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Intersection of Macrophage and Fibroblast Responses in Salivary Gland Fibrotic Injury

Award Number: F31DE035014
ORGANIZATION: NATIONAL INSTITUTE OF DENTAL AND CRANIOFACIAL RESEARCH
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 03/24/2026
PERIOD OF PERFORMANCE END DATE: 03/23/2029

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Intersection of Macrophage and Fibroblast Responses in Salivary Gland Fibrotic Injury - Abstract Fibrosis is a multisystemic disease that can affect many tissues and result in a loss of function in organs. Fibrosis can be caused by many factors including radiation treatment for cancers, tumors, or autoimmune diseases. In the salivary glands, fibrosis leads to dysbiosis of the oral microbiome, an increase in oral infections, difficulty in digestion of food and an overall reduction in the quality of life. Understanding the progression of fibrosis and how it affects human health is a crucial step for designing effective therapeutics. I hypothesize that during an injury response, macrophages produce higher levels of transforming growth factor beta 1, which drives the expression of myofibroblast genes in fibroblasts leading to a fibrotic phenotype. Disruption of this signaling axis by using TGFβR2 knockout mice will lead to a decrease in tissue fibrosis. To study the development of fibrosis, I use the ductal ligation model to induce a fibrotic phenotype in mouse submandibular glands. Using single cell RNA-sequencing (scRNA-seq) I will lineage trace Pdgfrα expressing fibroblast cells at early time points (1, 3, and 7 days) post ligation using Pdgfra-creERT2;R26tdT double transgenic mice. Afterwards, I will move to knocking out TGFβR2 specifically in the fibroblast cells using Pdgfra-creERT2;Tgfbr2fl/fl mice and evaluate the tissue at 7 days post ligation using immunohistochemistry (IHC) and histological staining. Then, I will first use scRNA-seq to determine the proportion of macrophages present in fibrotic SMGs tissue that express TGFβ cytokines and how this changes over the course of the ligation injury. Using CellChat, I will predict the pathways that mediate communication between the macrophages and the fibroblasts. To study interactions between diverse cell populations, I will use a SMG organoid model allowing us to study the interactions between cells. First, I will add primary macrophages into an organoid co-culture consisting of epithelial, Pdgfrα+ fibroblasts and macrophages. I will then use IHC to determine the expression of myofibroblast markers and fibrillar proteins as a readout for fibrosis. Lastly, I will add knockdown TGFβR2 fibroblasts into the organoid co-culture to determine whether there is a change in fibrosis levels.


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 = $35,571 )
2026	2026	RESEARCH FOUNDATION FOR THE STATE UNIVERSITY OF NEW YORK, THE	1400 WASHINGTON AVE	ALBANY	NY	12222	ALBANY	USA	Oral Diseases and Disorders Research	000	1	3/24/2026	NEW	$35,571
2026	2026	RESEARCH FOUNDATION FOR THE STATE UNIVERSITY OF NEW YORK, THE	1400 WASHINGTON AVE	ALBANY	NY	12222	ALBANY	USA	Oral Diseases and Disorders Research	001	1	3/24/2026	NEW	$0
														Subtotal = $35,571

Grand Total All Awards = $35,571

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Intersection of Macrophage and Fibroblast Responses in Salivary Gland Fibrotic Injury

Award Number: F31DE035014

ORGANIZATION: NATIONAL INSTITUTE OF DENTAL AND CRANIOFACIAL RESEARCH

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 03/24/2026

PERIOD OF PERFORMANCE END DATE: 03/23/2029

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