Antibody Responses Against S. Aureus in Atopic Dermatitis
Abstract and Introduction
Abstract
Background: Staphylococcus aureus plays a role in the pathogenesis of atopic dermatitis (AD), possibly via the expression of various virulence antigens. An altered antibody response towards these antigens might contribute to inflammation.
Objectives: To provide an overview of the varying prevalences and odds of antibody responses against S. aureus antigens in patients with AD.
Methods: Data were systematically obtained from Embase, MEDLINE, Web of Science, Scopus, Cochrane, PubMed and Google Scholar up to 12 February 2016. We selected all original observational and experimental studies assessing antistaphylococcal antibodies in serum of patients with AD. Prevalences and odds ratios (ORs) of IgE, IgG, IgM and IgA against S. aureus in patients with AD vs. healthy controls were pooled using the random–effects model. We calculated I 2 statistics to assess heterogeneity and rated study quality using the Newcastle–Ottawa Scale.
Results: Twenty–six articles (2369 patients) were included, of which 10 were controlled studies. Study quality was fair to poor. Patients with AD had higher prevalences of IgE against staphylococcal enterotoxin (SE)A (OR 8·37, 95% confidence interval 2·93–23·92) and SEB (OR 9·34, 95% confidence interval 3·54–24·93) compared with controls. Prevalences of antistaphylococcal IgE were 33% for SEA, 35% for SEB and 16% for toxic shock syndrome toxin–1. However, study heterogeneity and imprecision should be taken into consideration when interpreting the results. Data on IgG, IgM and IgA, as well as other antigens, are limited.
Conclusions: 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.
Introduction
Atopic dermatitis (AD) is a multifactorial disorder that arises from interactions between immune dysregulations, genetic predisposition, skin barrier defects and environmental factors.[1,2] Both lesional and nonlesional skin and the noses of patients with AD are more likely to be colonized with Staphylococcus aureus compared with healthy controls.[3] Recent studies have shown that the abundance of S. aureus is associated with AD severity, suggesting a causal role for S. aureus in the pathogenesis of AD.[2,4–9] However, the exact mechanisms by which S. aureus aggravates inflammation in AD are not fully understood.[10]
Staphylococcus aureus expresses a variety of virulence factors that could contribute to AD inflammation. Based on their biological function, these antigens can be divided in four groups: (i) microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) such as clumping factor A, which helps S. aureus adhere to the host cells; (ii) cell–membrane–damaging molecules such as alpha toxin, which can induce keratinocyte cell death; (iii) household enzymes such as lipase, which provides cell nutrition; and (iv) immune–modulating proteins (superantigenic and nonsuperantigenic).[10–13] The latter include the group of staphylococcal superantigens, which have the ability to activate mast cells and T cells directly, resulting in the release of proinflammatory cytokines.[14–16] Expression of these S. aureus antigens varies between the different S. aureus isolates. However, it has proven difficult to identify associations between the genetic composition of S. aureus strains and AD.[17–22]
Evaluation of the antibody response to these S. aureus antigens gives an indication of the antigens that are expressed by the bacterium in vivo and will give insight into how the immune system of patients with AD counteracts these antigens. This might help us to understand the role of S. aureus in AD pathogenesis, as well as the mechanisms by which S. aureus causes inflammation. Since 1982, several studies have reported serum antibodies against S. aureus in patients with AD.[23–35] However, the prevalences of antistaphylococcal antibodies in these studies vary widely. This is probably due to low sample sizes and different methods used to detect antibodies [e.g. enzyme–linked immunosorbent assay (ELISA) or AlaSTAT]. Moreover, studies often focus on few antigens and/or antibody classes.
The aim of this systematic review was to provide an overview of the pooled prevalences and odds of antibodies (IgE, IgG, IgM and IgA) against S. aureus antigens in serum of patients with AD compared with healthy controls. Additionally, we reviewed the relationship between AD severity and anti–S. aureus antibodies.
posted by dermatica at
July 30, 2018
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