Increased number of CD34+ cells in nasal mucosa of allergic rhinitis patients: inhibition by a local corticosteroid.
BACKGROUND
Eosinophils develop from CD34+ haematopoietic progenitor cells. Allergen exposure in susceptible individuals is known to induce a local eosinophilic inflammation, but the effect on progenitor cells is much less understood.


OBJECTIVE
We aimed to evaluate how allergen exposure affects the number of tissue CD34+ cells and CD34+ eosinophils in allergic rhinitis (AR) patients and whether any such effect is influenced by local corticosteroid treatment. Also, we evaluated changes in the number of CXC receptor 4-positive cells (CXCR4+), since the CXCR4 ligand (stromal cell-derived factor-1 (SDF-1)) is a potent chemoattractant for haematopoietic progenitors.


METHODS
In a double-blind, randomized study, pollen-sensitized AR patients were treated with a nasal corticosteroid fluticasone propionate (FP, 200 microg/day) or placebo throughout the pollen season. Nasal biopsies were taken before and during the season. CD34 and CXCR4 were stained using immunohistochemistry.


RESULTS
The pollen season significantly increased the number of CD34+ cells, CD34+/CXCR4+ cells and CD34+ eosinophils in placebo-treated patients, but not in FP-treated patients. The mean pollen season-induced increase in CD34+ cells, CD34+/CXCR4+ cells and CD34+ eosinophils in FP-treated patients was lower compared with placebo-treated patients.


CONCLUSIONS
A pollen season increases the number of CD34+ cells in nasal tissue accompanied by an increase in the number of CD34+/CXCR4+ haematopoietic progenitors and also the number of CD34+ eosinophils in subjects with AR. Treatment with a local corticosteroid provides protection against this pollen-induced increase in tissue CD34+ cells and CD34+ eosinophils possibly via inhibition of allergen-induced CXCR4-mediated recruitment of CD34+ haematopoietic progenitors into airways and their further differentiation into eosinophils within the tissue.
Sergejeva
S
S
The Lung Pharmacology Group, Department of Respiratory Medicine and Allergology, Institute of Internal Medicine, Göteborg University, Gothenburg, Sweden.
Malmhäll
C
C
Lötvall
J
J
Pullerits
T
T
D000293:Adolescent; D000328:Adult; D000485:Allergens; D000730:Androstadienes / Q000627:therapeutic use*; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D018952:Antigens, CD34 / Q000276:immunology*; D054377:Chemokine CXCL12; D019743:Chemokines, CXC / Q000032:analysis; D004804:Eosinophils / Q000276:immunology; D000068298:Fluticasone; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D009297:Nasal Mucosa / Q000276:immunology*; D009299:Nasal Provocation Tests; D019718:Receptors, CXCR4 / Q000032:analysis; D006255:Rhinitis, Allergic, Seasonal / Q000188:drug therapy / Q000276:immunology*; D018709:Statistics, Nonparametric; D013234:Stem Cells / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*
D000485:Allergens; D000730:Androstadienes; D000893:Anti-Inflammatory Agents; D018952:Antigens, CD34; C515255:CXCL12 protein, human; D054377:Chemokine CXCL12; D019743:Chemokines, CXC; D019718:Receptors, CXCR4; D000068298:Fluticasone