Late-phase response in allergic rhinitis is characterized by tissue eosinop
hilia and influx of CD4(+) T-cells. IL-16 and MIP-la are highly chemotactic
on T-cells and on eosinophils. Both IL-16 and MIP-1 alpha have been demons
trated to be up-regulated after challenge in the late-phase response in var
ious atopic conditions other than allergic rhinitis. The aim of our study w
as to determine the expression of IL-16 and MIP-1 alpha in nasal secretions
following allergen challenge in allergic rhinitis, and to compare these wi
th characteristic late-phase mediators such as IL-5 and ECP. Nasal secretio
ns of 14 allergic volunteers challenged intranasally by their specific alle
rgen M ere studied from 20 minutes to 8 hours after allergen challenge. Nas
al secretions were analyzed by routine ELISA for IL-16, MIP-1 alpha, IL-5,
and ECP. IL-16 and MIP-1 alpha increased significantly in nasal secretions
of challenged allergic patients in the late-phase response. IL-16 revealed
highest amounts 5 hours after challenge, whereas MIP-1 alpha peaked at 7 ho
urs. Both correlated significantly (r = 0.917 p < 0.05) at 6 hours. IL-5 an
d ECP peaked between 6 and 8 hours and correlated significantly (r = 0.951,
p < 0.01) at 6 hours as well. Our data demonstrate that IL-16 and MIP-la a
re expressed in the late phase response in allergic rhinitis in a more or l
ess similar kinetic like IL-5 and ECP. They are suggested to be responsible
for the observed influx of eosinophils (IL-5, IL-16, and MIP-1 alpha) and
CD4(+) T-cells (IL-16 and MIP-1 alpha) into the challenged allergic mucosa.