Specific immunoglobulin E for staphylococcal enterotoxins in nasal polyps from patients with aspirin‐intolerant asthma

Abstract

SummaryBackground 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 recepters (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 (Po0.02), 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 5 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. Conclusion These findings suggest that staphylococcal superantigens may drive local eosinophilic inflammation in nasal polyp tissue, and that this is exacerbated in subjects with AIA.

Clinical Significance of Immunoglobulin E Responses to Staphylococcal Superantigens in Patients with Aspirin-Exacerbated Respiratory Disease

“…IgE antibodies to SAg have been described in nasal polyp tissue and linked to local polyclonal IgE production and eosinophilic inflammation, which is often associated with severe asthma and aspirin hypersensitivity [13,14,27]. More recently, a study identified that serum SAg-specific IgE antibodies are risk factors for asthma, particularly severe asthma, although the presence of specific IgE to grass pollen or house-dust mite allergen was not an independent risk factor for asthma or asthma severity [11].…”

“…In addition, a few reports have demonstrated the presence or increased level of specific IgE to SAg in nasal polyp tissue of patients with aspirin-exacerbated respiratory disease (AERD). However, the presence of serum-specific IgE to SAg and its clinical relevance in patients with AERD has been reported only rarely [12,13,14,15]. Considering that chronic eosinophilic inflammation is a key feature of upper and lower airway inflammation in AERD, we hypothesized that SAg might be relevant to eosinophilic airway inflammation in patients with AERD [16].…”

Quantitative analysis of Staphylococcal enterotoxin B expression and its levels in patients with chronic rhinosinusitis with or without nasal polyps

“…[12] In patients with CRS, specific immunoglobulin (Ig) E responses to S. aureus exotoxins were detected. [13] It was also reported that the SAgs may contribute to glucocorticoid insensitivity. [14] Up to 30% of the nasal cavities of the population are colonized by S. aureus and 5-10% of the isolates secrete a SAg: SEB.…”

Atopy in Patients with Bronchiectasis: More than Coincidence

“…Staphylococcus infection, which is another narcotizing lung disease and a significant cause of bronchiectasis (Tsang and Tipoe 2004) can induce IL-5 stimulation and play a role as a cofactor in the pathogenesis of atopic disease (Heaton et al 2003). A role of staphylococcal superantigens in atopic dermatitis has been defined and similar mechanisms might be relevant in airway diseases including asthma (Bachert et al 2002;Suh et al 2004).…”