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Investigating Murine Intestinal Helminth Heligmosomoides polygyrus Amelioration of Depigmentation in a Mouse Model of Vitiligo

Award Number: F30AI200413
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 08/12/2026
PERIOD OF PERFORMANCE END DATE: 08/11/2030

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Investigating Murine Intestinal Helminth Heligmosomoides polygyrus Amelioration of Depigmentation in a Mouse Model of Vitiligo - ABSTRACT Vitiligo is an autoimmune disorder characterized by the targeted destruction of skin melanocytes leading to persistent patches of skin depigmentation. A ubiquitous and historical disease, vitiligo produces disfiguring discoloration often seen on the face, neck, hands arms, shoulders, torso, hips, knees, and feet of patients, with serious consequences for quality of life. Treatments for the disease are limited, and there is a large demand for novel therapeutic approaches. Research in animal models and human patients has demonstrated that environmental exposures and illnesses have a significant effect on autoimmune activity in the skin. While the exact triggers for autoimmunity remain unclear, emerging evidence suggested that the intestinal environment (including microbes and parasites) may play an important role in regulating disease activity. To investigate this, we studied the mouse parasite Heligmosomoides polygyrus bakeri in an established mouse model of vitiligo. Surprisingly, we found that the parasite consistently prevented any symptoms of the disease. In preliminary experiments, we discovered that a STAT6 knockout mouse line (incapable of mounting an anti-parasite type 2 immune response) did not alter the parasite’s effect on vitiligo. This meant that H. polygyrus inhibits vitiligo through a previously undiscovered pathway independent of a type 2 response in helminthiasis. I believe that this pathway is mediated either by worm secretions or by parasite-induced changes to the host microbiome. Aim 1 seeks to identify the effects of worm secretions, collectively termed HES, on vitiligo pathogenesis, with a particular focus on a previously-characterized TGF-β mimic known to induce systemic regulatory T cell populations. These regulatory T cells may play an important role in suppressing vitiligo. Aim 2 seeks to characterize the connection between parasite-induced microbiome community alterations and disease progression, exploring microbiome community structure, the consequences of dysbiosis, production of short- chain fatty acids, and impacts on circulating cytokines. Completing this project would lay the groundwork for a novel mechanism for vitiligo treatment, as well as advance our understanding of host-parasite interactions in the context of the gut-immune-skin axis.


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 = $38,312 )
2026	2026	UNIVERSITY OF MASSACHUSETTS MEDICAL SCHOOL	55 LAKE AVE N	WORCESTER	MA	01655	WORCESTER	USA	Allergy and Infectious Diseases Research	000	1	8/10/2026	NEW	$38,312
2026	2026	UNIVERSITY OF MASSACHUSETTS MEDICAL SCHOOL	55 LAKE AVE N	WORCESTER	MA	01655	WORCESTER	USA	Allergy and Infectious Diseases Research	001	1	8/10/2026	NEW	$0
														Subtotal = $38,312

Grand Total All Awards = $38,312

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Investigating Murine Intestinal Helminth Heligmosomoides polygyrus Amelioration of Depigmentation in a Mouse Model of Vitiligo

Award Number: F30AI200413

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 08/12/2026

PERIOD OF PERFORMANCE END DATE: 08/11/2030

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