L. Tabordabarata et al., EFFECT OF CETIRIZINE AND PREDNISOLONE ON CELLULAR INFILTRATION AND CYTOKINE MESSENGER-RNA EXPRESSION DURING ALLERGEN-INDUCED LATE CUTANEOUSRESPONSES, Clinical and experimental allergy, 26(1), 1996, pp. 68-78
Background The ability of cetirizine to inhibit eosinophil infiltratio
n into the sites of allergen-induced cutaneous late-phase reactions is
controversial. A previous skin biopsy study gave negative results wit
h 15 mg of cetirizine as a single dose. Objective To confirm these fin
dings we have used cetirizine (30 mg daily) for 5 days and compared th
e results with prednisolone (20 mg daily for 5 days) as a positive con
trol. The effect of these agents on mRNA positive cells for interleuki
n-3 (IL-3), interleukin-4, interleukin-5 and granulocyte/macrophage-co
lony stimulating factor (GM-CSF) was also evaluated. Methods A double-
blind, placebo-controlled cross-over study (n = 12) was followed. Afte
r each treatment 30 biological units (BUs) of Dermatophagoides pterony
ssinus or Phleum pratense were injected intradermally and the early (1
5 min) and late-phase response sizes (6 and 24 h) were measured. Skin
biopsies were taken at 24 h for immunocytochemistry and in situ hybrid
ization. Results Cetirizine but not prednisolone inhibited the early-p
hase response (37%, P = 0.004). In contrast prednisolone, but not ceti
rizine, significantly inhibited the size of the late-phase reaction at
24 h (70%, P = 0.021). This was associated with significant decreases
in total (MBP+) and activated (EG2+) eosinophils (P = 0.019 and 0.014
, respectively), as compared with placebo. There were also clear but n
on-significant reductions in interleukin-3, interleukin-4, interleukin
-5 and granulocyte/macrophage-colony stimulating factor mRNA+ cells. C
onclusion Prednisolone, but not cetirizine, inhibited both the magnitu
de of the allergen-induced late-phase response and the accompanying lo
cal eosinophil infiltration. These corticosteroid effects were associa
ted with a reduction in cells expressing mRNA for 'TH2-type' cytokines
.