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Investigating the role of T cell-derived acetylcholine during Influenza A Virus infection

Award Number: F31AI197827
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 10/21/2026
PERIOD OF PERFORMANCE END DATE: 10/20/2027

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Investigating the role of T cell-derived acetylcholine during Influenza A Virus infection - ABSTRACT The neurotransmitter acetylcholine regulates a diverse range of physiological functions and it is known that immune cells can respond to and synthesize acetylcholine in response to viral infections. Within the influenza A virus (IAV) infected lung, T cells are recruited to combat the infection. Upon an IAV infection activated T cells induce the gene choline acetyltransferase (chat) which results in the production of acetylcholine. I have found that aged mice are less likely to survive IAV infection and have fewer chat+ IAV-specific T cells than young mice. However, it is unclear why this decrease happens in aging mice. Humans over the age of 65 become hyper susceptible to IAV infection, while this is traditionally attributed to the changes in the immune landscape and quiescence of the immune system, little is known if there are other contributing factors. Using a mouse model wherein chat is not expressed in T cells I found that young mice that cannot produce T cell-derived acetylcholine have decreased survival and defective recovery from IAV infection. However, these mice clear IAV normally and have no differences in T cell infiltration into the lungs. Instead, I found that inflammation in the lungs is sustained well after viral clearance when T cells cannot produce acetylcholine. While this inflammation could be driven by many immune cell types, the only significantly elevated immune cell type in the lungs are neutrophils. Neutrophil depletion in vivo in the mice unable to synthesize T cell-derived acetylcholine rescues recovery. Additionally, the in vitro presence of acetylcholine prevents neutrophil migration toward a chemoattractant. This observation indicates a direct effect of T cell-derived acetylcholine on neutrophils. Taken together, these results suggest that acetylcholine-producing T cells are a critical source of acetylcholine in the lung during recovery from influenza infection. This proposal seeks to understand if (1) epigenetic changes are responsible for the decrease in chat expression in aged mice, (2) inhibiting the breakdown of acetylcholine can rescue weight recovery, and (3) how neutrophils are being directly impacted by T cell-derived acetylcholine. Based on my preliminary studies I hypothesize that acetylcholine plays a central role in recovery from viral infection. This hypothesis will be tested in the following aims.


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 = $47,914 )
2026	2026	UNIVERSITY OF OKLAHOMA	865 RESEARCH PKWY STE 560	OKLAHOMA CITY	OK	73104	OKLAHOMA	USA	Allergy and Infectious Diseases Research	000	1	4/27/2026	NEW	$47,914
														Subtotal = $47,914

Grand Total All Awards = $47,914

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Investigating the role of T cell-derived acetylcholine during Influenza A Virus infection

Award Number: F31AI197827

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 10/21/2026

PERIOD OF PERFORMANCE END DATE: 10/20/2027

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