Universität zu Köln

Bucker, R., Krug, S. M., Moos, V., Bojarski, C., Schweiger, M. R., Kerick, M., Fromm, A., Janssen, S., Fromm, M., Hering, N. A., Siegmund, B., Schneider, T., Barmeyer, C. and Schulzke, J. D. (2018). Campylobacter jejuni impairs sodium transport and epithelial barrier function via cytokine release in human colon. Mucosal Immunol., 11 (2). S. 474 - 486. NEW YORK: NATURE PUBLISHING GROUP. ISSN 1935-3456

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Abstract

Campylobacter jejuni is the most prevalent cause of foodborne bacterial enteritis worldwide. Patients present with diarrhea and immune responses lead to complications like arthritis and irritable bowel syndrome. Although studies exist in animal and cell models, we aimed at a functional and structural characterization of intestinal dysfunction and the involved regulatory mechanisms in human colon. First, in patients' colonic biopsies, sodium malabsorption was identified as an important diarrheal mechanism resulting from hampered epithelial ion transport via impaired epithelial sodium channel (ENaC) beta- and gamma-subunit. In addition, barrier dysfunction from disrupted epithelial tight junction proteins (claudin-1, -3, -4, -5, and -8), epithelial apoptosis, and appearance of lesions was detected, which cause leak-flux diarrhea and can perpetuate immune responses. Importantly, these effects in human biopsies either represent direct action of Campylobacter jejuni (ENaC impairment) or are caused by proinflammatory signaling (barrier dysfunction). This was revealed by regulator analysis from RNA-sequencing (cytometric bead array-checked) and confirmed in cell models, which identified interferon-gamma, TNF alpha, IL-13, and IL-1 beta. Finally, bioinformatics' predictions yielded additional information on protective influences like vitamin D, which was confirmed in cell models. Thus, these are candidates for intervention strategies against C. jejuni infection and post-infectious sequelae, which result from the permissive barrier defect along the leaky gut.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Bucker, R. UNSPECIFIED UNSPECIFIED UNSPECIFIED Krug, S. M. UNSPECIFIED UNSPECIFIED UNSPECIFIED Moos, V. UNSPECIFIED UNSPECIFIED UNSPECIFIED Bojarski, C. UNSPECIFIED UNSPECIFIED UNSPECIFIED Schweiger, M. R. UNSPECIFIED UNSPECIFIED UNSPECIFIED Kerick, M. UNSPECIFIED UNSPECIFIED UNSPECIFIED Fromm, A. UNSPECIFIED UNSPECIFIED UNSPECIFIED Janssen, S. UNSPECIFIED UNSPECIFIED UNSPECIFIED Fromm, M. UNSPECIFIED UNSPECIFIED UNSPECIFIED Hering, N. A. UNSPECIFIED UNSPECIFIED UNSPECIFIED Siegmund, B. UNSPECIFIED UNSPECIFIED UNSPECIFIED Schneider, T. UNSPECIFIED UNSPECIFIED UNSPECIFIED Barmeyer, C. UNSPECIFIED UNSPECIFIED UNSPECIFIED Schulzke, J. D. UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-193952
DOI:	10.1038/mi.2017.66
Journal or Publication Title:	Mucosal Immunol.
Volume:	11
Number:	2
Page Range:	S. 474 - 486
Date:	2018
Publisher:	NATURE PUBLISHING GROUP
Place of Publication:	NEW YORK
ISSN:	1935-3456
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language NF-KAPPA-B; INTESTINAL INFLAMMATION; CLAUDIN-2 EXPRESSION; ESCHERICHIA-COLI; DISTENDING TOXIN; TIGHT JUNCTIONS; CL-SECRETION; CELLS; INFECTION; ACTIVATION Multiple languages Immunology Multiple languages
Refereed:	Yes
URI:	http://kups.ub.uni-koeln.de/id/eprint/19395