S. aureus enterotoxin sensitization associated with asthma outcomes

Key takeaways:

• Sensitization to S. aureus enterotoxin but not aeroallergens was linked to higher exacerbation rates.
• Patients with specific S. aureus enterotoxin IgE had higher fractional exhaled nitric oxide.

By measuring specific IgE against Staphylococcus aureus enterotoxin, physicians may identify patients with more asthma exacerbations, according to a study published in The Journal of Allergy and Clinical Immunology: In Practice.

Patients with these sensitizations also may have more nasal polyposis and chronic sinusitis, lower lung function, and more intense type 2 inflammation, Florence Scheich, MD, PhD, respiratory physician at CHU Liège Sart-Tilman, University of Liège, and colleagues wrote.

The prospective study comprised 110 adults with asthma (mean age, 53 years; 61% women; mean BMI, 26.7 kg/m²), including 12% who were current smokers, 30% with chronic rhinosinusitis and 25% with comorbid nasal polyposis.

The researchers characterized participants as atopic if they had at least one positive sIgE test for a common aeroallergen (AA) such as cat, dog, house dust mites, grass pollen, tree pollen or a mixture of molds. Participants also were tested for sensitization to S. aureus enterotoxin (SE).

Overall, 59% were sensitized to an AA, and 50% were sensitized to SE. More specifically, the researchers classified participants into four groups, including:

• no sensitization to AA or SE (n = 22; 20%);
• sensitization to AA but not to SE (n = 33; 30%);
• sensitization to SE but not to AA (n = 23; 21%); and
• sensitization to AA and SE (n = 32; 29%).

The patients who were sensitized to SE but not AA had later onset of asthma, a higher number of pack-years in their smoking history, more exacerbations during the previous year, higher fractional exhaled nitric oxide and total serum IgE levels, and lower ratios of FEV₁ to forced vital capacity, in addition to more frequent chronic rhinosinusitis and nasal polyps, than patients who were sensitized to AA but not to SE.

The patients sensitized to AA and SE both had the highest total serum IgE levels.

Those patients with AA sensitization but no SE sensitization had earlier asthma onset, lower exacerbation rates, less intense smoking history with 79% reporting that they were not smokers, and better lung function, the researchers found.

The patients who were not sensitized to AA or SE had smoking histories of 18.8 person-years — which the researchers characterized as the most intense among the full cohort — as well as more airflow obstruction, the lowest total serum IgE levels and the lowest rates of ear, nose and throat comorbidities.

The researchers also excluded participants who had received treatment with biologics and measured sputum supernatant levels of IgE, IL-5 and IL-4 among 14 patients who were sensitized to SE and 40 who were not, without accounting for sensitization to AA.

The patients with SE sensitization had higher levels of sputum IgE and sputum IL-5 as well as similar levels of sputum IL-4 when compared with the patients who were not sensitized to SE.

With one-third to one-half of the general population of patients sensitized to SE, the researchers wrote, physicians who are treating patients with asthma should measure SE sIgE during the phenotype process.

Patients who are sensitized to SE but not to AA have later onset of disease and higher rates of exacerbations, chronic rhinosinusitis and nasal polyps, in addition to more severe airway obstruction, which could have implications for treatment.

The researchers also noted that patients who are sensitized to SE have higher FeNO, sputum IgE and sputum IL-5 levels, including associations with serum IgE levels that were well above those observed in patients who were sensitized to AA but not SE.

By measuring SE sIgE, the researchers wrote, clinicians can identify risks for these outcomes and design treatment accordingly.