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The role of Prostaglandin E2 in Listeria monocytogenes induced CD8+ T-cell priming

Award Number: R21AI187635
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: 11/12/2024
PERIOD OF PERFORMANCE END DATE: 10/31/2026

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The role of Prostaglandin E2 in Listeria monocytogenes induced CD8+ T-cell priming - Abstract: Recognition of invading pathogens by the innate immune system triggers a series of signaling cascades that together program an appropriate adaptive immune response. Listeria monocytogenes is a Gram positive, intracellular pathogen that triggers robust innate immune responses upon escape from the phagosome into the host cell cytosol. Cytosolic innate immune recognition of L. monocytogenes ultimately results in priming of a robust protective immune response mediated by CD8+ T-cells. We recently demonstrated that production of the eicosanoid prostaglandin E2 following L. monocytogenes escape to the cytosol is essential for optimal CD8+ T-cell priming. How PGE2 is induced in response to cytosolic L. monocytogenes and how it subsequently promotes cell mediated immunity are currently unknown. We will take an unbiased approach to identify bacterial determinants of PGE2 induction using an established bacterial transposon mutant screen. In parallel we will use ex vivo dendritic cell-T-cell co- culture models to define the signaling pathways and cell types upon which PGE2 acts to promote CD8+ T-cell priming. Finally, using both pharmacologic agonists and antagonists as well as tissue specific PGE2 receptor knockout mice we will assess the role of specific PGE2 signaling pathways in CD8+ T- cell mediated protective immunity. Upon completion of these aims we will have identified how phagocytes produce PGE2 in response to cytosolic L. monocytogenes and will have identified bacterial mutants that induce altered levels of PGE2. We will have determined how PGE2 modulates dendritic cells and/or T-cell signaling to promote CD8+ T-cell priming and cell mediated immunity. Finally, we will have identified small molecules that improve T-cell responses in combination with L. monocytogenes-based vaccines. Future studies will focus on determining the conservation of PGE2 production as a response to cytosolic bacterial infection and whether PGE2 signaling promotes immunity in the context of L.monocytogenes stimulated anti-tumor immunity. Additional future studies will use the information generated here to determine if altering PGE2 signaling could improve the generation of CD8+ T-cells in response to other vaccine platforms such as mRNA-based vaccines.


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 = $226,590 )
2026	2026	UNIVERSITY OF WISCONSIN SYSTEM	21 N PARK ST STE 6301	MADISON	WI	53715	DANE	USA	Allergy and Infectious Diseases Research	000	2	11/24/2025	NON-COMPETING CONTINUATION	$226,590
														Subtotal = $226,590

Issue Date FY: 2025 ( Subtotal = $182,084 )
2025	2025	UNIVERSITY OF WISCONSIN SYSTEM	21 N PARK ST STE 6301	MADISON	WI	53715	DANE	USA	Allergy and Infectious Diseases Research	000	1	11/12/2024	NEW	$182,084
														Subtotal = $182,084

Grand Total All Awards = $408,674

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The role of Prostaglandin E2 in Listeria monocytogenes induced CD8+ T-cell priming

Award Number: R21AI187635

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: 11/12/2024

PERIOD OF PERFORMANCE END DATE: 10/31/2026

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