Károly Dublecz

Campylobacter infection in chickens modulates the intestinal epithelial barrier function

Asymptomatic carriage of Campylobacter jejuni is highly prevalent in chicken flocks. Thus, we investigated whether chronic Campylobacter carriage affects chicken intestinal functions despite the absence of clinical symptoms. An experiment was carried out in which commercial chickens were orally infected with C. jejuni (1 × 108 CFU/bird) at 14 days of life. Changes in ion transport and barrier function were assessed by short-circuit current (Isc) and transepithelial ion conductance (Gt) in Ussing chambers. Gt increased in cecum and colon of Campylobacter-infected chicken 7 d post-infection (DPI), whereas Gt initially decreased in the jejunum at 7 DPI and increased thereafter at 14 DPI. The net charge transfer across the epithelium was reduced or tended to be reduced in all segments, as evidenced by a decreased Isc. Furthermore, the infection induced intestinal histomorphological changes, most prominently including a decrease in villus height, crypt depth and villus surface area in the jejunum at 7 DPI. Furthermore, body mass gain was decreased by Campylobacter carriage. This study demonstrates, for the first time, changes in the intestinal barrier function in Campylobacter-infected chickens and these changes were associated with a decrease in growth performance in otherwise healthy-appearing birds.

Composition of diet modifies colonization dynamics of Campylobacter jejuni in broiler chickens

To evaluate the impact of diet composition on colonization dynamics of Camp. jejuni and on related physiological parameters in the chicken intestine.

Effect of combined treatment with aflatoxin B1 and T-2 toxin and metabolites on some production traits and lipid peroxide status parameters of broiler chickens.

Three groups of cockerels were fed with a control diet, with a diet contaminated with T-2 and HT-2 toxin (0.31 and 0.26 mg/kg) or with that containing a combination of T-2 and HT-2 toxin (0.32 and 0.25 mg/kg) and aflatoxin B1 (AFB1, 0.38 mg/kg) for 21 days. Body weight gain and feed conversion ratio did not differ significantly among the groups. Malondialdehyde concentration of the liver was lower in the group fed the diet contaminated with the combination of T-2 + HT-2 toxin and aflatoxin B1 as compared to the control group or the group fed T-2 + HT-2 toxins. Reduced glutathione (GSH) content of the liver was lower in the T-2 + HT-2 group than in the group fed a combination of T-2, HT-2 and aflatoxin. Reduced glutathione content of the heart was higher in the T-2 + HT-2 group than in the control group. Mycotoxin contamination had no effect on glutathione peroxidase (GSH-Px) activity in comparison to the control, but significantly lower GSH-Px activity was found in the heart of chickens in the T-2 + HT-2 + AFB1 group than in the T-2 + HT-2 group. In this study, T-2 + HT-2 toxin and aflatoxin B1 contamination of the diets did not affect the production traits adversely and did not exert additive effects on lipid peroxidation and on the glutathione redox system.

Clinical signs and progression of lesions in the gizzard are not influenced by inclusion of ground oats or whole wheat in the diet following experimental infection with pathogenic fowl adenovirus serotype 1

In the present study the effects of dietary gizzard stimulation on the development and severity of adenoviral gizzard erosion were investigated. For this purpose, specific pathogen-free broilers were divided into six groups, investigating the influence of an oat-containing diet with higher fibre content, a whole wheat-containing diet and a control diet of nearly identical composition, but containing ground wheat. For each feed administered, one group of birds was experimentally infected on the 10th day of age by the oral route with virulent fowl adenovirus serotype 1 (FAdV-1), recently proven to induce gizzard erosions, while the respective negative control groups remained uninfected. Experimental feed was administered from 2 days post-infection onwards. No significant differences on gizzard health or in weight gain could be detected between uninfected control groups or between FAdV-1 infected groups that received different experimental feed. However, independent of the supplied diet, a significantly reduced weight gain was noted from 7 days post-infection onwards in FAdV-1 infected broilers compared to uninfected birds that received the same diet. Macroscopically, discolouration and erosion of the koilin layer and inflammation of the gizzard mucosa were observed in all FAdV-1 infected groups. Histologically, necrosis, degeneration of gizzard epithelial cells and multiple basophilic intranuclear inclusion bodies were observed. In summary, after experimental infection with FAdV-1 development of gizzard erosion in chickens was not influenced by the feeding regimes investigated. Therefore, it is unlikely that dietary gizzard stimulation influences the outcome of adenoviral gizzard erosion in vertically infected broilers.

Effect of feeding different oils on plasma corticosterone in broiler chickens

A study was conducted to examine the effects of different oils on the plasma corticosterone concentrations of broiler chickens fed ad libitum or deprived of feed for 24 hours. A total of 36 Ross broilers were randomly assigned to one of three dietary treatments at 10 days of age and fed a grower diet supplemented with 60 g/kg soybean oil (rich in linoleic acid, C18:2n-6), linseed oil (rich in a-linolenic acid, C18:3n-3) or fish oil (rich in C14:0, C16:0, C16:1n-7, C20:1n-9; eicosapentaenoic acid and docosahexaenoic acid, EPA, C20:5n-3 and DHA, C22:6n-3), respectively, for 18 days. Dietary supplementation of fish oil resulted in lower (P < 0.05) baseline plasma corticosterone levels of chickens fed ad libitum for 18 days compared to soybean and linseed oil supplementations. Feed deprivation for 24 h induced a significant (P < 0.05) increase in corticosterone concentration in every treatment group compared to the ad libitum-fed birds. The hormone levels of feed-deprived birds did not differ significantly among groups fed diets supplemented with different oils.

Nutritional modulation of intestinal drug-metabolizing cytochrome P450 by butyrate of different origin in chicken

Intestinal cytochrome P450 (CYP) enzymes play key role in the first pass metabolism of orally ingested xenobiotics, providing a primary metabolic barrier, being of special importance in maintaining animal health and production. This study was aimed to investigate how intestinal drug-metabolizing CYPs can be modulated by nutritional factors in broiler chicken. We investigated the effects of the natural growth promoter (n-)butyrate of different origin (feed supplementation of protected or non-protected forms and/or inducing caecal microbial production by supporting higher level of dietary non-starch polysaccharides [NSP]) on the activity of duodenal CYPs. To observe the connection between intestinal CYP activity and butyrate concentration, the distribution of differently originated butyrate was also assessed by measuring its concentration in various intestinal segments and different vessels of portal and systemic circulation. Butyrate of different origin showed varying distribution properties as being absorbed from different parts of the gastrointestinal tract. Intestinal CYP1A and CYP2H2 activities were increased by dietary butyrate supplementation and by the increased caecal microbial butyrate production, while CYP3A37 activity was minimally influenced by microbial butyrate only. The present study proved that both dietary and microbial butyrate could alter the activity of CYPs in the duodenal epithelium. Our findings suggest that intestinal CYPs could be induced not only by the intestinal luminal butyrate, but also from basolateral side, by the already absorbed butyrate. Such action of butyrate can be of special importance from food safety and pharmacotherapeutic point of view as it may modify the metabolism and intestinal kinetics of simultaneously applied xenobiotics.

Effects of butyrate on the insulin homeostasis of chickens kept on maize- or wheat-based diets

The aim of the present study was to investigate the effects of butyrate as a feed supplement on the expression of insulin signalling proteins as potent regulators of metabolism and growth in Ross 308 broiler chickens fed maize- or wheat-based diets. Both diets were supplemented with non-protected butyrate (1.5 and 3.0 g/kg of diet, respectively) or with protected butyrate (0.2 g/kg of diet); the diet of the control groups was prepared without any additives (control). On day 42 of life, systemic blood samples were drawn for analyses of glucose and insulin concentrations, and tissue samples (liver, gastrocnemius muscle and subcutaneous adipose tissue) were taken for Western blotting examinations. The expression of key insulin signalling proteins (IRβ, PKCζ and mTOR) was assessed by semiquantitative Western blotting from the tissues mentioned. The type of diet had a remarkable influence on the insulin homeostasis of chickens. The wheat-based diet significantly increased IRβ and mTOR expression in the liver as well as mTOR and PKCζ expression in the adipose tissue when compared to animals kept on a maize-based diet. IRβ expression in the liver was stimulated by the lower dose of non-protected butyrate as well, suggesting the potential of butyrate as a feed additive to affect insulin sensitivity. Based on the results obtained, the present study shows new aspects of nutritional factors by comparing the special effects of butyrate as a feed additive and those of the cereal type, presumably in association with dietary non-starch polysaccharide- (NSP-) driven enteric shortchain fatty acid release including butyrate, influencing insulin homeostasis in chickens. As the tissues of chickens have physiologically lower insulin sensitivity compared to mammals, diet-associated induction of the insulin signalling pathway can be of special importance in improving growth and metabolic health.