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*
Department of Medical Specialities, Southampton General Hospital, Southampton, Hampshire, United Kingdom; and
Washington University, St. Louis, MO 63110
The bronchial epithelium is a source of both 
and 
chemokines
and, uniquely, of secretory component (SC), the extracellular
ligand-binding domain of the polymeric IgA receptor. Ig superfamily
relatives of SC, such as IgG and 2-macroglobulin, bind
IL-8. Therefore, we tested the hypothesis that SC binds IL-8, modifying
its activity as a neutrophil chemoattractant. Primary bronchial
epithelial cells were cultured under conditions to optimize SC
synthesis. The chemokines IL-8, epithelial neutrophil-activating
peptide-78, growth-related oncogene , and RANTES were released
constitutively by epithelial cells from both normal and asthmatic
donors and detected in high m.w. complexes with SC. There were no
qualitative differences in the production of SC-chemokine complexes by
epithelial cells from normal or asthmatic donors, and in all cases this
was the only form of chemokine detected. SC contains 15%
N-linked carbohydrate, and complete deglycosylation with
peptide N-glycosidase F abolished IL-8 binding. In
micro-Boyden chamber assays, no IL-8-dependent neutrophil chemotactic
responses to epithelial culture supernatants could be demonstrated. SC
dose-dependently (IC50 
0.3 nM) inhibited the neutrophil
chemotactic response to rIL-8 (10 nM) in micro-Boyden chamber assays
and also inhibited IL-8-mediated neutrophil transendothelial migration.
SC inhibited the binding of IL-8 to nonspecific binding sites on
polycarbonate filters and endothelial cell monolayers, and therefore
the formation of haptotactic gradients, without effects on IL-8 binding
to specific receptors on neutrophils. The data indicate that in the
airways IL-8 may be solubilized and inactivated by binding to
SC.
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