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Enteric nervous system-macrophage interactions in Hirschsprung-associated enterocolitis

Award Number: F30DK143703
ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 09/01/2025
PERIOD OF PERFORMANCE END DATE: 08/31/2028

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Enteric nervous system-macrophage interactions in Hirschsprung-associated enterocolitis - Abstract/Project Summary: The gut is richly innervated by a dense network of intrinsic neurons and glia called the enteric nervous system (ENS). The ENS controls most aspects of bowel function including motility, blood flow, epithelial function, and immune cell activities. In 1:5000 children the ENS is missing from the distal bowel, a birth defect called Hirschsprung disease (HSCR). Children with HSCR are prone to HSCR associated enterocolitis (HAEC), a life-threatening colon inflammation. Although there are treatments for HAEC, many children have ongoing symptoms and the mechanisms underlying the enterocolitis remains poorly understood. In particular, how the absence of the ENS affects local immune cells and mechanisms of ENS-immune cell interactions are largely unexplored. Preliminary results in our murine HSCR model reveal increased macrophage infiltration of the distal colon that lacks ENS and changes in macrophage morphology that suggest altered macrophage function and roles for macrophage in colitis of the HSCR bowel. To find new ways to prevent HAEC, we will test the hypothesis that bowel macrophage phenotype changes in response to vasoactive intestinal peptide (VIP) or the absence of VIP signaling. VIP is an abundant ENS neurotransmitter that induces anti-inflammatory effects in diverse immune cell subtypes. We also will determine if reducing macrophage abundance or skewing macrophage toward an anti-inflammatory phenotype will reduce colitis severity in a HSCR model. These studies will provide new insight into neuro-immune interactions in the context of a HSCR disease model, and these results may suggest new strategies to treat or prevent HAEC.


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 = $38,129 )
2026	2026	TRUSTEES OF THE UNIVERSITY OF PENNSYLVANIA, THE	3451 WALNUT ST	PHILADELPHIA	PA	19104	PHILADELPHIA	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	2	8/25/2026	NON-COMPETING CONTINUATION	$38,129
														Subtotal = $38,129

Issue Date FY: 2025 ( Subtotal = $54,538 )
2025	2025	TRUSTEES OF THE UNIVERSITY OF PENNSYLVANIA, THE	3451 WALNUT ST STE 440A	PHILADELPHIA	PA	19104	PHILADELPHIA	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	001	1	8/29/2025	NEW	$0
2025	2025	TRUSTEES OF THE UNIVERSITY OF PENNSYLVANIA, THE	3451 WALNUT ST STE 440A	PHILADELPHIA	PA	19104	PHILADELPHIA	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	1	8/29/2025	NEW	$54,538
														Subtotal = $54,538

Grand Total All Awards = $92,667

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Enteric nervous system-macrophage interactions in Hirschsprung-associated enterocolitis

Award Number: F30DK143703

ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 09/01/2025

PERIOD OF PERFORMANCE END DATE: 08/31/2028

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