"This reduction could contribute to the clinical efficacy of this class of medications in the treatment of childhood obstructive sleep apnea syndrome," they wrote.

Some studies have shown that intranasal corticosteroid therapy -- used predominantly in allergic rhinitis and nasal polyposis -- has been shown to improve mild obstructive sleep apnea in children. That's accomplished, some have theorized, via an upregulation of T-regulatory cells and increased secretion of IL-10.

To explore the exact mechanism of the relationship, the researchers conducted a randomized prospective study of 24 children ages 2 to 12 who were having an adenotonsillectomy for obstructive sleep apnea. All were patients at a pediatric otolaryngology practice in a children's hospital.

Among those children, 11 were given 55 mcg per nostril of fluticasone furoate nasal spray every day for two weeks before adenotonsillectomy; 13 did not get the treatment.

Baroody and colleagues hypothesized that giving the drug would increase levels of T-regulatory cells and boost secretion of IL-10, while at the same time downregulating secretion of pro-inflammatory cytokines.

Their finding of no significant differences in the number of CD4, CD25, or FOXP3 cells or transforming growth factor beta-positive cells could be related to the small sample size or because the relationship may not be mediated by T cells as expected, the researchers wrote.

In explaining the significantly lower levels of IL-6 in treated patients, they wrote that it "is certainly plausible to speculate that the mechanism of action of intranasal corticosteroids is mediated via a reduction in the production of IL-6 by adenoid lymphocytes that, in turn, leads to decreased growth and differentiation of these adenoid cells and a decrease in adenoid size."

Or, they said, the decrease in IL-6 simply leads to a drop in pro-inflammatory effects, which would help mitigate the condition.