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The role of Toll-Like Receptor-9 in type II epithelial cells and fibroblasts during influenza and S. aureus coinfection

Award Number: F31HL179788
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 05/01/2026
PERIOD OF PERFORMANCE END DATE: 04/30/2029

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The role of Toll-Like Receptor-9 in type II epithelial cells and fibroblasts during influenza and S. aureus coinfection - Project Abstract Evidence from pandemics and seasonal epidemics indicates that influenza is associated with bacterial coinfections which increases morbidity and mortality. One of the most common bacteria found in coinfection is Staphylococcus aureus, and Methicillin resistant staphylococcus aureus (MRSA) is a newer strain that is resistant to methicillin antibiotics which has made infections more difficult to treat. Viruses and bacteria are recognized by extra-cellular or intracellular pattern recognition receptors (PRRs). Toll like receptor 9 (TLR9) is a class of PRRs that senses bacterial and viral DNA containing unmethylated cytosine-guanidine motifs. TLRs have been associated with exacerbation of disease and increase inflammation during infections. Most research to date has investigated the function of TLR9 in immune cells, but the function of TLR9 in non-immune cells is much less understood. Studies from our laboratory have shown that TRL9 knockout mice fare better during coinfection suggesting that TLR9 is associated with more inflammation and poor survival outcomes. Additionally, we have preliminary data indicating that TLR9 expression in structural cells is detrimental during coinfection. In this proposal we seek to identify the role of TLR9 in lung structural cells, mainly epithelial cells and fibroblasts, during coinfection with influenza virus and MRSA. We have preliminary data showing that TLR9 is upregulated in epithelial cells and fibroblasts following influenza virus infection, and mice that lack TLR9 only in epithelial cells have a decreased bacterial burden following coinfection indicating improvement in disease burden. In this proposal my central hypothesis is that upregulation of TLR9 in epithelial cells and/or fibroblasts post-IAV alters cytokine production to impair alveolar macrophage phagocytosis and killing of MRSA and results in increased bacterial burden and lung injury during coinfection. This hypothesis will be tested through two specific aims: 1) Assess the upregulation of TLR9 in lung alveolar epithelial type II cells post-IAV and its effects on innate host responses during coinfection with IAV and MRSA and 2) Investigate the upregulation of TLR9 in lung fibroblasts post-IAV and its effects on macrophage antibacterial function during coinfection with IAV and MRSA. Experiments for these aims will be completed with the use of genetically engineered mouse models, cells derived from such mice, and in vitro assays to study the effect of TLR9 on macrophage phagocytosis and killing of MRSA. The results from these innovative studies may inform treatments that help improve coinfection outcomes. Completion of this proposal will also allow me to receive rigorous training in experimental design, implementation, and interpretation that will help me become a successful, independent scientist.


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 = $50,114 )
2026	2026	REGENTS OF THE UNIVERSITY OF MICHIGAN	1109 GEDDES AVE STE 3300	ANN ARBOR	MI	48109	WASHTENAW	USA	Lung Diseases Research	000	1	4/13/2026	NEW	$50,114
2026	2026	REGENTS OF THE UNIVERSITY OF MICHIGAN	1109 GEDDES AVE STE 3300	ANN ARBOR	MI	48109	WASHTENAW	USA	Lung Diseases Research	001	1	4/13/2026	NEW	$0
														Subtotal = $50,114

Grand Total All Awards = $50,114

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The role of Toll-Like Receptor-9 in type II epithelial cells and fibroblasts during influenza and S. aureus coinfection

Award Number: F31HL179788

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 05/01/2026

PERIOD OF PERFORMANCE END DATE: 04/30/2029

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