Tuesday, October 21, 2025 10/21/2025

Protective adaptive immune mechanisms after cardiac arrest

Award Number: R01HL173118
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 04/02/2024
PERIOD OF PERFORMANCE END DATE: 01/31/2029

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Protective adaptive immune mechanisms after cardiac arrest - Cardiac arrest induces a systemic inflammatory response. Several studies have demonstrated that increased sustained inflammation is associated with poor outcomes, suggesting a possible role for anti-inflammatory and immunomodulatory therapies. However, these studies have focused on mechanisms that promote inflammation without considering protective mechanisms that are also mediated by the immune cells. Our preliminary data from human patients with cardiac arrest revealed an association between the higher number of CD73-expressing lymphocytes and favorable outcomes. CD73 is a key enzyme in the generation of adenosine, a purine nucleoside that is characterized by potent anti-inflammatory properties. Our new preliminary data generated using a mouse model of cardiac arrest and resuscitation suggest that CD73- expressing lymphocytes play a role in the control of local inflammation in the heart and brain tissues. In Specific Aim 1, we will determine the functional significance of adoptive cell therapy using protective CD73- expressing lymphocytes after an ischemia and reperfusion injury in a mouse model of cardiac arrest and cardiopulmonary resuscitation. In Specific Aim 2, we will test the hypothesis that CD73-expressing lymphocytes form T cell-monocyte complexes and promote the differentiation of monocytes toward anti- inflammatory macrophages. In Specific Aim 3, we will define molecular mechanisms involved in the formation of anti-inflammatory lymphocyte-macrophages complexes. Our new data will determine the contribution of cardiac arrest-induced inflammatory response in the heart and brain tissue damage and identify CD73/adenosine/adenosine receptors axis as a potential therapeutic approach to improve outcomes after global ischemia and reperfusion injury.


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: 2025 ( Subtotal = $644,111 )
2025	2025	MAINEHEALTH	110 FREE ST	PORTLAND	ME	04101	CUMBERLAND	USA	Cardiovascular Diseases Research	001	2	8/27/2025	NON-COMPETING CONTINUATION	$64,411
2025	2025	MAINEHEALTH	110 FREE ST	PORTLAND	ME	04101	CUMBERLAND	USA	Cardiovascular Diseases Research	000	2	12/24/2024	NON-COMPETING CONTINUATION	$579,700
														Subtotal = $644,111

Issue Date FY: 2024 ( Subtotal = $644,111 )
2024	2024	MAINEHEALTH	110 FREE ST	PORTLAND	ME	04101	CUMBERLAND	USA	Cardiovascular Diseases Research	000	1	4/2/2024	NEW	$579,700
2024	2024	MAINEHEALTH	110 FREE ST	PORTLAND	ME	04101	CUMBERLAND	USA	Cardiovascular Diseases Research	001	1	5/31/2024	NEW	$64,411
														Subtotal = $644,111

Grand Total All Awards = $1,288,222

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Protective adaptive immune mechanisms after cardiac arrest

Award Number: R01HL173118

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 04/02/2024

PERIOD OF PERFORMANCE END DATE: 01/31/2029

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