Intestinal Barrier in Post-<i>Campylobacter jejuni</i> Irritable Bowel Syndrome
Background: <i>Campylobacter jejuni</i> (<i>C. jejuni</i>) is one of the most common causes of bacterial gastroenteritis worldwide. One sequela of this infection is the development of post-infectious irritable bowel syndrome (PI-IBS). It has been suggested that a dysfunctiona...
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-02-01
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| Series: | Biomolecules |
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| Online Access: | https://www.mdpi.com/2218-273X/13/3/449 |
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| author | Sholpan Omarova Karem Awad Verena Moos Christoph Püning Greta Gölz Jörg-Dieter Schulzke Roland Bücker |
| author_facet | Sholpan Omarova Karem Awad Verena Moos Christoph Püning Greta Gölz Jörg-Dieter Schulzke Roland Bücker |
| author_sort | Sholpan Omarova |
| collection | DOAJ |
| description | Background: <i>Campylobacter jejuni</i> (<i>C. jejuni</i>) is one of the most common causes of bacterial gastroenteritis worldwide. One sequela of this infection is the development of post-infectious irritable bowel syndrome (PI-IBS). It has been suggested that a dysfunctional intestinal barrier may promote IBS development. We aimed to test this hypothesis against the background of the leaky gut concept for low-grade inflammation in PI-IBS. Methods: We identified patients with persistent PI-IBS symptoms after <i>C. jejuni</i> infection. During sigmoidoscopy, forceps biopsies were obtained for electrophysiological measurements of epithelial transport and barrier function in miniaturized Ussing devices. <i>C. jejuni</i> absence was checked by PCR and cytokine production with immunohistochemistry. Results: In PI-IBS, the epithelial resistance of the colon epithelium was unaltered, reflecting an intact paracellular pathway. In contrast, temperature-dependent horseradish peroxidase (HRP, 44 kDa) permeation increased. Short-circuit current (Isc) reflecting active anion secretion and ENaC-dependent electrogenic sodium absorption was unaffected. Early endosome antigen-1 (EEA1) and IL-4 levels increased. <i>C. jejuni</i> is not incorporated into the resident microbiota of the colon mucosa in PI-IBS. Conclusions: In PI-IBS after <i>C. jejuni</i> infection, macromolecule uptake via endocytosis was enhanced, leading to low-grade inflammation with pro-inflammatory cytokine release. The findings will allow <i>C. jejuni</i>-induced pathomechanisms to be targeted during infection and, thereafter to reduce sequelae such as PI-IBS. |
| first_indexed | 2024-03-11T06:53:00Z |
| format | Article |
| id | doaj.art-ddaf1b3fc17e454ead32bb2de7386bdd |
| institution | Directory Open Access Journal |
| issn | 2218-273X |
| language | English |
| last_indexed | 2024-03-11T06:53:00Z |
| publishDate | 2023-02-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biomolecules |
| spelling | doaj.art-ddaf1b3fc17e454ead32bb2de7386bdd2023-11-17T09:51:27ZengMDPI AGBiomolecules2218-273X2023-02-0113344910.3390/biom13030449Intestinal Barrier in Post-<i>Campylobacter jejuni</i> Irritable Bowel SyndromeSholpan Omarova0Karem Awad1Verena Moos2Christoph Püning3Greta Gölz4Jörg-Dieter Schulzke5Roland Bücker6Clinical Physiology, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, 12203 Berlin, GermanyClinical Physiology, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, 12203 Berlin, GermanyDepartment of Gastroenterology, Infectious Diseases and Rheumatology, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, 12203 Berlin, GermanyDepartment of Veterinary Medicine, Center for Veterinary Public Health, Institute of Food Safety and Food Hygiene, Freie Universität Berlin, 14163 Berlin, GermanyDepartment of Veterinary Medicine, Center for Veterinary Public Health, Institute of Food Safety and Food Hygiene, Freie Universität Berlin, 14163 Berlin, GermanyClinical Physiology, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, 12203 Berlin, GermanyClinical Physiology, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, 12203 Berlin, GermanyBackground: <i>Campylobacter jejuni</i> (<i>C. jejuni</i>) is one of the most common causes of bacterial gastroenteritis worldwide. One sequela of this infection is the development of post-infectious irritable bowel syndrome (PI-IBS). It has been suggested that a dysfunctional intestinal barrier may promote IBS development. We aimed to test this hypothesis against the background of the leaky gut concept for low-grade inflammation in PI-IBS. Methods: We identified patients with persistent PI-IBS symptoms after <i>C. jejuni</i> infection. During sigmoidoscopy, forceps biopsies were obtained for electrophysiological measurements of epithelial transport and barrier function in miniaturized Ussing devices. <i>C. jejuni</i> absence was checked by PCR and cytokine production with immunohistochemistry. Results: In PI-IBS, the epithelial resistance of the colon epithelium was unaltered, reflecting an intact paracellular pathway. In contrast, temperature-dependent horseradish peroxidase (HRP, 44 kDa) permeation increased. Short-circuit current (Isc) reflecting active anion secretion and ENaC-dependent electrogenic sodium absorption was unaffected. Early endosome antigen-1 (EEA1) and IL-4 levels increased. <i>C. jejuni</i> is not incorporated into the resident microbiota of the colon mucosa in PI-IBS. Conclusions: In PI-IBS after <i>C. jejuni</i> infection, macromolecule uptake via endocytosis was enhanced, leading to low-grade inflammation with pro-inflammatory cytokine release. The findings will allow <i>C. jejuni</i>-induced pathomechanisms to be targeted during infection and, thereafter to reduce sequelae such as PI-IBS.https://www.mdpi.com/2218-273X/13/3/449<i>Campylobacter jejuni</i>irritable bowel syndromepost-infectious irritable bowel syndromebarrier functionpermeabilityantigen entry |
| spellingShingle | Sholpan Omarova Karem Awad Verena Moos Christoph Püning Greta Gölz Jörg-Dieter Schulzke Roland Bücker Intestinal Barrier in Post-<i>Campylobacter jejuni</i> Irritable Bowel Syndrome Biomolecules <i>Campylobacter jejuni</i> irritable bowel syndrome post-infectious irritable bowel syndrome barrier function permeability antigen entry |
| title | Intestinal Barrier in Post-<i>Campylobacter jejuni</i> Irritable Bowel Syndrome |
| title_full | Intestinal Barrier in Post-<i>Campylobacter jejuni</i> Irritable Bowel Syndrome |
| title_fullStr | Intestinal Barrier in Post-<i>Campylobacter jejuni</i> Irritable Bowel Syndrome |
| title_full_unstemmed | Intestinal Barrier in Post-<i>Campylobacter jejuni</i> Irritable Bowel Syndrome |
| title_short | Intestinal Barrier in Post-<i>Campylobacter jejuni</i> Irritable Bowel Syndrome |
| title_sort | intestinal barrier in post i campylobacter jejuni i irritable bowel syndrome |
| topic | <i>Campylobacter jejuni</i> irritable bowel syndrome post-infectious irritable bowel syndrome barrier function permeability antigen entry |
| url | https://www.mdpi.com/2218-273X/13/3/449 |
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