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The role of skin commensal Micrococcus luteus in immune signaling and skin health

Award Number: K99AR087549
ORGANIZATION: NATIONAL INSTITUTE OF ARTHRITIS & MUSCULOSKELETAL & SKIN DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP
PERIOD OF PERFORMANCE START DATE: 07/02/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2028

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The role of skin commensal Micrococcus luteus in immune signaling and skin health - 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.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $101,414 )
2026	2026	THE REGENTS OF THE UNIVERSITY OF COLORADO	13001 E 17TH PL STE F428	AURORA	CO	80045	ADAMS	USA	Arthritis, Musculoskeletal and Skin Diseases Research	000	1	7/2/2026	NEW	$101,414
														Subtotal = $101,414

Grand Total All Awards = $101,414

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The role of skin commensal Micrococcus luteus in immune signaling and skin health

Award Number: K99AR087549

ORGANIZATION: NATIONAL INSTITUTE OF ARTHRITIS & MUSCULOSKELETAL & SKIN DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP

PERIOD OF PERFORMANCE START DATE: 07/02/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2028

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