Atopic asthma is characterized by inflammatory responses of the airway
and is associated with up-regulation of Th2 cytokines, notably IL-4 a
nd IL-5. A recently described human cytokine, IL-13, is a potent in vi
tro modulator of various cell types, including monocytes, B cells, and
endothelial cells. Similar to IL-4, it is also involved in the induct
ion of IgE synthesis. However, the in vivo expression and function of
IL-13 and its relation to disease remain to be defined. Using a segmen
tal allergen challenge model, we have examined the in vivo expression
of IL-13 in the bronchoalveolar ravage (BAL) cells of atopic patients.
We found a significant enhancement of both IL-13 transcripts and secr
eted proteins in the allergen-challenged BAL compared with the saline-
challenged control sites of asthmatic and rhinitic patients. In contra
st, the expression of IL-13 transcripts was not detected in the BAL of
two normal subjects challenged with the same dose of ragweed allergen
. The cellular source of IL-13 mRNA was identified in the mononuclear
cell fraction of the allergen-challenged BAL. The allergen-induced qua
ntitative differences in the level of transcripts were confirmed by co
mpetitive PCR assays. These results suggest that the significant incre
ase in IL-13 in the allergen-challenged BAL is primarily from the mono
nuclear cells and is involved in the regulation of allergen-induced la
te phase inflammatory responses.