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Abstract
The skin functions as a physical barrier against entry of pathogens while concomitantly supporting a myriad of commensal organisms. The characterization of these microbial communities has enhanced our knowledge of the ecology of organisms present in normal skin, and studies have begun to illuminate the intimate relationship between the host and resident microbes. The cutaneous innate and adaptive immune responses can modulate skin microbiota, while simultaneously, the microbiota educates the host immune system. A crucial element of the innate immune response is mast cells, which reside strategically in tissues that are commonly exposed to the external environment, such as the skin and mucosae. Mast cells are present on the frontline of defense against pathogens, suggesting they may play an important role in fostering the host-microbiota relationship. In this review, we highlight findings regarding the interaction between skin microbiota and mast cells and the resulting outcomes in skin homeostasis.
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Figure 1.
The network in skin microbiome and mast cells. S. epidermidis-derived LTA reinforces the clearance of virus (e.g., vaccinia virus) by increasing antimicrobial peptide, cathelicidin, in mast cells. LTA also promote mast cell maturation by triggering SCF in KC. S. aureus derived peptidoglycan can stimulate KC to produce TGF-β which lead to mast cells recruitment to the dermis in atopic dermatitis. The other byproduct of S. aureus, δ-toxin directly induce mast cells degranulation in the pathogenesis of atopic dermatitis. Phenol-soluble modulins produced by S. epidermidis can selectively inhibit S. aureus. The lipophilic yeast, Malassezia sympodialis can activate mast cells and exacerbate the inflammatory response in atopic dermatitis. C. albicans is frequently presented in psoriasis patients and correlate with disease severity. Mast cells produce cytokines, chemokine, and ROS in response to C. albicans. LTA, lipoteichoic acid; KC, keratinocytes; SCF, stem cell factor; TGF-β, transforming growth factor beta
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