NIH grant: The role of skin commensal Micrococcus luteus in immune signaling and skin health (1K99AR087549-01)

retained text

NIH grant 1K99AR087549-01: The role of skin commensal Micrococcus luteus in immune signaling and skin health
Institute: {'code': 'AR', 'abbreviation': 'NIAMS', 'name': 'National Institute of Arthritis and Musculoskeletal and Skin Diseases', 'admin_org_id': '12500006', 'admin_funding_url': ''}. PI: Flavia Gisela Costa. Award: $101414.
Start: 2026-07-02T00:00:00.
PROJECT SUMMARY
 The skin is the largest organ of the human body, and host to a complex microbiome. The skin
disease atopic dermatitis (AD), or eczema, affects approximately 10-30% of children and results in skin
damage, infections, itching, and reduced quality of life. AD often precedes other allergic diseases such
as asthma, in a phenomenon termed “the atopic march”. Pathology of AD typically includes stimulation
of T helper 2 (TH2) and T helper 22 (TH22) signaling, skin infections by pathogen Staphylococcus
aureus, and reduction of microbial diversity on the skin. Current FDA-approved treatments include
monoclonal antibodies that target the receptors IL-4R and IL-13R, blocking TH2-mediated signaling.
Additionally, prior work has shown that the skin commensal Staphylococcus epidermidis inhibits S.
aureus virulence and modulates T helper 1 (TH1) inflammatory immune signaling, suggesting that skin
commensals serve a protective role on the skin both by modulating host signaling and inhibiting
pathogen virulence. Understanding the contributions of skin commensals to skin health will be
crucial to identifying treatments and preventative strategies for diseases like AD.
 During my postdoc, I have advanced our understanding of S. aureus colonization of the skin
through development of an in vitro growth model, transcriptional analysis of S. aureus in skin
colonization models, and decoding the mechanism of S. aureus-induced itch. For my future research,
I will study how skin commensals can prevent S. aureus infections and improve skin health. In
support of this work, I have confirmed prior observations that the skin commensal, Micrococcus luteus,
blocks TH2-mediated signaling in skin epithelial cells. Additionally, I have identified an M. luteus strain
encoding an uncharacterized antimicrobial with activity against S. aureus. To demonstrate the role of
M. luteus in skin immune signaling and inhibition of S. aureus, I propose to 1) Identify and characterize
novel antimicrobials produced by M. luteus, and 2) Identify the M. luteus factor that blocks TH2-mediated
signaling in keratinocytes and investigate the mechanism of inhibition. This work will advance our
knowledge of the role of M. luteus on the skin, rely on my expertise in bacterial genetics and
biochemistry, and provide training in immunology and genomic analysis. Additionally, the career
training plan outlined in this proposal will prepare me for a future position at a research-intensive
institution understanding the role of the skin microbiome in skin health to generate new approaches for
AD treatments and other skin disorders.

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