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Gastrointestinal Colonization Mechanisms of Carbapenem-Resistant?Enterobacter hormaechei

Award Number: R21AI202631
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 09/01/2026
PERIOD OF PERFORMANCE END DATE: 08/31/2028

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Gastrointestinal Colonization Mechanisms of Carbapenem-Resistant?Enterobacter hormaechei - Summary Title: Gastrointestinal Colonization Mechanisms of Carbapenem-Resistant Enterobacter hormaechei Carbapenem-resistant Enterobacteriaceae (CRE) pose an escalating public health problem. In 2019, the CDC classified CRE as an “urgent threat,” its highest level of concern. Among them, the Enterobacter cloacae complex (ECC) is a major cause of hospital-acquired infections, particularly in neonates, preterm infants, and immunocompromised patients. Carbapenem-resistant Enterobacter species are highly prevalent in the United States, associated with severe, hard-to-treat infections. They are especially concerning due to their role in fatal late-onset neonatal sepsis and life-threatening disease in vulnerable adults. Despite their clinical importance, the mechanisms underlying ECC colonization and pathogenesis remain poorly defined. The gastrointestinal tract is a critical reservoir for CRE, promoting persistence, nosocomial transmission, and systemic spread. Fundamental unanswered questions remain about how Enterobacter spp. establish colonization, which nutrients sustain them during colonization, what adherence factors enable attachment, and how they disseminate from the intestinal barrier. Addressing these gaps is essential for developing strategies to block colonization and prevent invasive infection. A neonatal mouse model was developed to mimic the preterm infant gut. In this model, carbapenem-resistant Enterobacter hormaechei, the most clinically relevant ECC pathogen, demonstrated efficient colonization predominantly in the colon. Colonic mucin can serve as a key nutrient source, and two essential metabolic pathways were uncovered that sustain growth on mucin. These findings suggest that E. hormaechei uses host-derived mucus glycans and associated metabolic pathways to promote its survival, colonization, and persistence within the gut. Exploitation of host mucus is hypothesized to serve as a primary nutrient strategy regulating colonization, predisposing colonized individuals to risk of disseminated E. hormaechei infection. To test this hypothesis, and to explore mucus as a signal inducing the expression colonization and pathogenicity traits, the proposed research will integrate mechanistic studies in the neonatal mouse with human intestinal organoid-derived epithelial monolayers (HIODEM) containing mucus- secreting goblet cells, closely mimicking the human gut. The findings will inform strategies to prevent transmission, reducing the burden of drug-resistant infections. Specific Aim 1: Determine mechanisms by which colonic mucus serves as a nutrient source for E. hormaechei in a neonatal mouse model. Specific Aim 2: Uncover colonization mechanisms of E. hormaechei using a human intestinal organoid model.


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 = $436,309 )
2026	2026	MICHIGAN STATE UNIVERSITY	426 AUDITORIUM RD RM 360	EAST LANSING	MI	48824	INGHAM	USA	Allergy and Infectious Diseases Research	000	1	8/28/2026	NEW	$436,309
														Subtotal = $436,309

Grand Total All Awards = $436,309

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Gastrointestinal Colonization Mechanisms of Carbapenem-Resistant?Enterobacter hormaechei

Award Number: R21AI202631

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 09/01/2026

PERIOD OF PERFORMANCE END DATE: 08/31/2028

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