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Immune Mechanisms Linking Intensive CareUnit Sleep Disruption to Pneumonia

Award Number: F32HL188862
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 02/10/2027
PERIOD OF PERFORMANCE END DATE: 02/09/2028

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Immune Mechanisms Linking Intensive CareUnit Sleep Disruption to Pneumonia - ABSTRACT Bacterial pneumonia acquired in the intensive care unit (ICU) is the most common hospital-acquired infection and a major cause of acute lung injury and mortality among critically ill patients. Although multiple risk factors have been identified, most are inherent to life-supportive care and therefore unmodifiable. Sleep disruption, however, is nearly universal in the ICU and represents a promising modifiable contributor to infection risk. In the general population, disordered sleep increases susceptibility to pneumonia, yet how the profound and distinctive sleep disruption experienced by ICU patients impairs pulmonary host defense remains unknown. Addressing this gap could uncover new biological targets to prevent ICU-acquired pneumonia. To investigate this question, our laboratory developed a murine model of ICU-associated sleep fragmentation (ICU-SF) that closely replicates the features of disrupted sleep in critically ill patients. Applying this model to a Streptococcus pneumoniae pneumonia murine model (Sp), our laboratory published that ICU-SF impairs bacterial clearance and exacerbates lung injury. Using this combined ICU-SF-Sp model, I have generated preliminary data showing that ICU-SF selectively reduces lung γδT17 cells—an unconventional T-cell subset that provides rapid, IL-17A-dependent antibacterial defense—without affecting other IL-17A-producing lymphocytes, implicating γδT17 cells as a focus of ICU-SF engendered immune vulnerability. The central hypothesis of this proposal is that ICU-SF inhibits the accumulation of pulmonary γδT17 cells during infection, thereby impairing IL-17A-mediated antibacterial defenses and predisposing to bacterial pneumonia and acute lung injury. Specific Aim 1 will define how ICU-SF inhibits γδT17 cell accumulation by assessing effects on thymic output, recruitment from extrapulmonary sites, migration into lung tissue, proliferation, and apoptosis. Specific Aim 2 will determine whether impaired γδT17 cell-mediated antibacterial defenses explain ICU-SF-induced susceptibility to pneumonia, using recombinant IL-17A administration and adoptive γδT17-cell transfer to assess restoration of antibacterial function and disease outcomes. This work will elucidate fundamental sleep- immune mechanisms that govern susceptibility to bacterial pneumonia in critical illness. The proposed training integrates advanced immunophenotyping, adoptive transfer, and cytokine-based manipulation within a novel ICU-SF model, providing me with a strong foundation for an independent research career investigating immune mechanisms of acute lung 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: 2026 ( Subtotal = $84,148 )
2026	2026	THE JOHNS HOPKINS UNIVERSITY	3400 N CHARLES ST	BALTIMORE	MD	21218	BALTIMORE CITY	USA	Lung Diseases Research	000	1	8/13/2026	NEW	$84,148
														Subtotal = $84,148

Grand Total All Awards = $84,148

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Immune Mechanisms Linking Intensive CareUnit Sleep Disruption to Pneumonia

Award Number: F32HL188862

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 02/10/2027

PERIOD OF PERFORMANCE END DATE: 02/09/2028

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