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Increase Steady State Levels of Polymeric Ig Receptor mRNA in Human Airway and Intestinal Epithelial Cells1
Infectious Diseases Research Laboratory, Veterans Affairs Medical Center, and Department of Internal Medicine, University of Iowa, Iowa City, IA 52242
Delivery of IgA to the mucosal surface occurs via transcytosis of
polymeric IgA (pIgA) across the epithelium, a process mediated by the
pIgR. Several factors increase pIgR expression in human epithelial
cells, including IL-4 and IFN-
. Using an RNase protection assay, we
found that IL-4 and IFN- increase steady state levels of pIgR mRNA
in both human intestinal (HT29) and airway (Calu-3) epithelial cells.
Time course studies in HT29 clone 19A cells showed that with each
cytokine alone and with both together: 1) there was a significant lag
before mRNA levels increased; 2) maximal levels were not reached until
48–72 h after the addition of cytokines; 3) mRNA levels remained
elevated in the continued presence of cytokines; and 4) addition of
actinomycin D or removal of cytokines led to decreases in mRNA levels
with a half-life of 
20–28 h. Cytokine-dependent increases in steady
state levels of pIgR mRNA were inhibited by cycloheximide and by
protein tyrosine kinase inhibitors but not by inhibitors of protein
kinase C or cAMP-dependent protein kinase A. Both IFN- and IL-4
increased expression of the inducible transcription factor IFN
regulatory factor-1 (IRF-1), but levels of IRF-1 only weakly correlated
with levels of pIgR mRNA, suggesting that additional transcription
factors are required. These studies provide additional insights into
the mechanisms by which cytokines regulate expression of the pIgR, a
central player in mucosal immunity.
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