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Microbiota-gamma delta IEL-Paneth cell axis in host antimicrobial response

Award Number: R21AI171959
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 06/01/2022
PERIOD OF PERFORMANCE END DATE: 05/31/2025

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Microbiota-gamma delta IEL-Paneth cell axis in host antimicrobial response - PROJECT SUMMARY. Maintenance of an intact intestinal barrier is critical to prevent microbial activation of mucosal immunity. gd intraepithelial lymphocytes (IEL) migrate extensively within the epithelial compartment to serve as a first line of defense against luminal antigens and invasive enteric microbes, and have been implicating in regulating Paneth cell secretion of antimicrobial peptides. Although microbial-derived molecules contribute to gd IEL homeostasis, specific commensal bacteria have yet to be associated with alterations in gd IEL number and/or function. Moreover, the extent to which gd IEL-mediated signaling influences Paneth cell function has yet to be explored. In preliminary data generated for this application, we identified 5 amplicon sequence variants (ASV) that are strongly associated with the expansion of gd IELs under homeostatic conditions. We also show that epithelial cells isolated from WT mice with an expanded gd IEL compartment also exhibit a significant upregulation of genes involved in Paneth cell antimicrobial peptide production and secretion. Therefore, this proposal seeks to identify the contribution of individual commensals to the expansion of the gd IEL compartment and determine the extent of gd IEL-Paneth cell crosstalk in WT mice exhibiting this hyperproliferative phenotype. Using an integrated approach that combines unique mouse models and cutting edge imaging technologies both in vitro and in vivo, these studies will be the first to identify the contribution of individual commensals in the amplification of gd IEL proliferation and surveillance behavior, and elucidate whether gd IELs directly promote Paneth cell function. Developing a better understanding of the microbiota-gd IEL-Paneth cell axis may identify novel therapeutic targets to aid in host defense and help maintain remission in Crohn’s disease patients.


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: 2024 ( Subtotal = $0 )
2024	2023	ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI	1 GUSTAVE L LEVY PL	NEW YORK	NY	10029	NEW YORK	USA	Allergy and Infectious Diseases Research	001	2	4/18/2024	CHANGE OF GRANTEE / TRAINING INSTITUTION / AWARDING INSTITUTION	$140,993
2024	2022	RUTGERS, THE STATE UNIVERSITY	185 S ORANGE AVE	NEWARK	NJ	07103	ESSEX	USA	Allergy and Infectious Diseases Research	000	1	4/18/2024	NEW	-$140,993
														Subtotal = $0

Issue Date FY: 2023 ( Subtotal = $210,490 )
2023	2023	ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI	ONE GUSTAVE L LEVY PL	NEW YORK	NY	10029	NEW YORK	USA	Allergy and Infectious Diseases Research	001	2	5/17/2023	CHANGE OF GRANTEE / TRAINING INSTITUTION / AWARDING INSTITUTION	$210,490
2023	2022	RUTGERS THE STATE UNIVERSITY OF NEW JERSEY	185 S ORANGE AVE	NEWARK	NJ	07103	ESSEX	USA	Allergy and Infectious Diseases Research	000	1	5/17/2023	NEW	$0
														Subtotal = $210,490

Issue Date FY: 2022 ( Subtotal = $228,017 )
2022	2022	RUTGERS, THE STATE UNIVERSITY OF NEW JERSEY	185 S ORANGE AVE	NEWARK	NJ	07103	ESSEX	USA	Allergy and Infectious Diseases Research	000	1	5/25/2022	NEW	$228,017
														Subtotal = $228,017

Grand Total All Awards = $438,507

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Microbiota-gamma delta IEL-Paneth cell axis in host antimicrobial response

Award Number: R21AI171959

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 06/01/2022

PERIOD OF PERFORMANCE END DATE: 05/31/2025

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