Epithelial–immune crosstalk with the skin microbiota in homeostasis and atopic dermatitis – a mini review

Abstract

The skin is a complex and dynamic ecosystem, wherein epithelial cells, immune cells and the skin microbiota actively interact and maintain barrier integrity and functional immunity. Skin microbes actively tune the functions of the resident immune cells. Dysbiosis – alterations in the resident microbiota – leads to the dysregulation of host immunity. Microbiome analyses in humans and dogs with atopic dermatitis (AD) have shown shifts in microbial diversity, and in particular, an increased proportion of staphylococci. Monogenic diseases that manifest AD‐like symptoms provide insights into the pathogenesis of AD and the mechanisms of dysbiosis, from both the epithelial and immunological perspectives. The symbiotic relationships between the host and microbiota must be maintained constitutively. Detailed mechanisms of how host immunity regulates commensal bacteria in the steady state have been reported. The skin harbours multiple tissue‐resident immune cells, including both innate and adaptive immune cells. Recent studies have highlighted the fundamental role of innate lymphoid cells (ILCs) in the maintenance of barrier functions and tissue homeostasis. ILCs directly respond to tissue‐derived signals and are instrumental in barrier immunity. Epithelial cells produce alarmins such as thymic stromal lymphopoietin (TSLP) and interleukins (IL)‐33 and IL‐25, all of which activate group 2 ILCs (ILC2s), which produce type 2 cytokines, such as IL‐5 and IL‐13, boosting type 2 immune reactions. Dysregulation of the epithelial–ILC crosstalk results in allergic inflammation. This review highlights our understanding of the active interactions between the host epithelial and immune cells, and microbiota, providing a foundation for novel therapeutic strategies for inflammatory skin diseases.

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“…4e ). In particular, Staphylococcus correlates closely to FLG , SPINK5 , and DSG1 , all of which are related with epithelial barriers (stratum corneum and junctional barriers) 38 . Also, microbes belong to Carnobacteriaceae , Lactobacillaceae , Nanosynbacteraceae , and Weeksellaceae families showed high correlation with both barrier and immune genes ( CDSN, DSP, DSG1, SPINK5, FLG , and JAK1 ), whereas common skin microbes from Dermatophilaceae and Dermabacteraceae families showed no correlation.…”

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“…Influences include disease status, inflammation, household, sex, body site and breed. There is likely to be mutual interaction between skin barrier function, cutaneous immunity and the microbiome 26 . Loss of diversity leads to staphylococcal, Malassezia and Pseudomonas spp.…”

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“…Obesity, diabetes mellitus, cancer, cardiovascular diseases and neuroinflammatory disorders (like, for example, neuropathic pain and depression) are just a few examples of human and pet diseases with clear differences in fecal bacterial composition compared to healthy conditions [37,[50][51][52][53][54][55]. Not to mention that aside from the gut microbiome, the skin and oral microbiome are becoming increasingly involved in other human and pet disorders, such as atopic dermatitis [56,57] and periodontal diseases [58,59].…”