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Investigating long-term immune dysfunction following exposure to perinatal inflammation

Award Number: F30AI188816
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 04/08/2026
PERIOD OF PERFORMANCE END DATE: 04/07/2028

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Investigating long-term immune dysfunction following exposure to perinatal inflammation - ABSTRACT Chorioamnionitis is infection and/or inflammation of the fetal membranes and the placenta and is one of the most common complications during pregnancy. Chorioamnionitis is an independent risk factor for several im- mune-mediated morbidities, including neonatal sepsis, chronic lung disease of prematurity, and asthma devel- opment in childhood. Although the risks associated with chorioamnionitis are severe, our understanding of the impact of this perinatal inflammatory exposure on offspring immune cell function remains incomplete. Current treatment approaches for chorioamnionitis are non-specific, including broad spectrum antibiotics and supportive care, which may independently increase the risk of asthma development. Therefore, there is a critical need to identify new therapeutic targets that address the underlying immune alterations that occur during chorioamni- onitis. This proposal investigates the central hypothesis that fetal interleukin (IL)-1 receptor (IL-1R) signaling drives chorioamnionitis-induced bacterial tolerance in neonatal offspring by upregulating the toll-like receptor (TLR) regulator Tollip. This hypothesis is supported by published data demonstrating that chorioamnionitis is dependent on IL-1 and that chorioamnionitis results in post-birth neonatal hyporesponsiveness to bacteria in animals and in humans. My robust preliminary data demonstrates that murine chorioamnionitis-exposed neona- tal offspring have hyporesponsive splenic macrophages, decreased systemic inflammation, and decreased mor- tality during neonatal E. coli sepsis. Additionally, murine chorioamnionitis-exposed neonatal macrophages dis- play increased chromatin accessibility at the promoter of Tollip, which is associated with increased gene expres- sion. The overall objective of my proposal is to determine how chorioamnionitis impacts offspring innate im- mune function and leads to an increased risk of immune-mediated morbidities. I will address this objective through two specific aims that test 1) the role of IL-1R signaling and 2) the role of Tollip in chorioamnionitis- associated neonatal hyporesponsiveness. Upon completion of this project, the expected outcome is that the mechanism(s) underlying chorioamnionitis-induced alterations in macrophage antibacterial responses will be better understood. The broader impact is that this project has the potential to alter current clinical practice by informing therapeutic and preventative approaches for chorioamnionitis that will address the underlying inflam- matory insult.


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 = $43,212 )
2026	2026	THE UNIVERSITY OF IOWA	105 JESSUP HALL	IOWA CITY	IA	52242	JOHNSON	USA	Allergy and Infectious Diseases Research	000	1	4/8/2026	NEW	$43,212
2026	2026	THE UNIVERSITY OF IOWA	105 JESSUP HALL	IOWA CITY	IA	52242	JOHNSON	USA	Allergy and Infectious Diseases Research	001	1	4/8/2026	NEW	$0
														Subtotal = $43,212

Grand Total All Awards = $43,212

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Investigating long-term immune dysfunction following exposure to perinatal inflammation

Award Number: F30AI188816

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 04/08/2026

PERIOD OF PERFORMANCE END DATE: 04/07/2028

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