Effects of delayed feeding, sodium butyrate and glutamine on intestinal permeability in newly-hatched broiler chickens

The aim of the current study was to investigate the effects of delayed feeding, and supplementation with sodium butyrate or glutamine in drinking water, on intestinal permeability (IP) in young broiler chickens. Newly-hatched male chickens (Ross 308) were allocated to four groups comprising Control, 24 h delayed fed (DF), DF supplemented with sodium butyrate (0.1%) in the drinking water and DF supplemented with glutamine (1%) in the drinking water. On days 2, 4 and 7, twelve birds per group were randomly selected, weighed and orally gavaged with fluorescein isothiocyanate dextran (FITC-d) at 2.2 mg / ml / chicken. Serum FITC-d concentration was analysed by spectrophotometry while serum diamine oxidase and D-lactic acid concentrations were analysed by microplate reader. FITC-d concentrations in the Control and DF groups were not statistically different on any day, suggesting that delayed feeding did not affect IP. Additionally, sodium butyrate increased IP compared to DF and Control on day 2 only (p

Mucin Gene mRNA Levels in Broilers Challenged with 'Eimeria' and/or 'Clostridium perfringens'

The effects of 'Eimeria' (EM) and 'Clostridium perfringens' (CP) challenges on the mRNA levels of genes involved in mucin (Muc) synthesis (Muc2, Muc5ac, Muc13, and trefoil family factor-2 [TFF2]), inflammation (tumor necrosis factor alpha [TNF-α] and interleukin-18 [IL-18]), and metabolic processes (cluster of differentiation [CD]36) in the jejunum of broilers were investigated. Two parallel experiments involving 1) EM challenge and 2) EM and CP challenges were conducted. The first experiment was a 2 x 2 study with 12 birds per treatment (N 5 48) involving fishmeal substitution (25%) in the diet (FM) and EM challenge. The treatments were: Control (FM2, EM2), Fishmeal (FM+, EM2), EM challenge (FM2, EM+), and fishmeal substitution and EM challenge (FM+, EM+). The second experiment was a 2 x 2 x 2 experiment with six birds per treatment (N = 5 48) involving fishmeal (FM2, FM+), 'Eimeria' (EM2, EM+), and 'C. perfringens' (CP2, CP+). In both arms of the study, male broilers were given a starter diet for the whole period of 16 days, except those assigned to FM+, where 25% of the starter ration was replaced with fishmeal from days 8 to 14. EM inoculation was performed on day 9 and CP inoculation on days 14 and 15. The EM challenge birds were euthanatized for sampling on day 13; postmortem examination and sampling for the 'Eimeria' plus 'C. perfringens' challenge arm of the study were on day 16. In the 'Eimeria' challenge arm of the study, fishmeal supplementation significantly suppressed the mRNA levels of TNF-α, TFF2, and IL-18 pre-CP inoculation but simultaneously increased the levels of Muc13 and CD36 mRNAs. Birds challenged with Eimeria exhibited increased mRNA levels of Muc13, Muc5ac, TNF-a, and IL-18. In the 'Eimeria' and 'C. perfringens' challenge arm, birds exposed to EM challenge exhibited significantly lower mRNA levels of Muc2 and CD36. The mRNA levels of CD36 were also significantly suppressed by CP challenge. Our results showed that the transcription of mucin synthesis genes in the jejunum of broilers is modulated by fishmeal inclusion in the diet. Furthermore, we show for the first time suppression of CD36 mRNA levels in the intestine of broilers challenged with 'Eimeria' or 'C. perfringens'

Evaluation of fatty acid metabolism and innate immunity interactions between commercial broiler, F1 layer × broiler cross and commercial layer strains selected for different growth potentials

Abstract Background The broiler industry has undergone intense genetic selection over the past 50 yr. resulting in improvements for growth and feed efficiency, however, significant variation remains for performance and growth traits. Production improvements have been coupled with unfavourable metabolic consequences, including immunological trade-offs for growth, and excess fat deposition. To determine whether interactions between fatty acid (FA) metabolism and innate immunity may be associated with performance variations commonly seen within commercial broiler flocks, total carcass lipid %, carcass and blood FA composition, as well as genes involved with FA metabolism, immunity and cellular stress were investigated in male birds of a broiler strain, layer strain and F1 layer × broiler cross at d 14 post hatch. Heterophil: lymphocyte ratios, relative organ weights and bodyweight data were also compared. Results Broiler bodyweight (n = 12) was four times that of layers (n = 12) by d 14 and had significantly higher carcass fat percentage compared to the cross (n = 6; P = 0.002) and layers (P = 0.017) which were not significantly different from each other (P = 0.523). The carcass and whole blood FA analysis revealed differences in the FA composition between the three groups indicating altered FA metabolism, despite all being raised on the same diet. Genes associated with FA synthesis and β-oxidation were upregulated in the broilers compared to the layers indicating a net overall increase in FA metabolism, which may be driven by the larger relative liver size as a percentage of bodyweight in the broilers. Genes involved in innate immunity such as TLR2 and TLR4, as well as organelle stress indicators ERN1 and XBP1 were found to be non-significant, with the exception of high expression levels of XBP1 in layers compared to the cross and broilers. Additionally there was no difference in heterophil: lymphocytes between any of the birds. Conclusions The results provide evidence that genetic selection may be associated with altered metabolic processes between broilers, layers and their F1 cross. Whilst there is no evidence of interactions between FA metabolism, innate immunity or cellular stress, further investigations at later time points as growth and fat deposition increase would provide useful information as to the effects of divergent selection on key metabolic and immunological processes

Effects of delayed feeding, sodium butyrate and glutamine on intestinal permeability in newly-hatched broiler chickens

The aim of the current study was to investigate the effects of delayed feeding, and supplementation with sodium butyrate or glutamine in drinking water, on intestinal permeability (IP) in young broiler chickens. Newly-hatched male chickens (Ross 308) were allocated to four groups comprising Control, 24 h delayed fed (DF), DF supplemented with sodium butyrate (0.1%) in the drinking water and DF supplemented with glutamine (1%) in the drinking water. On days 2, 4 and 7, twelve birds per group were randomly selected, weighed and orally gavaged with fluorescein isothiocyanate dextran (FITC-d) at 2.2 mg / ml / chicken. Serum FITC-d concentration was analysed by spectrophotometry while serum diamine oxidase and d-lactic acid concentrations were analysed by microplate reader. FITC-d concentrations in the Control and DF groups were not statistically different on any day, suggesting that delayed feeding did not affect IP. Additionally, sodium butyrate increased IP compared to DF and Control on day 2 only (p < 0.05), while glutamine increased IP on all days, compared to DF and Control (p < 0.05). Diamine oxidase and d-lactic acid concentrations of all groups were not statistically different

Mechanisms Contributing to the Comorbidity of COPD and Lung Cancer

Lung cancer and chronic obstructive pulmonary disease (COPD) often co-occur, and individuals with COPD are at a higher risk of developing lung cancer. While the underlying mechanism for this risk is not well understood, its major contributing factors have been proposed to include genomic, immune, and microenvironment dysregulation. Here, we review the evidence and significant studies that explore the mechanisms underlying the heightened lung cancer risk in people with COPD. Genetic and epigenetic changes, as well as the aberrant expression of non-coding RNAs, predispose the lung epithelium to carcinogenesis by altering the expression of cancer- and immune-related genes. Oxidative stress generated by tobacco smoking plays a role in reducing genomic integrity, promoting epithelial-mesenchymal-transition, and generating a chronic inflammatory environment. This leads to abnormal immune responses that promote cancer development, though not all smokers develop lung cancer. Sex differences in the metabolism of tobacco smoke predispose females to developing COPD and accumulating damage from oxidative stress that poses a risk for the development of lung cancer. Dysregulation of the lung microenvironment and microbiome contributes to chronic inflammation, which is observed in COPD and known to facilitate cancer initiation in various tumor types. Further, there is a need to better characterize and identify the proportion of individuals with COPD who are at a high risk for developing lung cancer. We evaluate possible novel and individualized screening strategies, including biomarkers identified in genetic studies and exhaled breath condensate analysis. We also discuss the use of corticosteroids and statins as chemopreventive agents to prevent lung cancer. It is crucial that we optimize the current methods for the early detection and management of lung cancer and COPD in order to improve the health outcomes for a large affected population

Mechanisms Contributing to the Comorbidity of COPD and Lung Cancer

Lung cancer and chronic obstructive pulmonary disease (COPD) often co-occur, and individuals with COPD are at a higher risk of developing lung cancer. While the underlying mechanism for this risk is not well understood, its major contributing factors have been proposed to include genomic, immune, and microenvironment dysregulation. Here, we review the evidence and significant studies that explore the mechanisms underlying the heightened lung cancer risk in people with COPD. Genetic and epigenetic changes, as well as the aberrant expression of non-coding RNAs, predispose the lung epithelium to carcinogenesis by altering the expression of cancer- and immune-related genes. Oxidative stress generated by tobacco smoking plays a role in reducing genomic integrity, promoting epithelial-mesenchymal-transition, and generating a chronic inflammatory environment. This leads to abnormal immune responses that promote cancer development, though not all smokers develop lung cancer. Sex differences in the metabolism of tobacco smoke predispose females to developing COPD and accumulating damage from oxidative stress that poses a risk for the development of lung cancer. Dysregulation of the lung microenvironment and microbiome contributes to chronic inflammation, which is observed in COPD and known to facilitate cancer initiation in various tumor types. Further, there is a need to better characterize and identify the proportion of individuals with COPD who are at a high risk for developing lung cancer. We evaluate possible novel and individualized screening strategies, including biomarkers identified in genetic studies and exhaled breath condensate analysis. We also discuss the use of corticosteroids and statins as chemopreventive agents to prevent lung cancer. It is crucial that we optimize the current methods for the early detection and management of lung cancer and COPD in order to improve the health outcomes for a large affected population