Nasal eosinophilia and IL-5 mRNA expression in seasonal allergic rhinitis induced by natural allergen exposure: effect of topical corticosteroids.
BACKGROUND
Nasal allergen provocation in patients with allergic rhinitis leads to expression of the proeosinophilic cytokines IL-5 and GM-CSF and tissue eosinophilia.


OBJECTIVE
We sought to examine the effect of natural seasonal allergen exposure on IL-5 and GM-CSF mRNA expression and nasal eosinophilia and to evaluate the effects of topical corticosteroid therapy on these responses.


METHODS
Nasal biopsy specimens were collected from 46 grass pollen-sensitive patients with seasonal rhinitis before the grass pollen season. A second biopsy specimen was collected during the pollen season, by which time patients had received 6 weeks treatment with either fluticasone propionate (200 micro(g) twice daily) or placebo nasal spray.


RESULTS
Fluticasone treatment was clinically effective (P <.005). Patients receiving placebo, but not fluticasone, showed increased numbers of epithelial and submucosal EG2+ eosinophils (P <.005) and IL-5 and GM-CSF mRNA-expressing cells (P <.0001) during the pollen season. Colocalization experiments showed that greater than 80% of IL-5 mRNA-expressing cells were submucosal CD3+ T cells in both groups. The numbers of submucosal CD3+ T cells did not increase during the pollen season or decrease with fluticasone treatment. Fluticasone also inhibited IL-5 secretion by grass pollen-stimulated peripheral blood T cells from patients with seasonal rhinitis (n = 5, inhibitory concentration of 50% = 10(-9) to 10(-10) mol/L).


CONCLUSIONS
These results suggest that topical corticosteroids may reduce eosinophilia in seasonal rhinitis by inhibiting T cell IL-5 production.
Masuyama
K
K
Upper Respiratory Medicine, Imperial College School of Medicine at the National Heart and Lung Institute, London, United Kingdom.
Till
S J
SJ
Jacobson
M R
MR
Kamil
A
A
Cameron
L
L
Juliusson
S
S
Lowhagen
O
O
Kay
A B
AB
Hamid
Q A
QA
Durham
S R
SR
D000281:Administration, Intranasal; D000730:Androstadienes / Q000008:administration & dosage / Q000627:therapeutic use*; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D001706:Biopsy; D017252:CD3 Complex / Q000032:analysis; D002478:Cells, Cultured; D004802:Eosinophilia / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D000068298:Fluticasone; D005938:Glucocorticoids; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000096:biosynthesis / Q000235:genetics; D006801:Humans; D017403:In Situ Hybridization; D015848:Interleukin-5 / Q000096:biosynthesis* / Q000235:genetics; D009297:Nasal Mucosa / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D006109:Poaceae; D011058:Pollen; D012333:RNA, Messenger / Q000378:metabolism*; D006255:Rhinitis, Allergic, Seasonal / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D012882:Skin Tests; D013601:T-Lymphocytes / Q000737:chemistry / Q000276:immunology
D000730:Androstadienes; D000893:Anti-Inflammatory Agents; D017252:CD3 Complex; D005938:Glucocorticoids; D015848:Interleukin-5; D012333:RNA, Messenger; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D000068298:Fluticasone