Topical steroid treatment of allergic rhinitis decreases nasal fluid TH2 cytokines, eosinophils, eosinophil cationic protein, and IgE but has no significant effect on IFN-gamma, IL-1beta, TNF-alpha, or neutrophils.
BACKGROUND
Topical treatment with glucocorticoids (GCs) is known to decrease eosinophils but not neutrophils in patients with allergic rhinitis.


OBJECTIVE
We sought to examine whether the differential effects of GC treatment on eosinophils and neutrophils are mirrored by differential effects on T(H)1/T(H)2 cytokines and the neutrophil-associated cytokines IL-1beta and TNF-alpha.


METHODS
Differential counts of eosinophils and neutrophils in nasal fluids from 60 children with seasonal allergic rhinitis treated with a topical GC were examined after staining with May-Grünwald-Giemsa stain. Nasal fluid levels of IFN-gamma, IL-4, IL-6, IL-10, IL-1beta, and TNF-alpha were examined with ELISA, and IgE and eosinophil cationic protein (ECP) levels were examined with RIA.


RESULTS
After GC treatment, there was a statistically significant decrease of the T(H)2 cytokines IL-4, IL-6, and IL-10, as well as ECP and IgE. By contrast, there were no significant changes of the levels of IFN-gamma, IL-1beta, TNF-alpha, or neutrophils. In the GC-treated patients IL-1beta and TNF-alpha levels correlated with neutrophils and ECP, and IL-1beta correlated with eosinophils. Furthermore, ECP correlated with both eosinophils and neutrophils. Neither IL-1beta nor TNF-alpha correlated with IgE. Patients with high neutrophil counts after GC treatment were found to have significantly higher eosinophil counts and ECP than patients with low counts.


CONCLUSIONS
The beneficial effects of topical treatment with GC in patients with allergic rhinitis could be attributed to downregulation of T(H)2 cytokines, with an ensuing decrease of eosinophils, ECP, and IgE. It is possible that neutrophils could counteract the beneficial effects of GCs by releasing the proinflammatory cytokines IL-1beta and TNF-alpha.
Benson
M
M
Department of Pediatrics and Clinical Virology, Sahlgrenska University Hospital, Göteborg.
Strannegård
I L
IL
Strannegård
O
O
Wennergren
G
G
D000287:Administration, Topical; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001798:Blood Proteins / Q000378:metabolism*; D019819:Budesonide / Q000627:therapeutic use; D002648:Child; D016207:Cytokines / Q000378:metabolism*; D047091:Eosinophil Granule Proteins; D004804:Eosinophils / Q000166:cytology / Q000187:drug effects; D005938:Glucocorticoids; D006801:Humans; D007073:Immunoglobulin E / Q000378:metabolism; D007371:Interferon-gamma / Q000378:metabolism*; D007375:Interleukin-1 / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007958:Leukocyte Count / Q000187:drug effects; D009297:Nasal Mucosa / Q000166:cytology* / Q000276:immunology / Q000378:metabolism*; D009504:Neutrophils / Q000737:chemistry* / Q000187:drug effects; D006255:Rhinitis, Allergic, Seasonal / Q000188:drug therapy*; D012260:Ribonucleases; D018418:Th2 Cells / Q000737:chemistry; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D001798:Blood Proteins; D016207:Cytokines; D047091:Eosinophil Granule Proteins; D005938:Glucocorticoids; D007375:Interleukin-1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D015847:Interleukin-4; D007073:Immunoglobulin E; D019819:Budesonide; D007371:Interferon-gamma; D012260:Ribonucleases