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Microbial Balance in Skin and Atopic Dermatitis

Microbial balance and chronic skin inflammation in atopic dermatitis

Microbe communities on the skin and chronic skin inflammation
Microbe communities on the skin and chronic skin inflammation

Microbial Balance in Skin and Atopic Dermatitis

In the realm of dermatology, the microbiome - the community of microorganisms living on our skin - plays a crucial role in the development and severity of eczema, particularly atopic dermatitis.

One specific group of bacteria, Staphylococcus, is often found at higher levels on the skin of people with eczema. This overgrowth of Staphylococcus aureus (S. aureus) leads to a disruption of the skin barrier, triggering inflammatory immune responses and promoting secondary infections.

The impaired skin barrier function in eczema creates a favorable environment for S. aureus colonization. With increased skin pH and reduced antimicrobial peptides like defensins, S. aureus thrives, producing toxins and biofilms that damage the skin further. These toxins, such as α-toxin and δ-toxin, activate a Th2-mediated immune response involving cytokines IL-4 and IL-13, exacerbating skin barrier damage and worsening eczema severity.

Patients with eczema have much higher rates of S. aureus colonization (~90%) compared to healthy individuals (~5%), and colonization correlates strongly with more severe disease. S. aureus enterotoxins act as superantigens, stimulating local skin inflammation and allergic sensitization, increasing the risk of other allergic conditions like food allergies and asthma.

Overgrowth of S. aureus increases the risk of secondary bacterial infections (impetigo, cellulitis) and complicates eczema management. Treatments targeting reduction of S. aureus skin colonization, such as topical antibiotics or dilute bleach baths, help decrease infection risk and inflammation.

The interplay between microbial dysbiosis, barrier dysfunction, and immune activation creates a pathological loop in which S. aureus overgrowth drives eczema worsening and poor barrier repair.

Improvements in eczema symptoms following treatment are often followed by a decrease in the abundance of S. aureus on the skin. However, managing S. aureus colonization is not without challenges. The concept of a 'healthy skin microbiome' is not clearly defined, and the effectiveness of treatments like dilute bleach baths has been called into question.

A new approach to treating eczema, bacteriotherapy, or the replacement of beneficial bacteria, is currently in the clinical trial stage. Preliminary results have been mixed, with some showing improvement and others not.

In people with eczema, S. aureus density was higher on lesions than on skin without lesions and was found to be significantly linked to the severity of eczema symptoms. Overgrowth of S. aureus and other bacterial species can lead to reductions in the amount of commensal bacterial species and lower microbial diversity.

Despite these challenges, understanding the role of S. aureus in eczema development and severity is a significant step towards developing targeted treatments and improving the quality of life for those affected by this condition. In addition to managing S. aureus colonization, using emollients and treating skin inflammation is generally recommended for people with eczema to help repair the skin barrier.

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