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Cardiac Macrophage Plasticity in Sepsis-induced Cardiomyopathy

Award Number: R21AI178434
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: 06/22/2023
PERIOD OF PERFORMANCE END DATE: 05/31/2026

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Cardiac Macrophage Plasticity in Sepsis-induced Cardiomyopathy - Project Summary Sepsis is a leading cause of death in critical care units. Our long-term research goal is to understand the mechanisms of sepsis-induced multi-organ failure and to identify potential new therapeutic opportunities for this devastating clinical condition. Studies proposed in this application are designed to elucidate novel pathological functions of an immunometabolism regulator, growth hormone secretagogue receptor (GHS-R), in sepsis-induced cardiomyopathy using preclinical models. Recent studies revealed that macrophages localized in the heart are originated from different sources. With diversified functions ranging from reparative to inflammatory, the dynamics of changing these macrophage subsets forms a diagram of cardiac macrophage plasticity. Our ongoing investigation have obtained exciting preliminary evidence showing that GHS-R is a critical cellular switch that reprograms macrophage polarization to an inflammatory state. Furthermore, in a newly generated genetic mouse model, our data showed that ablation of myeloid linage macrophage-specific GHS-R attenuated systemic inflammation and improved heart function in response to endotoxemia challenge, which benefits were well associated with responses in metabolism, mitochondria, and autophagy in the heart. In this exploratory project, we will use in vitro and in vivo approaches to test the hypothesis that macrophage GHS-R reprograms cardiac macrophage plasticity and stimulates inflammation during sepsis (aim 1). We will further address whether macrophage GHS-R stimulates mitochondrial deficiencies, metabolic perturbations, and maladaptive autophagy in the heart during sepsis (aim 2). Together, this investigation is expected not only to advance the fundamental understanding of sepsis pathology but also to evaluate whether targeting GHS-R signal improves cardiac outcomes in sepsis, laying a scientific foundation for future development of novel therapies.


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 = $0 )
2025	2024	LOYOLA UNIVERSITY OF CHICAGO	2160 S 1ST AVE	MAYWOOD	IL	60153	COOK	USA	Allergy and Infectious Diseases Research	000	2	3/4/2025	NON-COMPETING CONTINUATION	$0
														Subtotal = $0

Issue Date FY: 2024 ( Subtotal = $233,878 )
2024	2024	LOYOLA UNIVERSITY OF CHICAGO	2160 S 1ST AVE	MAYWOOD	IL	60153	COOK	USA	Allergy and Infectious Diseases Research	000	2	5/14/2024	NON-COMPETING CONTINUATION	$233,878
														Subtotal = $233,878

Issue Date FY: 2023 ( Subtotal = $199,129 )
2023	2023	LOYOLA UNIVERSITY OF CHICAGO	2160 S 1ST AVE	MAYWOOD	IL	60153	COOK	USA	Allergy and Infectious Diseases Research	000	1	6/22/2023	NEW	$199,129
														Subtotal = $199,129

Grand Total All Awards = $433,007

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Cardiac Macrophage Plasticity in Sepsis-induced Cardiomyopathy

Award Number: R21AI178434

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: 06/22/2023

PERIOD OF PERFORMANCE END DATE: 05/31/2026

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