scholarly journals The Role of Immune Defects and Colonization ofStaphylococcus aureusin the Pathogenesis of Atopic Dermatitis

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Danuta Nowicka ◽  
Ewelina Grywalska

Atopic dermatitis (AD) is a condition with a complex and not fully understood etiology. In patients with AD, acute skin lesions are colonized by a greater number ofStaphylococcus aureus(S. aureus) bacteria than chronic lesions, clinically unchanged atopic skin, or the skin of healthy people. Mechanisms promoting skin colonization byS. aureusinclude complex interactions among several factors. Apart from increased adhesion ofS. aureusin atopic skin, defects of the innate immune response resulting in the lack of restriction of the growth of microorganisms also contribute to susceptibility to colonization by and infection withS. aureus. A deficiency in the endogenous antimicrobial peptides may be partly responsible for the susceptibility to colonization by and skin infection withS. aureusin patients with AD. Majority of isolatedS. aureusstains are able to produce exotoxins, which act as superantigens. Moreover, anti-S. aureus-specific IgE was identified and measured in patients with AD, revealing that its level corresponds to the severity of the disease. This review of the literature attempts to identify factors that are involved in the pathogenesis of AD-relatedS. aureusskin colonization. In the light of presented mechanisms, a reduction of colonization may become both causative and symptomatic treatment in AD.

Pathogens ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 71
Author(s):  
Danuta Nowicka ◽  
Karolina Chilicka ◽  
Iwona Dzieńdziora-Urbińska

Atopic dermatitis (AD) is a condition with a complex and unclear aetiology. Possible causes of AD encompass alterations in the structure and function of the epidermal barrier, disturbances in the skin microbiome, immune factors, allergens, bacterial and fungal infections as well as environmental and genetic factors. In patients with AD, acute skin lesions are colonized by a greater number of bacteria and fungi than chronic lesions, clinically unchanged atopic skin and the skin of healthy people. Mechanisms promoting skin colonization by pathogens include complex interplay among several factors. Apart from disturbances of the skin microbiome, increased adhesion in atopic skin, defects of innate immune response resulting in the lack of or restriction of growth of microorganisms also contribute to susceptibility to the skin colonization of and infections, especially with Staphylococcus aureus. This review of the literature attempts to identify factors that are involved in the pathogenesis of AD-related bacterial and fungal skin colonization. Studies on the microbiome, commensal microorganisms and the role of skin microorganisms in maintaining healthy skin bring additional insight into the treatment and prevention of AD. In the light of presented mechanisms, reduction in colonization may become both causative and symptomatic treatment in AD.


Author(s):  
Galina I. Smirnova

There are presented modern data describing the current understanding of the pathogenesis of atopic dermatitis (AD): a genetic predisposition to atopy, disruptions of epidermal barrier integrity and a cascade of immune responses, contributing allergic inflammation in the skin. There are both described several mechanisms of acute and chronic phases of AD, the main directions of pathogenetically substantiated treatment of AD in children and indicated the prospects of new preparations specific blockers of proinflammatory cytokines involved in the development of AD - crisaborole, apremilast, dupilumab, lebrikizumab, tralokinumab, tezepelumab. There is especially presented in details external therapy of atopic skin lesions in children with the use of means of modern dermatological cosmetics.


Biomolecules ◽  
2019 ◽  
Vol 9 (11) ◽  
pp. 697 ◽  
Author(s):  
Tae-Young Kim ◽  
No-June Park ◽  
Jonghwan Jegal ◽  
Sangho Choi ◽  
Sang Woo Lee ◽  
...  

Plants of the genus Wikstroemia have long been used as traditional medicines to treat diseases like pneumonia, rheumatism, and bronchitis. This study was designed to determine the effect of chamaejasmine, a biflavonoid present in W. dolichantha, on atopic dermatitis (AD)-like skin lesions in a 2,4-dinitrochlorobenzene (DNCB)-induced murine model of AD. Initially, we examined the anti-allergic activities of ten flavonoids from W. dolichantha by measuring β-hexosaminidase release from RBL-2H3 cells. Subsequently, an SKH-1 hairless mouse model of AD was developed based on the topical application of DNCB. Chamaejasmine (0.5%) or pimecrolimus (1%, positive control) were applied to dorsal skins of DNCB-sensitized AD mice for two weeks. Serum IL-4 and IgE levels were determined using enzyme-linked immunosorbent assay kits and transepidermal water loss (TEWL) and skin hydration were measured using a Tewameter TM210 and a SKIN-O-MAT, respectively. Of the ten flavonoids isolated from W. dolichantha, chamaejasmine most potently inhibited DNP-specific IgE-induced degranulation in RBL-2H3 cells. Topical administration of chamaejasmine attenuated the clinical symptoms of DNCB-induced dermatitis (i.e., itching, dryness, erythema, and edema). Histological analyses demonstrated that dermal thickness and mast cell infiltration in dermis were significantly reduced by chamaejasmine. In addition, 0.5% chamaejasmine inhibited DNCB-induced increases in total IL-4 and IgE levels in serum, improved skin barrier function, and increased epidermis moisture. Our findings suggest chamaejasmine might be an effective therapeutic agent for the treatment of atopic diseases.


2017 ◽  
Vol 14 (4-5) ◽  
pp. 30-39
Author(s):  
G I Smirnova

Modern data describing the current understanding of the pathogenesis of atopic dermatitis (AD): a genetic predisposition to atopy, disturbances of the intestinal microbiome, disruptions of epidermal barrier integrity and a cascade of immune responses, contributing allergic inflammation in the skin are presented. There are both described several mechanisms of acute and chronic phases of AD, the main directions of pathogenetically substantiated treatment of AD in children and indicated the prospects of new preparations specific blockers of proinflammatory cytokines involved in the development of AD - crisaborole, dupilumab, apremilast et al. External therapy of atopic skin lesions in AD children with modern dermatological cosmetics is presented.


Author(s):  
Suna Asilsoy ◽  
Serdar Al

Atopic dermatitis (AD) is a chronic skin disease caused by genetic and environmental factors. Often it begins in early childhood. It is located at the first step of the process we refer to as atopic march. This feature is a precursor of the development of other allergic diseases such as asthma and allergic rhinitis. Especially in patients with atopy of food and inhalant allergens, the occurrence of other atopic diseases is more common. Although the role of these sensitivities in AD is controversial, it has been determined that some patients may trigger eczematous skin lesions. In this report, the role of allergens in atopic dermatitis are reviewed in the light of current literature.


Dermatitis ◽  
2008 ◽  
Vol 19 (4) ◽  
pp. 218-238
Author(s):  
T. Uenishi ◽  
H. Sugiura ◽  
T. Tanaka ◽  
M. Uehara

2016 ◽  
Vol 65 (3) ◽  
pp. 253-259 ◽  
Author(s):  
Jacek Międzobrodzki

Staphylococcus aureus colonizes the mucous membrane of the nasal vestibule of a significant number of healthy people. These microorganisms are opportunistic pathogens, that in favorable conditions, may cause infections of various course, location or manifestation. Secondary infections emerge in cases when other risk factors contribute to such a change. One of the diseases during which S. aureus changes its saprophytic character to a pathogenic one is atopic dermatitis (AD), an allergic skin condition of a chronic and recurrent nature. Patients with AD are highly predisposed to secondary staphylococcal infections due to active S. aureus colonization of the stratum corneum, damage of the skin barrier or a defective immune response. Microorganisms present in skin lesions destroy the tissue by secreting enzymes and toxins, and additionally stimulate secondary allergic reactions. The toxins secreted by strains of S. aureus also act as superantigens and penetrate the skin barrier contributing to a chronic inflammation of the atopic skin lesions. The S. aureus species also releases proinflammatory proteins, including enzymes that cause tissue damage. When initiating treatment it is particularly important to properly assess that the onset of the secondary bacterial infection is caused by S. aureus and thus justifying the inclusion of antibiotic therapy. Depending on the severity and extent of the staphylococcal infection, topical antibiotics are used, usually mupirocin or fusidic acid, or general antibiotic treatment is introduced. Another therapeutic strategy without antibiotics has given a positive effect in patients.


2018 ◽  
Vol 9 (4) ◽  
pp. 643-652 ◽  
Author(s):  
T. Kawahara ◽  
N. Hanzawa ◽  
M. Sugiyama

Lactobacillus strains, a major group of lactic acid bacteria, are representative food microorganisms that have many potential beneficial effects via their interactions with immune and intestinal epithelial cells. However, little is known about the effect of Lactobacillus strains on atopic dermatitis via keratinocytes, which comprise the physical barrier of the skin. In this study, we report that Lactobacillus strains have a significant suppressive effect on tumour necrosis factor (TNF)-α-induced expression and production of thymus and activation-regulated chemokine (TARC), a T helper 2 cell chemokine responsible for atopic dermatitis, in human keratinocytes. An RNA interference study showed that the effect of Lactobacillus reuteri strain Japan Collection of Microorganisms (JCM) 1112, the most suppressive strain, depended on the presence of Toll-like receptor 2 and the induction of A20 (also known as TNF-α-induced protein 3) and cylindromatosis in HaCaT cells. Topical application of a water-soluble extract of homogenised JCM 1112 cells significantly suppressed the development of house dust mite-induced atopic skin lesions and TARC expression at the lesion sites in NC/Nga mice. Our study provides new insights into the use of Lactobacillus strains as suppressive agents against keratinocyte-involved atopic inflammation of the skin.


2020 ◽  
Vol 1 (1) ◽  
pp. 25-30
Author(s):  
Febrina Andarini ◽  
Nopriyati ◽  
Sarah Diba

The Human epithelium, including the epidermis produces antimicrobial peptide (AMP)as part of innate immunity. Cathelicidin and human β-defensins are the most AMPfound on the skin. This antimicrobial peptide has a role in the response of the naturalimmune system by becoming the front line of the defense system against infection. Thediscussion of this literature review will focus on cathelicidin and human β-defensin-1which are the main AMPs that affect atopic dermatitis and psoriasis. Antimicrobialpeptides are excessively produced in lesional psoriatic scales or rosacea in contrast tothe atopic skin that shows lower AMP levels when compared with psoriasis. Despitethe impaired skin barrier which facilitates potentially pathogenic microbes to colonizethe epidermis, patients with psoriasis surprisingly present a low frequency of skininfections, whereas patients with atopic dermatitis are predominantly susceptible toparticular cutaneous bacterial, fungal and viral infections. One possible explanation ofthe fact is the difference in the expression of AMPs. DA patients have fewer AMPexpression characteristics, especially cathelicidins LL-37 and HBD-2. Research onantimicrobial use can help reduce pathogen colonization so that clinical improvementof AD occurs. In the case of psoriasis, AMP expression increases, especially LL-37 andHBD-2, showing synergistic antimicrobial activity that is effective in eradicatingmicrobial colonization, so there is no strong evidence to support antibiotic use intreating psoriasis or in preventing disease.


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