This episode features Dr. Nathan Archer PhD from Johns Hopkins Medicine (USA), speaking about the skin microbiome and particular microorganisms that cause inflammation. The skin is a dynamic organ with the main functions of keeping moisture in and keeping the environment out. Overall, the skin environment is not very welcoming to microorganisms but some have adapted to thrive in the low pH environment. His research has found that certain bacteria that are normally considered commensals can become pathogenic when they start producing specific proteases that instigate inflammation on the skin. Acute inflammation that removes a bacterial exposure from the skin is beneficial, but chronic inflammation can be a major problem. Staphylococcus aureus is a bacterium that predominates in many inflammatory skin diseases and benefits from an inflammatory environment and disruption in the skin barrier; in turn, S. aureus is proinflammatory and uses proteases to drive skin inflammation. His lab is interested in understanding the connection between skin microorganisms and the ‘atopic march’ (progression of allergic diseases, including atopic dermatitis, through infancy and childhood). They found that S. aureus on the skin can exacerbate allergic reactions in the lungs, driving hard-to-treat neutrophilic asthma. His group is contributing to several strategies for preventing / treating skin and allergic diseases, including a vaccine for S. aureus; so far, vaccines against this bacterium have not succeeded because S. aureus has so many tools for avoiding human immune responses. However, a multivalent vaccine targeting multiple toxins that affect the immune system is currently being developed and is in Phase 1 clinical trials.
Episode abbreviations and links:
Paper on the contribution of microorganisms to normal skin function: Commensal Staphylococcus epidermidis contributes to skin barrier homeostasis by generating protective ceramidesResearch on the mechanisms of how S. aureus triggers skin inflammation: Staphylococcus aureus proteases trigger eosinophil-mediated skin inflammationStudy on the mechanisms by which S. aureus causes epithelial barrier damage: Quorum sensing between bacterial species on the skin protects against epidermal injury in atopic dermatitisReview article on how S. aureus contributes to skin inflammation: Staphylococcus aureus Proteases: Orchestrators of Skin InflammationConnection of skin microbes to allergic diseases: Epicutaneous Staphylococcus aureus initiates cross-tissue IL-36R signaling for neutrophilic lung inflammation in a model of the atopic marchTreatment approach for atopic dermatitis: Development of a human skin commensal microbe for bacteriotherapy of atopic dermatitis and use in a phase 1 randomized clinical trialAbout Dr. Nathan Archer PhD:
Dr. Nathan Archer is an Associate Professor at the Johns Hopkins School of Medicine Department of Dermatology. Dr. Archer’s research involves uncovering how skin microbes, especially the major human pathogen Staphylococcus aureus, exacerbate inflammatory skin diseases such atopic dermatitis as well as how host immunity protects against bacterial skin infections. His work involves the incorporation of immunological and “omic” approaches with preclinical models and clinical samples to reveal mechanistic insights with translational relevance to human disease. His long-term research goals are to develop novel host-directed therapies for the treatment of inflammatory skin disorders and skin infections. Dr. Archer has received funding from the NIH as well as from foundation and industry sources, including the Dermatology Foundation, LEO Foundation, and Pfizer. He has been an invited speaker at numerous international and national conferences with a focus on dermatology, immunology, and microbiology.