Cutaneous Microbiome Interactions in Chronic Inflammatory Skin Disorders

The skin is more than a barrier — it’s a thriving ecosystem. The cutaneous microbiome, composed of bacteria, fungi, viruses, and mites, plays a crucial role in maintaining skin health, defending against pathogens, and modulating immune responses. Disruption to this delicate microbial balance is increasingly recognised as a contributing factor in chronic inflammatory skin disorders, including atopic dermatitis, psoriasis, rosacea, and seborrhoeic dermatitis.

This article explores how microbial dysbiosis interacts with the skin’s immune system, impacts disease progression, and informs emerging therapeutic approaches.

The Skin Microbiome: A Dynamic Defence System

The healthy skin microbiome consists of diverse microbial communities that vary depending on the site (e.g. moist vs dry), individual genetics, environment, hygiene, and age. Key commensal organisms — such as Staphylococcus epidermidis, Cutibacterium acnes, and Malassezia spp. — help maintain barrier integrity, produce antimicrobial peptides, and communicate with immune cells to maintain tolerance.

When this ecosystem is disrupted (known as dysbiosis), pathogenic microbes may overpopulate, triggering inflammatory cascades, immune hypersensitivity, or barrier dysfunction.

Atopic Dermatitis and Staphylococcus aureus Overgrowth

Perhaps the most well-documented example of microbiome involvement in skin disease is atopic dermatitis (AD). During flare-ups, the abundance of Staphylococcus aureus significantly increases, often dominating the microbiome of lesional skin.

S. aureus exacerbates inflammation by:

• Producing superantigens that activate T-cells
• Releasing proteases that disrupt the epidermal barrier
• Outcompeting beneficial commensals like S. epidermidis

Restoring microbial balance through emollients, bleach baths, or probiotic-based topicals is now considered a key adjunct to standard corticosteroid and immunomodulator therapies.

Psoriasis and Microbial Shift Patterns

Although psoriasis is primarily a Th17/IL-23 driven autoimmune condition, microbial shifts in psoriatic lesions suggest a secondary but significant role of the microbiome. Research has identified decreased levels of Propionibacterium and increased levels of Streptococcus and Corynebacterium in psoriatic plaques.

These organisms may:

• Alter skin lipid metabolism
• Modulate keratinocyte behaviour
• Influence T-cell polarisation via antigen presentation

However, the exact causative versus associative role remains under investigation.

Rosacea, Demodex, and Inflammatory Amplification

Rosacea, particularly the papulopustular subtype, has been linked to increased densities of Demodex folliculorum mites, often accompanied by Bacillus oleronius, a bacterium found within Demodex.

Demodex mites may:

• Physically damage follicular units
• Trigger innate immune responses via TLR2 activation
• Exacerbate vasodilation and inflammatory lesion formation

Targeting Demodex through acaricidal agents like ivermectin has become an effective strategy for rosacea management.

Therapeutic Innovations: From Probiotics to Microbiome Transplants

With the microbiome’s role in skin disease now well established, emerging therapies aim to restore microbial homeostasis rather than merely suppress symptoms.

These include:

• Topical probiotics containing live commensals to compete with pathogens
• Postbiotics (non-living microbial components) to modulate immune signalling
• Prebiotics to promote the growth of beneficial flora
• Bacterial lysates and microbiome transplants (still experimental) for severe or refractory cases

Clinical trials continue to explore the safety, viability, and regulatory framework for these novel treatments.

Conclusion

Chronic inflammatory skin disorders are no longer viewed solely through the lens of immune dysfunction — they are increasingly understood as immune–microbial imbalances. The cutaneous microbiome is both a marker and a modulator of disease, and its manipulation represents a promising frontier in dermatological therapeutics.

Restoring balance, rather than merely eradicating pathogens, may hold the key to long-term remission and skin resilience.