Résumé
The microbiome consists of a diverse array of commensal microorganisms that reside at barrier sites of the human body and promote local immune homeostasis. While recent work has demonstrated that intestinal commensals can influence immunity throughout the body, the distal effects of other microbial communities have not been fully explored. Here we show that application of distinct human commensals to the skin of mice induces the accumulation of IL-17A-producing T cells in the lungs. The induction of these cells occurs in a manner that is partially dependent on both antigen presentation and IL-23 signaling. Response kinetics and adoptive transfer experiments suggest that the T cells migrate from the skin-draining lymph nodes, while transcriptional analysis has identified specific chemokine receptors that may facilitate trafficking to the lungs. Furthermore, in the context of pulmonary infection, cutaneous application of commensals promotes the production of IL-17A and recruitment of neutrophils to the lungs. This work demonstrates that the skin microbiome can enhance pulmonary immunity, but also has the potential to exacerbate inflammation through the production of IL-17A, thus providing a possible mechanism for why children with atopic dermatitis have an increased propensity to develop asthma, a progression commonly referred to as the “atopic march.”