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Defining the pathogenic roles of fibrin(ogen) during influenza A virus-induced lung injury

Award Number: F31HL182147
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 09/30/2025
PERIOD OF PERFORMANCE END DATE: 09/29/2026

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Defining the pathogenic roles of fibrin(ogen) during influenza A virus-induced lung injury - ABSTRACT Influenza A virus (IAV) is a major seasonal respiratory pathogen with pandemic potential. The total economic burden of IAV in the United States is estimated at $11.2 billion annually. Should a pandemic IAV strain emerge, the costs, both monetarily and in human life, would be expected to increase drastically. Lung injury during IAV infection results from a combination of viral infection of lung epithelial cells that causes damage and cell death, as well as excessive immune cell infiltration and activation as part of the host antiviral response. The coagulation system is activated as part of the innate immune response to IAV infection, leading to the conversion of the soluble fibrinogen to a fibrin matrix. Fibrin formation limits hemorrhage and vascular leakage of blood components into the airspace. However, excessive activation of coagulation leads to pathologic fibrin deposition both as extravascular fibrin deposition in the airway and within the vasculature as occlusive thrombi in the microvasculature. Both contribute to lung injury. Importantly, fibrin enhances inflammation by mediating signaling through leukocyte integrin αMβ2. We hypothesize that excessive fibrin deposition in the lung following IAV infection enhances leukocyte activation, increases inflammation, and contributes to lung injury. We will use an established IAV mouse infection model to test our hypothesis. We will determine the contribution of fibrin- driven leukocyte activation via αMβ2 (Aim 1) and the effect of reducing circulating fibrin(ogen) levels (Aim 2) on IAV-induced inflammation and lung injury). Successful completion of our aims will elucidate the pathogenic roles of fibrin in IAV-driven lung injury. In addition, this work will serve as a proof of concept that targeting fibrin may be a novel therapeutic strategy to reduce lung injury caused by other pathogens.


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 = -$35,589 )
2026	2025	UNIVERSITY OF NORTH CAROLINA AT CHAPEL HILL	104 AIRPORT DR STE 2200	CHAPEL HILL	NC	27599	ORANGE	USA	Lung Diseases Research	000	1	12/8/2025	NEW	-$35,589
														Subtotal = -$35,589

Issue Date FY: 2025 ( Subtotal = $35,589 )
2025	2025	UNIVERSITY OF NORTH CAROLINA AT CHAPEL HILL	104 AIRPORT DR STE 2200	CHAPEL HILL	NC	27599	ORANGE	USA	Lung Diseases Research	000	1	8/18/2025	NEW	$35,589
														Subtotal = $35,589

Grand Total All Awards = $0

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Defining the pathogenic roles of fibrin(ogen) during influenza A virus-induced lung injury

Award Number: F31HL182147

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 09/30/2025

PERIOD OF PERFORMANCE END DATE: 09/29/2026

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