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Mucosal and Microbiota Changes During Acute Campylobacteriosis

Mucosal and Microbiota Changes During Acute Campylobacteriosis

Status
Recruiting
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT03223077
Enrollment
150
Registered
2017-07-19
Start date
2014-10-31
Completion date
2027-06-01
Last updated
2026-08-07

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Irritable Bowel Syndrome

Keywords

Post infectious

Brief summary

Gastrointestinal (GI) infection with Campylobacter causes inflammation in the bowel and can change bacteria in the gut. Certain individuals with Campylobacter infection are also known to develop chronic bowel problems such as Irritable Bowel Syndrome (IBS). The researchers are doing this study to understand if changes in gut bacteria and gut mucosal lining during an acute infection can help identify individuals who might be at risk for developing problems in the future.

Detailed description

Gastrointestinal (GI) infections involving a variety of bacterial, viral, and parasitic pathogens predispose patients to post-infectious irritable bowel syndrome (PI-IBS) and other functional GI disorders1. Campylobacter is one of the top five organisms responsible for food-borne illnesses causing approximately 0.8 million cases annually2. Isolated C. jejuni infection has been associated with a PI-IBS risk of 9% to 13%3. Epidemiological studies have identified female gender, age \<60 years, smoking, enteritis severity, and pre-enteritis psychological stress as risk-factors for development of PI-IBS4. In a single study, variants in host genes TLR9, IL6, and CDH1 were identified as independent risk factors for development of PI-IBS after controlling for previously identified clinical risk factors5. In another study, host cytokines were looked at in relation to development of reactive arthritis and IBS following Campylobacter enteritis. The risk of acquiring clinical gastroenteritis with Campylobacter jejuni/coli was related to the INFG (+ 874A\>T) of intron 1. Polymorphisms in IL-18 and INFG were linked to the risk of post-infectious reactive arthritis, but not to PI-IBS6. However, this study was limited by assessment of only serum cytokine profile and not mucosal. A recent study has shown that fecal microbiota of patients with PI-IBS differs from that of healthy controls and resembles that of patients with IBS with diarrhea (IBS-D)7. The microbiota is altered during acute enteritis, but it is unclear if there are any signatures in acute microbiota alterations that can help predict development of PI-IBS following Campylobacter enteritis. Our overall goal with this study is to identify non-invasive and invasive host factors that can help predict the development of PI-IBS following Campylobacter enteritis.

Interventions

None listed

Sponsors

Mayo Clinic
Lead SponsorOTHER

Study design

Observational model
CASE_ONLY
Time perspective
PROSPECTIVE

Eligibility

Sex/Gender
ALL
Age
18 Years to 80 Years
Healthy volunteers
No

Inclusion criteria

* No abdominal surgery (except appendectomy and cholecystectomy) * Stool culture or Polymerase chain reaction (PCR) positive enteritis with Campylobacter

Exclusion criteria

* History of IBS, Irritable Bowel Disease (IBD) (Crohn's disease or ulcerative colitis), microscopic colitis or celiac disease. * History of gastroenteritis in six months prior to Campylobacter enteritis * Pregnancy

Design outcomes

Primary

MeasureTime frameDescription
Development of IBS is the endpoint.6 monthsNumber of Subjects Who Develop Irritable Bowel Syndrome After Campylobacter Infection

Countries

United States

Contacts

CONTACTMargaret K Breen-Lyles, BS
Breen-Lyles.Margaret@mayo.edu507-255-3520
PRINCIPAL_INVESTIGATORMadhusudan Grover, MBBS

Mayo Clinic

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Aug 8, 2026