable recruitment of eosinop
hils or neutrophils. This suggests that this disorder is related to ma
st cell-mediated changes.