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Selected Publication:

Type of publication: Journal Article
Type of document: Full Paper

Year: 2015

Authors: Awad, WA; Smorodchenko, A; Hess, C; Aschenbach, JR; Molnár, A; Dublecz, K; Khayal, B; Pohl, EE; Hess, M

Title: Increased intracellular calcium level and impaired nutrient absorption are important pathogenicity traits in the chicken intestinal epithelium during Campylobacter jejuni colonization.

Source: Appl Microbiol Biotechnol. 2015; 99(15):6431-6441



Authors Vetmeduni Vienna:

Awad Wageha
Hess Claudia
Hess Michael
Khayal Basel
Molnar Andor
Pohl Elena
Smorodchenko Alina

Vetmed Research Units
University Clinic for Poultry and Fish Medicine, Clinical Unit of Poultry Medicine
Institute of Animal Nutrition and Functional Plant Compounds
Institute of Physiology, Pathohysiology and Biophysics, Unit of Physiology and Biophysics


Project(s): Etablierung einer universitären Kooperation und eines transnationalen "Centre of Excellence" für Geflügel


Abstract:
Although a high number of chickens carry Campylobacter jejuni, the mechanistic action of colonization in the intestine is still poorly understood. The current study was therefore designed to investigate the effects of C. jejuni on glucose uptake, amino acids availability in digesta, and intracellular calcium [Ca(2+)]i signaling in the intestines of broiler chickens. For this, we compared: control birds (n = 60) and C. jejuni-infected birds (n = 60; infected orally with 1 × 10(8) CFU of C. jejuni NCTC 12744 at 14 days of age). Our results showed that glucose uptake was reduced due to C. jejuni infection in isolated jejunal, but not in cecal mucosa at 14 days postinfection (dpi). The decrease in intestinal glucose absorption coincided with a decrease in body weight gain during the 2-week post-infectious period. A reduction in the amount of the amino acids (serine, proline, valine, leucine, phenylalanine, arginine, histidine, and lysine) in ileal digesta of the infected birds at 2 and/or 7 dpi was found, indicating that Campylobacter utilizes amino acids as a carbon source for their multiplication. Applying the cell-permeable Ca(2+) indicator Fluo-4 and two-photon microscopy, we revealed that [Ca(2+)]i was increased in the jejunal and cecal mucosa of infected birds. The muscarinic agonist carbachol induced an increase in [Ca(2+)]i in jejunum and cecum mucosa of control chickens, a response absent in the mucosa of infected chickens, demonstrating that the modulation of [Ca(2+)]i by Campylobacter might be involved in facilitating the necessary cytoskeletal rearrangements that occur during the bacterial invasion of epithelial cells. In conclusion, this study demonstrates the multifaceted interactions of C. jejuni with the gastrointestinal mucosa of broiler chickens. For the first time, it could be shown that a Campylobacter infection could interfere with intracellular Ca(2+) signaling and nutrient absorption in the small intestine with consequences on intestinal function, performance, and Campylobacter colonization. Altogether, these findings indicate that Campylobacter is not entirely a commensal and can be recognized as an important factor contributing to an impaired chicken gut health.


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