J. Raud et al., ANTI-IGE-INDUCED ACCUMULATION OF LEUKOCYTES, MEDIATORS, AND ALBUMIN IN SKIN CHAMBER FLUID FROM HEALTHY AND ATOPIC SUBJECTS, Journal of allergy and clinical immunology, 97(5), 1996, pp. 1151-1163
The aim of this study ws to examine potential differences between heal
thy and atopic subjects with regard to IgE-mediated cutaneous inflamma
tion. For this purpose, we analyzed histamine, tryptase, leukotriene B
-4, albumin, eosinophils, and total leukocytes in skin chamber fluid a
fter challenge with anti-human IgE. We also measured gross skin reacti
vity (wheal, flare, and late-phase reactions), circulating IgE, and eo
sinophils, as well as the state of eosinophil activation. It was found
that despite having more circulating IgE, the skin responsiveness of
the atopic subjects did not differ significantly from that of the nona
topic subjects with respect to mediator release, albumin extravasation
, or total recruitment of leukocytes. Moreover, the sizes of anti-IgE-
induced wheal, flare, and late-phase reactions were very similar in th
e two groups. On the other hand, significant recruitment of eosinophil
s during the IgE-mediated reaction was more or less restricted to the
atopic group. Yet the recruited eosinophils, of which the majority was
in an early state of activation before degranulation, did not seem to
contribute significantly to the IgE-mediated delayed skin edema. Furt
hermore, the eosinophil count in anti-IgE chambers of the atopic subje
cts did not correlate with any of the other parameters monitored. Thus
because the anti-IgE-induced recruitment of eosinophils appeared to b
e unrelated to factors such as the number of peripheral blood eosinoph
ils, the degree of mast cell activation, the intensity of inflammatory
skin changes, and the level of circulating IgE, it is apparent that t
he mechanisms for and pathophysiologic role of IgE-mediated dermal eos
inophil accumulation in atopic subjects require further investigation.