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Core mechanisms that contribute to inhibition of wound healing in diabetic foot and venous leg ulcers

Award Number: F30DK132806
ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 06/01/2022
PERIOD OF PERFORMANCE END DATE: 05/31/2027

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Core mechanisms that contribute to inhibition of wound healing in diabetic foot and venous leg ulcers - Project Summary Diabetic foot ulcers (DFUs) and venous leg ulcers (VLUs) are prevalent chronic wounds with a debilitating impact on patient quality of life, morbidity, and mortality, imposing a major economic burden to healthcare systems worldwide. Effective treatments for chronic wounds are scarce. Their efficacy is further limited by the presence and recurrence of infection. While arising from different etiologies, both DFUs and VLUs share common features such as a hyperproliferative, non-migratory epidermis, fibrosis, decreased angiogenesis, and a de-regulated inflammatory response. In addition, a major common characteristic is a shift in the microbiome from benign commensal bacteria to an abundance of pathogens. Unfortunately, a lack of animal models that closely recapitulates the human chronic wound condition impedes the understanding of this complex host-microbiome interaction. Thus, our laboratory focuses on the analyses of human tissue samples to decipher core molecular pathways that contribute to the non-healing phenotype of DFUs and VLUs. We used tissue samples from DFUs and VLUs (n=19), RNAseq and bioinformatic analysis to determine a core chronic wound transcriptome common for both types of chronic wounds. Analyses of this novel and unique core chronic wound gene signature indicates suppression of two host response pathways that may be modulated by the microbiome: the aryl hydrocarbon receptor (AHR) signaling pathway and the signal transducer and activator of transcription 3 (STAT3) pathway. As these pathways have been implicated in host antimicrobial response, as well as cell migration, and proliferation, we postulate that suppression of the AHR and STAT3 signaling pathways is mediated by a dysregulated microbiome and impairs chronic wound healing. Thus, the goal of this proposal is to understand the mechanisms by which the wound microbiome modulates the AHR (Aim 1) and STAT3 (Aim 2) pathways in DFUs and VLUs. We will use an integrative approach that includes patients’ wound samples, primary human cells and human skin ex vivo wound infection models. By using patient-relevant wound models, we will greatly advance understanding of the mechanisms by which the wound microbiome modulates the host response in chronic wounds and contribute to the inhibition of healing. In turn, understanding the interaction of the microbiome with the AHR and STAT3 pathways will further identify novel therapeutic targets for wound infections. Prevention and treatment of wound infections will have a major impact on healing outcomes of both DFUs and VLUs, decreasing lower leg amputations, morbidity and mortality.


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 = $58,114 )
2026	2026	UNIVERSITY OF MIAMI	1320 S DIXIE HWY STE 1200	CORAL GABLES	FL	33146	MIAMI-DADE	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	5	4/27/2026	NON-COMPETING CONTINUATION	$58,114
														Subtotal = $58,114

Issue Date FY: 2025 ( Subtotal = $57,538 )
2025	2025	UNIVERSITY OF MIAMI	1320 S DIXIE HWY STE 1200	CORAL GABLES	FL	33146	MIAMI-DADE	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	4	5/9/2025	NON-COMPETING CONTINUATION	$56,974
2025	2025	UNIVERSITY OF MIAMI	1320 S DIXIE HWY STE 1200	CORAL GABLES	FL	33146	MIAMI-DADE	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	001	4	6/3/2025	NON-COMPETING CONTINUATION	$564
														Subtotal = $57,538

Issue Date FY: 2024 ( Subtotal = $56,974 )
2024	2024	UNIVERSITY OF MIAMI	1320 S DIXIE HWY STE 1200	CORAL GABLES	FL	33146	MIAMI-DADE	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	3	5/22/2024	NON-COMPETING CONTINUATION	$56,974
														Subtotal = $56,974

Issue Date FY: 2023 ( Subtotal = $52,694 )
2023	2023	UNIVERSITY OF MIAMI	1400 NW 10TH AVE	MIAMI	FL	33136	MIAMI-DADE	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	2	5/10/2023	NON-COMPETING CONTINUATION	$52,694
														Subtotal = $52,694

Issue Date FY: 2022 ( Subtotal = $51,752 )
2022	2022	UNIVERSITY OF MIAMI	1600 NW 10 AVE	MIAMI	FL	33136	MIAMI-DADE	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	001	1	4/26/2022	NEW	$0
2022	2022	UNIVERSITY OF MIAMI	1600 NW 10 AVE	MIAMI	FL	33136	MIAMI-DADE	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	1	4/26/2022	NEW	$51,753
2022	2022	UNIVERSITY OF MIAMI	1600 NW 10 AVE	MIAMI	FL	33136	MIAMI-DADE	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	002	1	7/8/2022	NEW	-$1
														Subtotal = $51,752

Grand Total All Awards = $277,072

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Core mechanisms that contribute to inhibition of wound healing in diabetic foot and venous leg ulcers

Award Number: F30DK132806

ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 06/01/2022

PERIOD OF PERFORMANCE END DATE: 05/31/2027

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