Аннотация:Neurohormones diffuse in sweat and epidermis leading skin bacterial microflora to be
largely exposed to these host factors. Bacteria can sense a multitude of neurohormones,
but their role in skin homeostasis was only investigated recently. The first study focused on
substance P (SP), a neuropeptide produced in abundance by skin nerve terminals. SP is
without effect on the growth of Gram-positive (Bacillus cereus, Staphylococcus aureus,
and Staphylococcus epidermidis) and Gram-negative (Pseudomonas fluorescens)
bacteria. However, SP is stimulating the virulence of Bacillus and Staphylococci. The
action of SP is highly specific with a threshold below the nanomolar level. Mechanisms
involved in the response to SP are different between bacteria although they are all
leading to increased adhesion and/or virulence. The moonlighting protein EfTu was
identified as the SP-binding site in B. cereus and Staphylococci. In skin nerve terminals,
SP is co-secreted with the calcitonin gene-related peptide (CGRP), which was shown to
modulate the virulence of S. epidermidis. This effect is antagonized by SP. Identification of
the CGRP sensor, DnaK, allowed understanding this phenomenon as EfTu and DnaK are
apparently exported from the bacterium through a common system before acting as SP
and CGRP sensors. Many other neuropeptides are expressed in skin, and their potential
effects on skin bacteria remain to be investigated. Integration of these host signals by the
cutaneous microbiota now appears as a key parameter in skin homeostasis.
Keywords: skin bacterial communication, substance P, calcitonin gene-related peptide, DnaK chaperone protein