Steroid treatment reduces allergic eosinophilic inflammation in rhinitis
MedWire News: Nasal steroid treatment in patients with allergic rhinitis reduces allergic eosinophilic inflammation within 5 days after institution of treatment, research shows.
The data suggest there is a role for the inhibition of CCL5-dependent cell recruitment, report Lena Uller (Lund University, Sweden) and colleagues.
Writing in the journal Respiratory Research, the authors state that it is assumed apoptosis of eosinophils is a central component of halting allergic airway disease.
Despite this assumption, it has not previously been demonstrated in human allergic airways in vivo.
The group hypothesized that the steroid-induced resolution of human airway eosinophilic inflammation involves inhibition of CCL5, a chemokine regulating eosinophil and lymphocyte traffic.
In this study, 21 patients with allergic rhinitis were treated with daily birch or grass pollen allergen challenges for up to 1 week, followed by a 2-week or longer washout. After treatment with the allergens, patients were given budesonide or placebo for 6 days and nasal biopsy histochemistry was obtained on the final day of treatment.
In the biopsies from placebo-treated patients, marked epithelial- and sub-epithelial eosinophilia remained 3 days after cessation of the allergen challenges. Compared with placebo, budesonide reduced tissue eosinophilia, and sub-epithelial eosinophilia more than epithelial eosinophilia.
In placebo-treated individuals, the intensity of CCL5 immunoreactivity was pronounced in the epithelium, including the glandular epithelium and in sub-epithelial tissue. In steroid-treated patients, CCL5 immunoreactivity was less than in the placebo group.
The reduced expression of CCL5, "occurring simultaneously to the reduced tissue eosinophilia, suggests that CCL5, with its proposed roles in eosinophil and lymphocyte recruitment, can be of special importance as pharmacological target," suggest Uller and colleagues.
General tissue cell apoptosis and epithelial cell proliferation were reduced by budesonide, but apoptotic eosinophils were not observed in any biopsies, regardless of treatment.
"In view of the established dogma it was most surprising that apoptotic eosinophils are not detected in the airway tissues at ongoing, spontaneous or drug-induced, resolution of the allergic airway inflammation," concludes the team.
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