Short chain fatty acid (SCFA) butyrate has various beneficial effects on the gut microbiota as well as on the overall health status and metabolism of the host organism. The modulatory role of butyrate on gut barrier integrity reflected by tight junction protein expression has been already described in mammalian species. However, there is limited information available regarding chickens. Therefore, the main aim of this study was to monitor the effects of protected butyrate on claudin barrier protein and monocarboxylate transporter 1 abundance in different gastrointestinal segments of chickens as well as the growth performance of broiler chickens. The effect of protected butyrate on the caecal microbiota was monitored by quantifying the concentrations of total eubacteria and key enzymes of butyrate production. Furthermore, intestinal SCFA concentrations were also measured. Based on the data obtained, protected butyrate increased the overall performance as well as the barrier integrity of various gut segments. Protected butyrate also positively affected the SCFA concentration and composition. These findings provide valuable insight into the complex effects of protected butyrate on broiler gut health, highlighting the beneficial effects in improving intestinal barrier integrity and performance parameters.

Heat stress is one of the most important issues in broiler flocks impairing animal health and productivity. On a cellular level, excess heat exposure can trigger heat shock response acting for the restoration of cell homeostasis by several mechanisms, such as affecting heat shock protein synthesis, redox homeostasis and pro-inflammatory cytokine production. The major aim of this study was to establish a novel avian hepatocyte—nonparenchymal cell co-culture as a model for investigating the cellular effects of heat stress and its interaction with inflammation in chicken liver. Cell fractions were isolated by differential centrifugation from a freshly perfused chicken liver, and hepatocyte mono-cultures as well as hepatocyte–nonparenchymal cell co-cultures (with cell ratio 6:1, hepatocytes to nonparenchymal cells, mimicking a milder hepatic inflammation) were prepared. Isolated and cultured cells were characterized by flow cytometry and immunocytochemistry applying hepatocyte- and macrophage-specific antibodies. Confluent cell cultures were exposed to 43 °C temperature for 1 or 2 h, while controls were cultured at 38.5 °C. The metabolic activity, LDH enzyme activity, reactive oxygen species (H₂O₂) production, extracellular concentration of heat shock protein 70 (HSP70), and that of the pro-inflammatory cytokines interleukin (IL-)6 and IL-8 were assessed. Shorter heat stress applied for 1 h could strongly influence liver cell function by significantly increasing catabolic metabolism and extracellular H₂O₂ release, and by significantly decreasing HSP70, IL-6, and IL-8 production on both cell culture models. However, all these alterations were restored after 2 h heat exposure, indicating a fast recovery of liver cells. Hepatocyte mono-cultures and hepatocyte—nonparenchymal cell co-cultures responded to heat stress in a similar manner, but the higher metabolic rate of co-cultured cells may have contributed to a better capability of inflamed liver cells for accommodation to stress conditions. In conclusion, the established new primary cell culture models provide suitable tools for studying the hepatic inflammatory and stress response. The results of this study highlight the impact of short-term heat stress on the liver in chickens, underline the mediatory role of oxidative stress in acute stress response, and suggest a fast cellular adaptation potential in liver cells.

Trichothecene mycotoxins such as T-2 toxin cause severe problems for agriculture, as well as for veterinary medicine. As liver is one of the key organs in metabolism, the main aim of our study was to investigate the immunomodulatory and cytotoxic effects of T-2 toxin, using primary hepatocyte mono-culture and hepatocyte—nonparenchymal cell (predominantly Kupffer cell) co-culture models of chicken. Cultures were exposed to 10 (T10 group), 100 (T100 group) and 1000 (T1000 group) nmol/L T-2 toxin treatment for 8 or 24 h. Alterations of cellular metabolic activity, the production of reactive oxygen species (extracellular H₂O₂), heat shock protein 70 (HSP70), and the concentration of different inflammatory cytokines such as interleukin (IL-)6 and IL-8 were investigated. Metabolic activity was intensely decreased by T-2 toxin administration in all of the cell culture models, in every applied concentration and incubation time. Concentrations of HSP70 and IL-8 were significantly increased in hepatocyte mono-cultures exposed to higher T-2 toxin levels (both in T100 and T1000 groups for HSP70 and in T1000 group for IL-8, respectively) compared to controls after 24 h incubation. Similarly, IL-6 levels were also significantly elevated in the T100 and T1000 groups in both of mono- and co-cultures, but only after 8 h of incubation time. In spite of the general harmful effects of T-2 toxin treatment, no significant differences were observed on reactive oxygen species production. Furthermore, the two cell culture models showed different levels of H₂O₂, HSP70, and IL-8 concentrations independently of T-2 toxin supplementation. In conclusion, the established primary cell cultures derived from chicken proved to be proper models to study the specific molecular effects caused by T-2 toxin. Metabolic activity and immune status of the different examined cell cultures were intensively affected; however, no changes were found in H₂O₂ levels.

Air pollution is a foremost public health problem worldwide. The pulmonary effects of air pollution have been well established for decades, and substantial epidemiological evidence is consistently showing that both acute and chronic exposure to air pollution is linked to cardiovascular morbidity and mortality. The underlying cause for this link is, however, still unknown, and many questions remain open. Most of the epidemiological studies focusing on health consequences of exposure to urban air used data from air monitoring stations or—when applying personal sampling or monitoring—measured a limited number of components to assess the exposure. On the other hand, studies conducting a decent exposure characterization and measuring a relatively large number of components with personal sampling had little or no focus on the effects and investigated only a few biomarkers. The number of research studies on this topic is huge, but at the same time, it seems as if there was no need for a comprehensive examination of the effects of urban air pollution on health. Researchers and research supporting organizations, in their fascination with the search for “novelty” and “beyond state-of-the-art”, do not seem to be aware of that they will never be able to assemble the whole picture from the puzzle pieces of research activities focusing only on certain aspects. Without a comprehensive investigation, we might never be able to answer such questions as (i) which of the urban air pollutants are forerunners in causing health effects, especially cardiovascular effects? (ii) Which biomarkers have the best predictor performance in early effects? (iii) Are there biomarkers or combinations of biomarkers that can help determine the degree of individual susceptibility and sensitivity and the dependence of these by different factors (e.g., age, gender, and physical activity)? The authors of this article aim to go through the already investigated—at the same time, essential—elements of the topic and propose a more comprehensive study, which, of course, can be expanded, debated, and improved.

The short-chain fatty acid butyrate, either in unprotected or protected form, is widely applied as a growth-promoting feed additive in poultry nutrition; however, its possible effects on the carcass composition of broilers have not been fully elucidated. Further, lowering dietary crude protein (CP) levels is an important issue in poultry farming, contributing to ecologically beneficial lower nitrogen excretion. The main aims of this study were to test how unprotected and protected forms of butyrate and decreased dietary CP content with essential amino acid (lysine, methionine, threonine, tryptophan) supplementation (“LP-EAA” diet) affect carcass parameters and the chemical composition of muscles in broilers. Ross 308 chickens were randomized to seven groups (n=10/group) receiving adequate CP-containing (normal protein, “NP”) or LP-EAA diets, both supplemented with or without unprotected sodium butyrate, and NP diets with different forms of protected sodium butyrate. Carcass traits were measured, and the chemical composition of pectoral and femoral muscles was analyzed at the age of 6 weeks. Carcass weight was significantly increased by the LP-EAA diet and all protected butyrate types tested, while the relative breast meat yield was significantly higher in LP-EAA than NP groups and in both unprotected and protected butyrate-supplemented chickens compared to controls. The protein content of the femoral muscle was significantly decreased, but its lipid content was significantly elevated by the LP-EAA diet and by all types of butyrate addition. However, no changes were detected in the chemical composition of pectoral muscle. In conclusion, breast meat production can be effectively stimulated by dietary factors, such as by reducing dietary CP content with essential amino acid supplementation and by applying butyrate as a feed additive, while its chemical composition remains unchanged, in contrast to the femoral muscle. The aforementioned nutritional strategies seem to be the proper tools to increase carcass yield and to alter meat composition of broilers, contributing to more efficient poultry meat production.

The intestinal microbiome of dogs can be influenced by a number of factors such as non-starch polysaccharides as well as some non-digestible oligo- and disaccharides. These molecules are only decomposed by intestinal anaerobic microbial fermentation, resulting in the formation of volatile fatty acids (VFAs), which play a central role in maintaining the balance of the intestinal flora and affecting the health status of the host organism. In the present study, the effects of lactulose and psyllium husk (Plantago ovata) were investigated regarding their influence on concentrations of various VFAs produced by the canine intestinal microbiome. Thirty dogs were kept on a standard diet for 15 days, during which time half of the animals received oral lactulose once a day, while the other group was given a psyllium-supplemented diet (in 0.67 and in 0.2 g/kg body weight concentrations, respectively). On days 0, 5, 10 and 15 of the experiment, feces were sampled from the rectum, and the concentration of each VFA was determined by GC-MS (gas chromatography–mass spectrometry). Lactulose administration caused a significant increase in the total VFA concentration of the feces on days 10 and 15 of the experiment (p = 0.035 and p < 0.001, respectively); however, in the case of psyllium supplementation, the concentration of VFAs showed a significant elevation only on day 15 (p = 0.003). Concentrations of acetate and propionate increased significantly on days 5, 10 and 15 after lactulose treatment (p = 0.044, p = 0.048 and p < 0.001, respectively). Following psyllium administration, intestinal acetate, propionate and n-butyrate production were stimulated on day 15, as indicated by the fecal VFA levels (p = 0.002, p = 0.035 and p = 0.02, respectively). It can be concluded that both lactulose and psyllium are suitable for enhancing the synthesis of VFAs in the intestines of dogs. Increased acetate and propionate concentrations were observed following the administration of both supplements; however, elevated n-butyrate production was found only after psyllium treatment, suggesting that the applied prebiotics may exert slightly different effects in the hindgut of dogs. These findings can be also of great importance regarding the treatment and management of patients suffering from intestinal disorders as well as hepatic encephalopathy due to portosystemic shunt.