Atopic dermatitis in adults: evaluation of peripheral blood mononuclear cells proliferation response to <i>Staphylococcus aureus</i> enterotoxins A and B and analysis of interleukin‐18 secretion

Orfali, Raquel Leão; Sato, Maria Notomi; Takaoka, Roberto; Azor, Mayce Helena; Rivitti, Evandro A.; Hanifin, Jon M.; Aoki, Valéria

doi:10.1111/j.1600-0625.2009.00842.x

Cited by 29 publications

(19 citation statements)

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“…19 It was demonstrated enhanced levels of IL-18 both in sera and culture supernatants under staphylococcal enterotoxin A stimuli in AD patients. 44 …”

Section: Pattern Recognition Receptors (Prr)mentioning

confidence: 99%

Skin barrier in atopic dermatitis: beyond filaggrin

Zaniboni

Samorano

Orfali

et al. 2016

An. Bras. Dermatol.

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Atopic dermatitis is a chronic inflammatory skin disease with a complex pathogenesis, where changes in skin barrier and imbalance of the immune system are relevant factors. The skin forms a mechanic and immune barrier, regulating water loss from the internal to the external environment, and protecting the individual from external aggressions, such as microorganisms, ultraviolet radiation and physical trauma. Main components of the skin barrier are located in the outer layers of the epidermis (such as filaggrin), the proteins that form the tight junction (TJ) and components of the innate immune system. Recent data involving skin barrier reveal new information regarding its structure and its role in the mechanic-immunological defense; atopic dermatitis (AD) is an example of a disease related to dysfunctions associated with this complex.

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“…19 It was demonstrated enhanced levels of IL-18 both in sera and culture supernatants under staphylococcal enterotoxin A stimuli in AD patients. 44 …”

Section: Pattern Recognition Receptors (Prr)mentioning

confidence: 99%

Skin barrier in atopic dermatitis: beyond filaggrin

Zaniboni

Samorano

Orfali

et al. 2016

An. Bras. Dermatol.

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“…When analyzing the role of S. aureus in AE, several factors have to be taken into account. First, there seem to be crucial factors for a preferential adherence and a continuous colonization on atopic skin (6); second, defense factors are impaired in atopic individuals including diminished defensin expression and polymorphisms in pattern recognition receptors (7–9); third, there is a preferential induction of IgE antibodies against staphylococcal components in atopic patients leading to aggravation of clinical symptoms (10); and fourth, many of the strains isolated from AE are producers of superantigens, which continuously stimulate the host immune system and thereby contribute as a distinct risk factor for the chronification and exacerbation of skin symptoms (11–13).…”

Section: Introductionmentioning

confidence: 99%

TNF receptor I on human keratinocytes is a binding partner for staphylococcal protein A resulting in the activation of NF kappa B, AP-1, and downstream gene transcription

Claßen

Kalali

Schnopp

et al. 2010

Experimental Dermatology

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Primary human keratinocytes and immortalized HaCaT cells were analysed for their capacity to bind purified staphylococcal protein A (SpA). Co-incubation with FITC-labelled SpA led to a dose-depending attachment. Pull-down experiments with cellular extracts revealed the TNFα receptor I (TNF RI) as binding partner on keratinocytes. Thus, we next looked for expression of this receptor in human epidermis and cultured keratinocytes. TNF RI is strongly expressed on all keratinocytes analysed, both at the mRNA and protein level and activation by SpA at optimal doses of 50-100 μg/ml resulted in the phosphorylation of the TNF RI downstream kinases MEK1/2, JNK1/2, and p38 subsequently leading to translocation of the p65 NF kappa B subunit and AP-1 into the nucleus. This translocation was then followed by increased expression of IL-8 and COX-2, two known NF kappa B-induced pro-inflammatory genes. To further test the relevance of our findings, we analysed in vitro production of over 100 strains isolated from atopic eczema showing that more than 85% of the tested strains produced extracellular SpA in substantial amounts. Thus, besides superantigens, haemolysins, and other cell wall components, Staphylococcus aureus exerts pro-inflammatory stimuli on human keratinocytes through the production of SpA signalling through TNF RI.

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“…Early recognition of their characteristic as superantigens promoted theoretical considerations that these microbial contaminants might contribute to the underlying causes of self-reactive autoimmune disease due to the nature of the interaction between the microbial superantigen and host cells [1,2]. The SEs have since been implicated in the induction of several human autoimmune exacerbations that include allergic airway disease [3,4], atopic dermatitis [5,6], inflammatory arthritic conditions [3], and colitis [7]. Indeed, patients exhibiting dust mite-induced allergic rhinitis or asthma demonstrate significant levels of IgE antibodies to SEA, SEB, and SEC [8] as well as elevated levels of serum eosinophil cationic protein, an indicator of asthma and rhinitis.…”

Section: The Staphylococcal Enterotoxins and Diseasementioning

confidence: 99%

Staphylococcal enterotoxins in the Etiopathogenesis of Mucosal Autoimmunity within the Gastrointestinal Tract

Principato

Qian

2014

Toxins

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The staphylococcal enterotoxins (SEs) are the products of Staphylococcus aureus and are recognized as the causative agents of classical food poisoning in humans following the consumption of contaminated food. While illness evoked by ingestion of the SE or its producer organism in tainted food are often self-limited, our current understanding regarding the evolution of S. aureus provokes the utmost concern. The organism and its associated toxins, has been implicated in a wide variety of disease states including infections of the skin, heart, sinuses, inflammatory gastrointestinal disease, toxic shock, and Sudden Infant Death Syndrome. The intricate relationship between the various subsets of immunocompetent T cells and accessory cells and the ingested material found within the gastrointestinal tract present daunting challenges to the maintenance of immunologic homeostasis. Dysregulation of the intricate balances within this environment has the potential for extreme consequences within the host, some of which are long-lived. The focus of this review is to evaluate the relevance of staphylococcal enterotoxin in the context of mucosal immunity, and the underlying mechanisms that contribute to the pathogenesis of gastrointestinal autoimmune disease.

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Atopic dermatitis in adults: evaluation of peripheral blood mononuclear cells proliferation response to Staphylococcus aureus enterotoxins A and B and analysis of interleukin‐18 secretion

Cited by 29 publications

References 47 publications

Skin barrier in atopic dermatitis: beyond filaggrin

Skin barrier in atopic dermatitis: beyond filaggrin

TNF receptor I on human keratinocytes is a binding partner for staphylococcal protein A resulting in the activation of NF kappa B, AP-1, and downstream gene transcription

Staphylococcal enterotoxins in the Etiopathogenesis of Mucosal Autoimmunity within the Gastrointestinal Tract

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