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Acidosis in pulmonary endothelial injury and repair

Award Number: R01HL160988
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 02/01/2022
PERIOD OF PERFORMANCE END DATE: 01/31/2027

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Acidosis in pulmonary endothelial injury and repair - PROJECT SUMMARY/ABSTRACT The proposed research plan focuses on improving our understanding of the effects of acidosis on pneumonia and establishing the conceptual basis for diagnostic and therapeutic translation. Acidosis is common in critically ill pneumonia patients, and is associated with high mortality. The pathophysiology of acidosis in pneumonia is poorly understood, and current therapies fail to improve major outcomes. Our studies have shown that pulmonary microvascular endothelial cells (PMVECs) utilize the carbonic anhydrase IX (CA IX) isoform to regulate pH, metabolism and migration. We also demonstrated that Pseudomonas aeruginosa infection of PMVECs induces release of cytotoxic amyloid proteins, which disrupts the alveolar capillary membrane. These cytotoxic amyloids induce soluble CA IX shedding from PMVECs which compromises their repair potential. Based on these preliminary studies, we test the hypothesis that P. aeruginosa infection induces cytotoxic amyloid production that leads to shedding of soluble CA IX in PMVECs, increasing lung injury. Specific aims test the hypotheses that: 1) CA IX is critical to the acid regulation, metabolism and migration of PMVECs and pulmonary endothelial barrier integrity; and, 2) P. aeruginosa infection elicits cytotoxic amyloid production, causing CA IX shedding in PMVECs, which increases lung injury. In vitro, we will use genetic approaches and endothelial cell functional assays to evaluate the effects of acidosis and the role of specific CA IX functional domains during physiologic and infectious conditions. In vivo and ex vivo, we will use acidosis, pneumonia and isolated lung perfusion mouse models to translate in vitro findings. Successful completion of this study will provide new insights into the mechanisms underlying acidosis in pneumonia and help identify CA IX and cytotoxic amyloids as biomarkers and therapeutic targets for pneumonia.


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 = $385,000 )
2026	2026	UNIVERSITY OF SOUTH ALABAMA	307 UNIVERSITY BLVD	MOBILE	AL	36688	MOBILE	USA	Lung Diseases Research	000	5	2/25/2026	NON-COMPETING CONTINUATION	$385,000
														Subtotal = $385,000

Issue Date FY: 2025 ( Subtotal = $385,000 )
2025	2025	UNIVERSITY OF SOUTH ALABAMA	307 N UNIVERSITY BLVD	MOBILE	AL	36608	MOBILE	USA	Lung Diseases Research	000	4	3/17/2025	NON-COMPETING CONTINUATION	$385,000
														Subtotal = $385,000

Issue Date FY: 2024 ( Subtotal = $385,000 )
2024	2024	UNIVERSITY OF SOUTH ALABAMA	307 N UNIVERSITY BLVD	MOBILE	AL	36608	MOBILE	USA	Lung Diseases Research	000	3	1/12/2024	NON-COMPETING CONTINUATION	$385,000
														Subtotal = $385,000

Issue Date FY: 2023 ( Subtotal = $385,000 )
2023	2023	UNIVERSITY OF SOUTH ALABAMA	307 UNIVERISTY BLVD 380 ADMINISTRATION BLDG	MOBILE	AL	36688	MOBILE	USA	Lung Diseases Research	000	2	1/24/2023	NON-COMPETING CONTINUATION	$385,000
														Subtotal = $385,000

Issue Date FY: 2022 ( Subtotal = $385,000 )
2022	2022	UNIVERSITY OF SOUTH ALABAMA	307 UNIVERISTY BLVD 380 ADMINISTRATION BLDG	MOBILE	AL	36688	MOBILE	USA	Lung Diseases Research	000	1	1/30/2022	NEW	$385,000
														Subtotal = $385,000

Grand Total All Awards = $1,925,000

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Acidosis in pulmonary endothelial injury and repair

Award Number: R01HL160988

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 02/01/2022

PERIOD OF PERFORMANCE END DATE: 01/31/2027

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