Baby’s skin bacteria: first impressions are long-lasting

The composition and function of skin bacteria and immune cells differ substantially in mammalian neonates versus adults. Although much remains to be understood about early-life skin immunity in humans, this period is demarcated by an increased capacity for tolerogenic function and a layered transition from innate-type lymphocytes to classical memory populations. The ability of microbes to durably tune immune composition or function is often referred to as 'immune imprinting' – this phenomenon is preferentially active early in life and, if missed, some immune education events cannot be reproduced later on. Growing evidence suggests that unique molecular interactions between commensal microbes and cells of the neonatal immune system have the potential to tip the balance between skin health and disease in adult life. Mechanistically, early life bacterial exposure can influence skin immune function via bacteria–bacteria interactions, bacteria–epithelial cell interactions, and/or bacteria–immune cell interactions. Only through separate, dedicated study of skin–bacteria crosstalk in the early developmental window can we understand the biology of pivotal events that impact on host–microbe symbiosis and skin immune function. The safe and successful use of live bacteria or bacteria-derived therapies to promote skin health or treat skin disease relies upon the ability to stably introduce key species and understand their direct and indirect effects on the composition of the skin microbial community. The strategy of targeting skin microbe–immune interactions in early life has the advantage of 'correcting course' before the stable establishment of microbial communities and/or immune cell populations, thereby not only treating but perhaps preventing skin disease. Early life is a dynamic period for skin microbial colonization and immune development. We postulate that microbial exposures in this period durably alter the skin immune trajectory and later disease susceptibility. Bacteria contribute to infant skin immune imprinting via interactions with microbes as well as with cutaneous epithelial and immune cells. Excellent research is underway at the skin microbiome–immune interface, both in deciphering basic mechanisms and implementing their therapeutic applications. As emphasized herein, focusing on the unique opportunities and challenges presented by microbial immune modulation in early life will be important. In our view, only through dedicated study of skin–microbe crosstalk in this developmental window can we elucidate the molecular underpinnings of pivotal events that contribute to sustained host–microbe symbiosis. Early life is a dynamic period for skin microbial colonization and immune development. We postulate that microbial exposures in this period durably alter the skin immune trajectory and later disease susceptibility. Bacteria contribute to infant skin immune imprinting via interactions with microbes as well as with cutaneous epithelial and immune cells. Excellent research is underway at the skin microbiome–immune interface, both in deciphering basic mechanisms and implementing their therapeutic applications. As emphasized herein, focusing on the unique opportunities and challenges presented by microbial immune modulation in early life will be important. In our view, only through dedicated study of skin–microbe crosstalk in this developmental window can we elucidate the molecular underpinnings of pivotal events that contribute to sustained host–microbe symbiosis. bacteria that are commonly found on skin; this group includes genera such as Corynebacterium and Cutibacterium. The prevalence of these bacteria on sebaceous sites such as the face, chest, and back increases during late puberty. a common inflammatory, allergic skin disorder with onset often in early life and that is characterized by flares typified by itching and redness, often associated with increases in S. aureus. a community of microbes that grow on surfaces encased in a tough matrix which is not easily removable from the surface. the outermost layer of the skin that comprises several layers of keratinocytes which terminally differentiate to form the stratum corneum. reversible changes in genetic information that are not encoded in the DNA sequence but are instead mediated by DNA methylation or histone modifications. These types of changes can occur in response to various environmental factors including microbes and alter the function of the cells in which they occur. these reside in the basal layer of the epidermis and the hair follicle bulge region; they help to maintain skin homeostasis and hair regeneration, and participate in repair of the epidermis after injury. bacteria that are commonly found on the skin. They are especially dominant in early life and include genera such as Staphylococcus and Streptococcus. species of microorganisms that establish a niche, early in life, at a given anatomical site in the body, which then influences the future composition of the microbiome at that site. the concept that specific immune interactions (e.g., with microbes) can durably alter the composition and/or function of the immune system in a way that alters subsequent immune responses. This has classically been intertwined with the molecular mechanism of epigenetic modification, but there are examples of imprinting that do not rely on this mechanism. epithelial cells of the skin that form the epidermis, including that portion which lines the hair follicles. molecules that are conserved and expressed across several species of microbes and that are recognized by pattern recognition receptors. the collective microbial composition, including but not restricted to, bacteria, viruses, and fungi, in any given anatomical niche. these are resident mainly in mucosal tissues, have a semi-invariant αβ T cell receptor, and are characterized by their innate-like properties. proteins that recognize and bind to conserved molecular patterns typically expressed by microbes. These proteins generally initiate signal transduction pathways upon binding their cognate molecules. a method of communication between bacteria via secreted molecules that in turn govern gene expression and foster community behavior. In Staphylococcus aureus, the accessory gene regulator (Agr) system is a key regulator of quorum-sensing behavior and related toxin production. a subset of CD4+ T cells defined by the transcription factor FoxP3; they play a key role in suppressing inflammation and preventing autoimmunity. Gram-positive skin bacteria of the Firmicutes phylum; these can asymptomatically colonize nares and skin, but are also a major cause of skin bacterial infections and are associated with flares of atopic dermatitis. one of several coagulase-negative Staphylococcus species that are commonly found on human skin. a subset of CD4+ effector T cells that are traditionally studied for their role in mounting immune responses to fight infection by intracellular pathogens and viruses via the production of IFN-γ. a subset of CD4+ effector T cells that are traditionally studied for their role in mounting immune responses to fight infection by extracellular parasites such as helminths; they are known producers of IL-4, IL-5, and IL-13. Overt production of these cytokines has been associated with allergic immune responses. a subset of CD4+ effector T cells that are deemed to have both protective and pathogenic roles; they are known producers of IL-17A and have a protective role against cutaneous bacterial infections (e.g., S. aureus). Th17-mediated inflammation has also been linked to disease pathology in skin conditions such as psoriasis.