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The Impact of Acid Ceramidase in Myeloid Cells on Intestinal Inflammation

Award Number: F31DK145020
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: 05/15/2026
PERIOD OF PERFORMANCE END DATE: 05/14/2028

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The Impact of Acid Ceramidase in Myeloid Cells on Intestinal Inflammation - Abstract Sphingolipids play significant roles in mediating inflammation in disease. Patients with inflammatory bowel disease (IBD) and colitis associated cancer (CAC) demonstrate elevated expression of various sphingolipid metabolism enzymes. Acid ceramidase (AC) is highly expressed in disease and deacylates ceramide generating the product for the generation of the bioactive lipid sphingosine 1-phosphate (S1P). Samples from patients with IBD and colorectal cancer, and animal models of colitis, have identified tissue infiltrating macrophages to be a likely source of elevated AC expression; however, the role of AC and immune cell sphingolipid metabolism in IBD remains understudied. The goal of this proposal aims to elucidate the role of myeloid cell derived AC in the progression of IBD and determine the role of AC in immune cell recruitment in IBD. Several studies have implicated sphingolipid metabolism in IBD and CAC using genetic manipulation or pharmacologic inhibitors in mouse models. Many of these studies have examined total body knockouts; however, the contribution of immune cell specific sphingolipid metabolism has not been thoroughly investigated. Our lab has demonstrated that loss of AC in myeloid cells protected mice from acute colitis using dextran sulfate sodium (DSS). The preliminary data presented in this proposal have extended these studies assessing myeloid specific loss of AC in a model of chronic colitis utilizing IL-10 deficient mice. The loss of AC protected from colonic inflammation, increased ceramide content, and reduced innate immune cell infiltrate. Furthermore, loss of AC in myeloid cells altered adaptive immune cell populations in the colon and peripheral tissues, potentially indicating a role for AC in cell- to-cell communication. Our findings have led us to hypothesize that loss of AC in myeloid cells impairs inflammatory signaling, and immune cell recruitment or maturation to alleviate chronic colitis. We therefore propose the following specific aims: Specific Aim 1: Determine the mechanism by which loss of AC protects from chronic colitis. Specific Aim 2: Determine the role of AC in T cell maturation and immune cell recruitment in colitis.


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 = $50,114 )
2026	2026	UNIVERSITY OF ARIZONA	845 N PARK AVE RM 538	TUCSON	AZ	85721	PIMA	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	1	5/15/2026	NEW	$50,114
2026	2026	UNIVERSITY OF ARIZONA	845 N PARK AVE RM 538	TUCSON	AZ	85721	PIMA	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	001	1	5/15/2026	NEW	$0
														Subtotal = $50,114

Grand Total All Awards = $50,114

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The Impact of Acid Ceramidase in Myeloid Cells on Intestinal Inflammation

Award Number: F31DK145020

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: 05/15/2026

PERIOD OF PERFORMANCE END DATE: 05/14/2028

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