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The impact of dysphagia driven aspiration on lung pathophysiology in an animal model of term and preterm infants

Award Number: R01HD117115
ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 08/20/2026
PERIOD OF PERFORMANCE END DATE: 05/31/2031

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The impact of dysphagia driven aspiration on lung pathophysiology in an animal model of term and preterm infants - Feeding and respiration are fundamental and critical life functions. Failure to keep liquid out of the airway, aspiration, can be problematic, even pathological. However, the exact relationship between frequency and amount of aspiration and subsequent lung pathology is unknown. One standard compensatory treatment is thickening liquids; yet aspiration of such fluids has not been evaluated as an additional health burden on developing lungs and associated vascular tissues. The gold standard for assessing aspiration during swallowing, videofluoroscopy, presents ethical concerns for collecting data in both normal and compromised human infants. What is missing from both clinical and animal model data is a direct measurement of the impact of aspiration on lung physiology and histology. The goal of the proposed project is to use our validated animal model for infant dysphagia to develop a predictive model that links feeding physiology, blood biomarkers, and the amount of aspiration with measurable changes in lung pathophysiology. We propose to quantify the response to varying levels of aspiration, in term (SA1) and preterm (SA2) infants on normal and thickened (SA3) milk. Our animal models can generate variation in performance that can predict the extent of lung damage. Our predictive model will include physiologic measurements, as well as the ability to clear the lungs following a feed, to assess their contribution to pulmonary damage. We will measure aspiration lung damage in vivo dynamically through high resolution videofluoroscopy and post-mortem gross and histological assays, as well as in vivo blood biomarkers of inflammation. We hypothesize, supported by our preliminary data, that there will be a dose relationship between the frequency and extent of aspiration and histologically measurable lung damage. We hypothesize that the degree of aspiration will predict the lung damage response but will be different in term and preterm infants. We also hypothesize that both term and preterm infants will aspirate less frequently on thickened milk, but the impact of thickeners on lung physiology will produce more lung damage, as it will be more difficult to clear such fluid post-feeding. The results from these experiments will determine the physiological impact of aspiration on the respiratory system in both term and preterm infants. We propose to quantify the impact of aspiration across infant development up to the time of weaning, something not possible in humans. Documenting the tissue level sequalae of aspiration, and its correlation with biomarkers, will provide the basis for subsequent clinical decisions on therapeutic interventions for infant airway protection.


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 = $626,200 )
2026	2026	NORTHEAST OHIO MEDICAL UNIVERSITY	4209 STATE ROUTE 44	ROOTSTOWN	OH	44272	PORTAGE	USA	Child Health and Human Development Extramural Research	000	1	8/24/2026	NEW	$626,200
														Subtotal = $626,200

Grand Total All Awards = $626,200

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The impact of dysphagia driven aspiration on lung pathophysiology in an animal model of term and preterm infants

Award Number: R01HD117115

ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 08/20/2026

PERIOD OF PERFORMANCE END DATE: 05/31/2031

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