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Yersiniabactin Precursor Escherichelin May Enhance Enterobacteriaceae Colonization and Pathogenicity in Inflamed Colon

Award Number: F31AI189082
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 10/16/2026
PERIOD OF PERFORMANCE END DATE: 10/15/2027

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Yersiniabactin Precursor Escherichelin May Enhance Enterobacteriaceae Colonization and Pathogenicity in Inflamed Colon - Project Summary. Microbial competition is a complex process that can act to protect the host from infection by pathogens. Probiotic Escherichia coli Nissle 1917 (EcN) competes with Salmonella enterica serovar Typhimurium (STm) using several strategies that include iron acquisition via siderophores and secretion of small antimicrobial proteins called microcins. Whether EcN also competes with STm and other pathogens for other metal nutrients, including zinc, is not well understood. The yersiniabactin gene cluster is a biosynthesis pathway that synthesizes and secretes yersiniabactin (Ybt), a metallophore originally described in Yersinia pestis. Ybt is found in a range of pathogenic Enterobacteriaceae, including E. coli. Adherent-invasive E. coli (AIEC) is a distinct and virulent pathovar associated with IBD and is a Ybt producer. Ybt is internalized via the outer membrane permease FyuA, and the inner membrane permease YbtX. The Ybt gene cluster expresses two main proteins: HMWP2 (encoded by irp2) and HMWP1 (encoded by irp1), where HMWP2 is upstream of HMWP1 and creates the Ybt precursor and small molecule metabolite HPTT-COOH, also termed escherichelin. It is unknown whether escherichelin contributes to growth and metal competition. Our central hypothesis is that escherichelin functions as a zincophore, contributing to Zn acquisition in commensal and pathogenic E. coli. In the case of EcN, we hypothesize that escherichelin production will provide a competitive advantage against STm during colitis. In the case of AIEC, we hypothesize that escherichelin will enhance colonization of this pathobiont, potentially exacerbating colitis. To address this knowledge gap, various knockouts will be created. To test this hypothesis my first aim is to use extracted escherichelin and the irp1 and irp2 mutants to elucidate whether escherichelin functions as a zincophore in vitro and in vivo. The growth advantage of escherichelin will be assessed in vivo by using a murine model of colitis. Next, growth curves will be performed in different media to measure the growth response when zinc is present. Additionally, a second aim will determine whether zinc acquisition via escherichelin enables EcN to compete with STm in the inflamed gut and in vitro. To answer this, mice will be co-infected with the EcN irp1 mutant and STm. Additionally, to investigate whether escherichelin boosts pathogenesis, AIEC infections with irp mutants will be performed. The outcome of this research will inform on metal competition in the gut during infection and inflammation and is necessary to understand potential microbe-based treatments and prophylaxis.


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 = $43,097 )
2026	2026	UNIVERSITY OF CALIFORNIA, SAN DIEGO	9500 GILMAN DR	LA JOLLA	CA	92093	SAN DIEGO	USA	Allergy and Infectious Diseases Research	000	1	4/16/2026	NEW	$43,097
														Subtotal = $43,097

Grand Total All Awards = $43,097

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Yersiniabactin Precursor Escherichelin May Enhance Enterobacteriaceae Colonization and Pathogenicity in Inflamed Colon

Award Number: F31AI189082

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 10/16/2026

PERIOD OF PERFORMANCE END DATE: 10/15/2027

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