Amazing stuff!
"... Now, new experiments in mice have revealed that stress makes it harder for certain skin cells to fight off bacteria—leaving the animals vulnerable to more severe infection with Staphylococcus aureus.
To induce stress, scientists confined the mice inside small tubes for three hours a day on three consecutive days, exposing them to S. aureus upon release. The restrained rodents produced more adrenaline, leading to higher levels of a stress-related protein called TGFβ. This protein interferes with specialized skin cells known as dermal fibroblasts and prevents them from making cathelicidin—an antimicrobial molecule that normally plays a key role in the skin’s defense system. As a result, the restrained mice ended up experiencing more severe infections, characterized by larger lesions. Blocking adrenaline or TGFβ, meanwhile, allowed the animals’ skin cells to mount a stronger defense against the bacteria."
From the editor's summary and abstract:
"Editor’s summary
Psychological stress affects multiple systems in mammals and is linked with greater susceptibility to bacterial infections. Chan et al. used a mouse model to show that psychological stress causes an impaired response to Staphylococcus aureus infection.
The defective response was associated with decreased dermal adipogenesis by fibroblasts and decreased production of the antimicrobial peptide cathelicidin (Camp) by these cells, thus enhancing susceptibility to S. aureus.
This brain-skin axis triggered by stress was mediated by adrenergic signaling and the production of TGFβ. These were critical for infection given that inhibiting adrenergic or TGFβ signaling restored normal host defense to S. aureus in stressed mice. ...
Abstract
Infections after psychological stress are a major health care problem.
Single-cell transcriptomics and lipidomic profiling in a mouse model of stress show that dermal fibroblasts undergoing adipogenesis have defective responses to Staphylococcus aureus skin infection.
Adrenalectomy or adrenergic inhibition restores the fibroblast adipogenic response to S. aureus and enables mice to effectively resist infection during stress. Increased susceptibility to S. aureus from stress is attributed to suppression of the antimicrobial peptide cathelicidin (Camp) because adrenaline directly inhibits Camp production by fibroblasts, and mice lacking Camp in fibroblasts do not increase infection after stress.
Transforming growth factor β (TGFβ) is induced by stress and adrenergic signaling, and inhibition of TGFβ or deletion of the TGFβ receptor on fibroblasts increases Camp expression and restores protection against infection.
Together, these data show that stress initiates a brain-skin axis mediated by TGFβ that impairs the immune defense function of dermal fibroblasts to produce the Camp antimicrobial peptide."
Psychological stress increases skin infection through the action of TGFβ to suppress immune-acting fibroblasts (open access)
Fig. 1. Psychological stress exacerbates skin infection by SA [Staphylococcus aureus].
No comments:
Post a Comment