Summary
Atopic dermatitis (AD) is a common type of eczema. The bacterium Staphylococcus (S.) aureus plays a role in AD, possibly via various substances that are part of the bacterium. In people with AD, how the body's immune system reacts to these substances might lead to the inflammation seen in AD. In this study, we provide an overview of what is known from current literature (e.g. studies published in medical journals) on the immune response (antibodies) against S. aureus substances (antigens) in AD patients compared to healthy controls (people without AD). Scientific literature was systematically obtained from different databases. We extracted data on how often (so‐called ‘prevalence’) antibodies of, among others, the IgE type directed against S. aureus can be found in AD patients. A weighted prevalence was calculated, as studies with more patients were regarded more relevant, and prevalence was compared between AD patients and healthy controls. Tests for differences between studies and overall study quality were done to interpret the robustness of the results. We included 26 publications with a total of 2369 patients. In 10 studies a control group (of people without AD) was also studied. Study quality was fair to poor. The weighted prevalence of IgE against S. aureus antigens was 33% for staphylococcal enterotoxin (SE) A, 35% for SEB and 16% for toxic shock syndrome toxin (TSST)‐1. Compared to healthy controls, AD patients had 8.37 times more IgE against SEA and 9.37 times more IgE against SEB. No significant difference was seen for IgE against TSST‐1. Interpretation of the results should take into account that there were some important differences in study design and the fact that the studies were generally small. In conclusion, AD patients more often show an IgE antibody response against the S. aureus antigens SEA and SEB compared to healthy controls. These findings show that S. aureus may have a role in AD.
Patients with AD more often show an IgE antibody response directed against S. aureus superantigens than healthy controls, supporting a role for S. aureus in AD pathogenesis.
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