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*
Section of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520;
Division of Pulmonary Medicine, Department of Internal Medicine, Hanyang University College of Medicine, Seoul, Korea; and
Division of Epidemiology and Virology, Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, VA 22908
Rhinovirus (RV) upper respiratory tract infections are
prototypic transient inflammatory responses. To address the mechanism
of disease resolution in these infections, we determined if RV
stimulated the production of the IL-1 receptor antagonist (IL-1ra) in
vivo and in vitro. In contrast to IL-1
and IL-1ß, immunoreactive
IL-1ra was readily detected in the nasal washings of normal human
volunteers. Symptomatic RV infection caused a small increase in
IL-1, a modest increase in IL-1ß, and an impressive increase in
IL-1ra. Maximal induction of IL-1 and IL-1ß was transiently noted
48 h after RV infection. In contrast, maximal induction of IL-1ra
was prolonged appearing 48–72 h after RV infection. These time points
corresponded to the periods of peak symptomatology and the onset of
symptom resolution, respectively. Western analysis of nasal washings
demonstrated that RV stimulated the accumulation of intracellular
IL-1ra type I in all and secreted IL-1ra in a subset of volunteers.
Unstimulated normal respiratory epithelial cells contained
intracellular IL-1ra type I mRNA and protein. RV infection increased
the intracellular levels and extracellular transport of this IL-1ra
moiety without causing significant changes in the levels of IL-1ra
mRNA. IL-1ra may play an important role in the resolution of RV
respiratory infections. RV stimulates epithelial cell IL-1ra
elaboration, at least in part, via a novel translational and/or
posttranslational mechanism.
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