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Redox mechanisms contributing to pathogenicity of Campylobacter jejuni

Award Number: R01AI195641
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: 05/01/2026
PERIOD OF PERFORMANCE END DATE: 03/31/2030

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Redox mechanisms contributing to pathogenicity of Campylobacter jejuni - Summary: Redox mechanisms contributing to pathogenicity of Campylobacter jejuni. Foodborne illnesses are a significant global health concern, with Campylobacter jejuni being a leading cause of bacterial infection through food. In 2023, the CDC reported an incidence rate of 19.3 cases per 100,000 people in the U.S. Symptoms of C. jejuni infection include diarrhea, abdominal pain, and fever. While the incubation period is typically two-five days, the mechanisms underlying C. jejuni pathogenicity and proliferation in the colon remain poorly understood. A major reason for this has been lack of an ideal model system. Ferrets effectively model human infections with C. jejuni, exhibiting hallmark signs of colitis with robust bacterial growth. Observed pathological effects include crypt hyperplasia, increased epithelial oxygenation, elevated undifferentiated Ki67+ cells in the lamina propria, reduced levels of the hypoxia regulator Hif-1α, and altered profiles of gut metabolites. Elevated lactate levels, originating likely from host cell aerobic glycolysis, suggest a more oxygenated gut, promoting C. jejuni growth via lactate as a carbon source, with oxygenation stimulating proposed de-repression of the C. jejuni lactate transporter lctP expression, which is proposed to be repressed by the redox-sensitive protein LctR in the hypoxic gut prior to inflammation. Critical questions about C. jejuni pathogenicity mechanisms remain unanswered, including how this microaerophilic bacterium manipulates gut physiology, creates favorable conditions for growth, and proliferates in the redox environment of the gut through aerobic or anaerobic respiratory pathways. Our central hypothesis: C. jejuni alters gut physiology, transforming its niche from oxygen-limiting to a more oxygenated (microaerobic) environment through the virulence factors cytolethal distending toxin (CDT) and effector Cia proteins. Anaerobic respiration is critical in the early, oxygen-limiting stage of infection, while aerobic respiration is required during later inflammation-induced oxygenated stage. We hypothesize that the redox regulator LctR is vital in regulating C. jejuni physiology, enabling fitness and adaptation to the gut’s dynamic redox environment. We will test these hypotheses by accomplishing the following specific aims: Specific Aim 1: Define the impact of aerobic and anaerobic respiration pathways on Campylobacter jejuni colonization of ferrets. Specific Aim 2: Determine the role of CDT and CiaD of C. jejuni on changes in gut physiology. Specific Aim 3: Characterize the function of the redox regulator LctR of C. jejuni. Completing these aims will advance the development of targeted therapies to reduce bacterial burden and alleviate disease symptoms.


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 = $2,145,032 )
2026	2026	MICHIGAN STATE UNIVERSITY	426 AUDITORIUM RD RM 360	EAST LANSING	MI	48824	INGHAM	USA	Allergy and Infectious Diseases Research	000	1	4/28/2026	NEW	$2,145,032
														Subtotal = $2,145,032

Grand Total All Awards = $2,145,032

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Redox mechanisms contributing to pathogenicity of Campylobacter jejuni

Award Number: R01AI195641

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: 05/01/2026

PERIOD OF PERFORMANCE END DATE: 03/31/2030

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