Persistent skin colonization with <i>Staphylococcus aureus</i> in atopic dermatitis: relationship to clinical and immunological parameters

Guzik, Tomasz J.; Bzowska, Monika; Kasprowicz, A; Czerniawska-Mysik, G; Wójcik, Kinga; Szmyd, D; Adamek-Guzik, T; Pryjma, J

doi:10.1111/j.1365-2222.2005.02210.x

Cited by 128 publications

(126 citation statements)

References 37 publications

(57 reference statements)

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“…Most affected individuals have S. aureus identifiable on skin swabs, often at very high density and more often present on lesional than nonlesional skin (16). Furthermore, S. aureus present on the skin of atopics is significantly more likely to express superantigen, and indeed the levels correlate with disease severity (17)(18)(19).…”

Section: Atopy ͉ T Cells ͉ Keratinocytes ͉ Staphylococcusmentioning

confidence: 97%

Bacterial superantigen facilitates epithelial presentation of allergen to T helper 2 cells

Ardern‐Jones

Black

Bateman

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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Although clinical and laboratory evidence support roles for both staphylococcal infection and environmental allergens in the pathogenesis of atopic dermatitis, human studies have largely considered these variables independently. We sought to test the hypothesis that staphylococcal superantigen influences the allergen-specific T cell response. We first mapped a Der p 1 epitope and used HLA DRB1*1501 class II tetramer-based cell sorted populations to show that specific CD4 ؉ T cells were able to recognize the peptide presented by HLA DR-matched keratinocytes. We observed that staphylococcal enterotoxin B (SEB) enhanced the IL-4 Der p 1-specific T cell response. This response was mediated by two synergistic mechanisms: first, SEB-induced IFN-␥ promoted class II and intercellular adhesion molecule-1 expression by presenting keratinocytes; and second, SEB-induced IL-4 directly amplified allergen-specific CD4 ؉ T cell production of many cytokines. We propose that handling of staphylococcal infection is a critical step in the amplification of the allergen-specific T cell response, linking two common disease associations and with implications for the prevention and treatment of atopic disease.T here is convincing evidence that allergic reactivity to environmental challenge has a role in the pathogenesis of atopic dermatitis (AD). For example, the histology of AD shares many features with classic allergic contact delayed-type hypersensitivity, including spongiosis and a dominant T cell inflammatory infiltrate that is distributed predominantly in a dermal, and to a lesser extent epidermal pattern. Approximately 80% of individuals with AD have circulating specific IgE recognizing one or more of house dust mite, cat, dog, grass, and other ubiquitous environmental allergens (1). In many studies, allergen-specific CD4 ϩ and CD8 ϩ T cells have been documented to be present in the peripheral blood and lesional skin of affected individuals and to produce diverse cytokines but with a frequent T helper 2 (Th2) dominance (2, 3). House dust mite extract application to the skin of individuals with AD can reproduce eczematous changes (4, 5), and allergen avoidance has been shown by some to be partially effective (6, 7). Keratinocytes have been shown to up-regulate HLA class II and intercellular adhesion molecule-1 (ICAM-1) in AD and other inflammatory dermatoses (8, 9) and also in response to injection of IFN-␥ into normal skin (10). However, in isolation, allergic reactivity to an environmental challenge does not explain all of the features of AD. Twenty percent of affected individuals do not generate IgE responses to such ubiquitous proteins, and it is unclear why disease incidence changes during age and between different geographical regions. The risk of disease is clearly influenced by genetic susceptibility factors, some of which affect the immune response, e.g., polymorphisms of the Fc R1 and IL-4R genes (11-13). However, it is becoming increasingly clear from the genetic studies that skin-specific genes, determining variables s...

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Section: Atopy ͉ T Cells ͉ Keratinocytes ͉ Staphylococcusmentioning

confidence: 97%

Bacterial superantigen facilitates epithelial presentation of allergen to T helper 2 cells

Ardern‐Jones

Black

Bateman

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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“…In both, children and adults with AD Th2 polarity, including IgE levels, eosinophilia and comorbidity of other allergic disorders is directly correlated with S. aureus colonization (45)(46)(47)(48). Furthermore, AD patients with a history of food allergy or asthma and sensitization(s) to common allergens are more likely to suffer from viral infections (49).…”

Section: Th2 Polarity In Allergic Diseases Correlates With Infectionsmentioning

confidence: 99%

Does allergy impair innate immunity? Leads and lessons from atopic dermatitis

Mrabet-Dahbi

Maurer

2010

Allergy

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To cite this article: Mrabet‐Dahbi S, Maurer M. Does allergy impair innate immunity? Leads and lessons from atopic dermatitis. Allergy 2010; 65: 1351–1356.AbstractHost defence responses against invading pathogens are well‐balanced, inflammatory processes of the innate and adaptive immune system. Impaired development or abnormal function of either system can result in failure to control pathogens and to clear infections. Infections have been claimed to modulate the onset and course of allergic diseases. This so‐called hygiene hypothesis is still an active area of research. In contrast, the effects of allergies on infections and pathogen‐directed immune responses are less well understood. Here, we have reviewed the existing evidence that allergies result in impaired innate immunity and we discuss recent observations that may explain why and how innate immunity is dysfunctional in allergic patients. With a focus on atopic dermatitis as a model of allergic disease, we speculate that one of the key features of allergic conditions, namely Th2 polarization, leads to several independent inhibitory effects on host defence and consequently to a higher risk of infections in allergic patients. A better understanding of impaired host defence and its mechanisms in allergic subjects will help to improve the management of these diseases.

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“…The majority of AD patients show superficial skin colonization by Staphylococcus aureus and increased expression of T helper type 2 (Th2) cytokines such as interleukin (IL)-4, IL-5 and IL-13 in their peripheral blood mononuclear cells (1). S. aureus can be isolated from 96-100% of skin lesions of AD patients, whereas only 0-10% of healthy individuals show skin colonization by this organism (2,3). We have also found that the incidence of S. aureus detection in the lesioned skin of AD patients is higher than that in non-lesioned skin, and that the S. aureus bacterial cell count in lesioned skin is significantly higher than that in non-lesioned skin (3).…”

Section: Introductionmentioning

confidence: 99%

Effects of Macrolide Antibiotics on Th1 Cell and Th2 Cell Development Mediated by Langerhans Cells

2016

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-Background:It is well known that Langerhans cells (LCs) work as the primary orchestrators in the polarization of the immune milieu towards a T helper type 1 (Th1) or a Th2 immune response. In this study, we investigated the effects of macrolide antibiotics on Th1 cell and Th2 cell development mediated by LCs. Methods: LC-like dendritic cells (LDCs) were generated from mouse bone marrow cells and used as substitutes for LCs. Mice were primed with ovalbumin (OVA) peptide-pulsed LDCs, which had been treated with each macrolide antibiotic, via the hind footpad. After 5 days, the cytokine response in the popliteal lymph nodes was investigated by enzyme-linked immunosorbent assay. The expression of cell surface molecules on LDCs was investigated using reverse transcriptase polymerase chain reaction. Results: Injection of OVA peptide-pulsed LDCs, which had been treated with josamycin or spiramycin, inhibited Th2 cell development as represented by down-regulation of interleukin (IL)-4 production as well as Th1 cell development as represented by downregulation of interferon (IFN)- production. This inhibition of Th1 cell and Th2 cell development was associated with suppression of CD86 and T-cell immunoglobulin and mucin domain-containing protein (TIM)-4 expression, respectively, in LDCs. Furthermore, Staphylococcus aureus strains isolated from skin lesions of patients with atopic dermatitis (AD) were more susceptible to josamycin than to spiramycin. Conclusions: These results suggest that topical application of josamycin to AD lesions colonized with S. aureus would be beneficial for control of AD by acting on both superficial S. aureus and epidermal LCs, and inhibiting the development of Th2 cells.

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Persistent skin colonization with Staphylococcus aureus in atopic dermatitis: relationship to clinical and immunological parameters

Abstract: Patients with AD differ in the ability to clear S. aureus from the skin during anti-inflammatory treatment, which appears to be related to the abnormalities in immunological parameters. Local antibiotic therapy should be considered only in patients with persistent S. aureus colonization.

Cited by 128 publications

References 37 publications

Bacterial superantigen facilitates epithelial presentation of allergen to T helper 2 cells

Bacterial superantigen facilitates epithelial presentation of allergen to T helper 2 cells

Does allergy impair innate immunity? Leads and lessons from atopic dermatitis

Effects of Macrolide Antibiotics on Th1 Cell and Th2 Cell Development Mediated by Langerhans Cells

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