Specific immunoglobulin E for staphylococcal enterotoxins in nasal polyps from patients with aspirin-intolerant asthma.
BACKGROUND
Nasal polyps infiltrated with eosinophils are commonly found in chronic asthmatic patients, more frequently in those with aspirin-intolerant asthma (AIA) than aspirin-tolerant asthma (ATA). Some studies have suggested a contribution of superantigens derived from Staphylococcus sp to nasal polyposis and eosinophilia, but their relative importance in AIA and ATA subjects is unknown.


OBJECTIVE
We investigated whether local production of specific IgE to staphylococcal enterotoxins A and B (SEA and SEB) and relationships with markers of eosinophilic inflammation differ in the nasal polyps of AIA and ATA subjects.


METHODS
Fifteen AIA subjects with positive responses to lysine-aspirin bronchoprovocation and 15 ATA subjects underwent polypectomy. Immunoassays were used to quantify eosinophil cationic protein (ECP), IL-5, mast cell tryptase, soluble IL-2 receptors (sIL-2R), total IgE, and specific IgE for SEA and SEB.


RESULTS
ECP levels in nasal polyp homogenates were higher in AIA subjects than in ATA subjects (P < 0.02), with no significant differences in tryptase, IL-5 or sIL-2R. Total IgE, and specific IgE to both SEA and SEB, were detectable in some nasal polyps from both subject groups, but median levels were markedly higher in AIA subjects than in ATA subjects (P = 0.04, 0.01, 0.05, respectively). Levels of specific IgE to SEA and SEB correlated significantly with levels of ECP and IL-5, but not those of tryptase or sIL-2R.


CONCLUSIONS
These findings suggest that staphylococcal superantigens may drive local eosinophilic inflammation in nasal polyp tissue, and that this is exacerbated in subjects with AIA.
Department of Allergy & Rheumatology, Ajou University School of Medicine, Suwon, Korea.
Y J
YJ
Suh
S H
SH
Yoon
A P
AP
Sampson
H J
HJ
Kim
S H
SH
Kim
D H
DH
Nahm
C H
CH
Suh
H S
HS
Park
D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects; D001241:Aspirin / Q000009:adverse effects; D001249:Asthma / Q000139:chemically induced / Q000276:immunology* / Q000382:microbiology; D015415:Biomarkers / Q000032:analysis; D004768:Enterotoxins / Q000276:immunology*; D047150:Eosinophil Cationic Protein / Q000032:analysis; D004802:Eosinophilia; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000032:analysis*; D015848:Interleukin-5 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009297:Nasal Mucosa / Q000276:immunology* / Q000382:microbiology; D009298:Nasal Polyps / Q000276:immunology* / Q000382:microbiology; D011961:Receptors, Fc / Q000276:immunology; D013205:Staphylococcal Protein A / Q000276:immunology; D013210:Staphylococcus / Q000378:metabolism*
D000894:Anti-Inflammatory Agents, Non-Steroidal; D015415:Biomarkers; D004768:Enterotoxins; C045281:IgA receptor; D015848:Interleukin-5; D011961:Receptors, Fc; D013205:Staphylococcal Protein A; D007073:Immunoglobulin E; D047150:Eosinophil Cationic Protein; D001241:Aspirin