Mucosal and Microbiota Changes During Acute Campylobacteriosis
| Status: | Recruiting |
|---|---|
| Conditions: | Irritable Bowel Syndrome (IBS), Infectious Disease |
| Therapuetic Areas: | Gastroenterology, Immunology / Infectious Diseases |
| Healthy: | No |
| Age Range: | 18 - 80 |
| Updated: | 11/16/2018 |
| Start Date: | October 31, 2014 |
| End Date: | June 30, 2022 |
| Contact: | Wendy J Sundt, BS |
| Email: | sundt.wendy@mayo.edu |
| Phone: | 507-293-4234 |
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.
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.
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.
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.
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
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