Project description:IntroductionPollutant gas emissions in the current production system of the livestock industry have negative influences on environment as well as the health of farm staffs and animals. Although ammonia (NH3) is considered as the primary and harmful gas pollutant in the rabbit farm, less investigation has performed to determine the toxic effects of house ammonia exposure on rabbit in the commercial confined barn.MethodsIn this study, we performed multi-omics analysis on rabbits exposed to high and low concentration of house ammonia under similar environmental conditions to unravel the alterations in nasal and colonic microbiota, pulmonary and colonic gene expression, and muscular metabolic profile.Results and discussionThe results showed that house ammonia exposure notably affected microbial structure, composition, and functional capacity in both nasal and colon, which may impact on local immune responses and inflammatory processes. Transcriptome analysis indicated that genes related to cell death (MCL1, TMBIM6, HSPB1, and CD74) and immune response (CDC42, LAMTOR5, VAMP8, and CTSB) were differentially expressed in the lung, and colonic genes associated with redox state (CAT, SELENBP1, GLUD1, and ALDH1A1) were significantly up-regulated. Several key differentially abundant metabolites such as L-glutamic acid, L-glutamine, L-ornithine, oxoglutaric acid, and isocitric acid were identified in muscle metabolome, which could denote house ammonia exposure perturbed amino acids, nucleotides, and energy metabolism. In addition, the widespread and strong inter-system interplay were uncovered in the integrative correlation network, and central features were confirmed by in vitro experiments. Our findings disclose the comprehensive evidence for the deleterious effects of house ammonia exposure on rabbit and provide valuable information for understanding the underlying impairment mechanisms.
Project description:Heat-induced stress has a significant impact on the health of broilers. It induces panting behavior and elevates oxygen consumption, leading to considerable strain on the broiler lungs. However, the precise effects of heat stress on lung injury, along with changes in the lung and gut microbiota, are not yet fully understood. In our study, Arbor Acres (AA) broilers were employed as a model to assess the efficacy of sodium butyrate (SB) in mitigating heat stress-induced lung injury, while concurrently exploring the potential role of lung and gut microbiota in this phenomenon. Heat stress negatively affected broilers, particularly leading to lung injury, which was alleviated by dietary supplementation with SB. However, antibiotic-induced dysbiosis of the microbiota diminished the protective effects of SB, highlighting the critical importance of gut microbiota homeostasis. Heat stress resulted in a reduction in lung microbial diversity and altered its composition, primarily due to the depletion of g_Clostridia and the proliferation of g_Staphylococcus. SB supplementation helped restore beneficial microbes and improved their adaptation to heat stress. Heat stress induced comparable effects on the gut microbiota, resulting in a decline in p_Firmicutes and an elevation in p_Bacteroidetes. However, SB supplementation effectively modulated these alterations in the gut microbiota, promoting a more beneficial microbial profile. Our findings highlighted the significant contributions of both lung and gut microbiota in maintaining homeostasis during heat stress. Moreover, SB administration demonstrated its efficacy in mitigating heat stress-induced lung injury in broilers. This study provides critical insights for developing dietary strategies to reduce heat stress and promote broiler health.
Project description:Enterococcus cecorum (EC) is one of the most relevant bacterial pathogens in modern broiler chicken production from an economic and animal welfare perspective. Although EC pathogenesis is generally well described, predisposing factors are still unknown. This study aimed to understand the effect of heat stress on the caecal microbiota, intestinal integrity, and EC pathogenesis. A total of 373 1-day-old commercial broiler chicks were randomly assigned to four groups: (1) noninoculated, thermoneutral conditions (TN); (2) noninoculated, heat stress conditions (HS); (3) EC-inoculated, thermoneutral conditions (TN + EC); and (4) EC-inoculated, heat stress conditions (HS + EC). Birds were monitored daily for clinical signs. Necropsy of 20 broilers per group was performed at 7, 14, 21, and 42 days post-hatch (dph). A trend towards enhanced and more pronounced clinical disease was observed in the EC-inoculated, heat-stressed group. EC detection rates in extraintestinal tissues via culture were higher in the HS + EC group (~19%) than in the TN + EC group (~11%). Significantly more birds were colonized by EC at 7 dph in the HS + EC group (100%) than in the TN + EC group (65%, p < 0.05). The caecal microbiota in the two EC-inoculated groups was significantly more diverse than that in the TN group (p < 0.05) at 14 dph, which may indicate an effect of EC infection. An influence of heat stress on mRNA expression of tight junction proteins in the caecum was detected at 7 dph, where all six investigated tight junction proteins were expressed at significantly lower levels in the heat stressed groups compared to the thermoneutral groups. These observations suggest that heat stress may predispose broilers to EC-associated disease and increase the severity thereof. Furthermore, heat stress may impair intestinal integrity and promote EC translocation.
Project description:The effects of early heat conditioning on the acute heat stress response in broilers were investigated via the growth performance, dopamine, serotonin, and corticosterone and the expression of heat shock proteins (HSP) and heat shock factors. One-day-old chicks (n = 144) were divided into 3 groups in a 35-d experiment (48 chicks per each group). Group 1 (C) was treated with an optimum temperature, group 2 (CH) was treated with 40°C ± 1°C on day 35 (5 h), and group 3 (HH) was treated with 40°C ± 1°C on day 5 (24 h) and day 35 (5 h). On day 7, the body weight gain was lower (P < 0.05) in HH than in C and CH. On day 35, the heat-treated groups (CH and HH) had lower weight gains than the C group (P < 0.05), whereas the feed conversion ratio was lower in HH (P < 0.05). Serum corticosterone was higher in CH than in C, but HH and C did not differ (P < 0.05). Liver HSP70 protein expression was higher in CH than HH and C (P < 0.05), which did not differ, and HSP40 protein expression was higher in CH than C (P < 0.05). These results suggest that early heat conditioning may reduce acute heat stress on broiler.
Project description:Heat stress (HS) can inhibit the growth performance of broilers and cause substantial economic losses. Alterations in bile acid (BA) pools have been reported to be correlated with chronic HS, yet the specific mechanism and whether it is related to gut microbiota remains unclear. In this study, 40 Rugao Yellow chickens were randomly selected and distributed into two groups (20 broilers in each group) when reaching 56-day age: a chronic heat stress group (HS, 36 ± 1 °C for 8 h per day in the first 7 days and 36 ± 1 °C for 24 h in the last 7 days) and a control group (CN, 24 ± 1 °C for 24 h within 14 days). Compared with the CN group, total BAs' serum content decreased, while cholic acid (CA), chenodeoxycholic acid (CDCA), and taurolithocholic acid (TLCA) increased significantly in HS broilers. Moreover, 12α-hydroxylase (CYP8B1) and bile salt export protein (BSEP) were upregulated in the liver, and the expression of fibroblast growth factor 19 (FGF19) decreased in the ileum of HS broilers. There were also significant changes in gut microbial composition, and the enrichment of Peptoniphilus was positively correlated with the increased serum level of TLCA. These results indicate that chronic HS disrupts the homeostasis of BA metabolism in broilers, which is associated with alterations in gut microbiota.
Project description:Global warming is one of the most common environmental challenges faced by cold-water fish farming. Intestinal barrier function, gut microbiota, and gut microbial metabolites are significantly altered under heat stress, posing serious obstacles to the healthy artificial culture of rainbow trout. However, the molecular mechanisms underlying intestinal injury in rainbow trout under heat stress remain unclear. In the present study, the optimal growth temperature for rainbow trout (16 °C) was used for the control group, and the maximum temperature tolerated by rainbow trout (24 °C) was used for the heat stress group, which was subjected to heat stress for 21 days. The mechanism of intestinal injury in rainbow trout under heat stress was explored by combining animal histology, 16S rRNA gene amplicon sequencing, ultra-high performance liquid chromatography-mass spectrometry, and transcriptome sequencing. The results showed that the antioxidant capacity of rainbow trout was enhanced under heat stress, the levels of stress-related hormones were significantly increased, and the relative expression of genes related to heat stress proteins was significantly increased, indicating that the heat stress model of rainbow trout was successfully established. Secondly, the intestinal tract of rainbow trout showed inflammatory pathological characteristics under heat stress, with increased permeability, activation of the inflammatory factor signaling pathway, and increased relative expression of inflammatory factor genes, suggesting that the intestinal barrier function was impaired. Thirdly, heat stress caused an imbalance of intestinal commensal microbiota and changes in intestinal metabolites in rainbow trout, which participated in the stress response mainly by affecting lipid metabolism and amino acid metabolism. Finally, heat stress promoted intestinal injury in rainbow trout by activating the peroxisome proliferator-activated receptor-α signaling pathway. These results not only expand the understanding of fish stress physiology and regulation mechanisms, but also provide a scientific basis for healthy artificial culture and the reduction of rainbow trout production costs.
Project description:BackgroundGlobal warming leading to heat stress (HS) is becoming a major challenge for broiler production. This study aimed to explore the protective effects of seaweed (Enteromorpha prolifera) polysaccharides (EPS) on the intestinal barrier function, microbial ecology, and performance of broilers under HS. A total of 144 yellow-feathered broilers (male, 56 days old) with 682.59 ± 7.38 g were randomly assigned to 3 groups: 1) TN (thermal neutral zone, 23.6 ± 1.8 °C), 2) HS (heat stress, 33.2 ± 1.5 °C for 10 h/d), and 3) HSE (HS + 0.1% EPS). Each group contained 6 replicates with 8 broilers per replicate. The study was conducted for 4 weeks; feed intake and body weights were measured at the end of weeks 2 and 4. At the end of the feeding trial, small intestine samples were collected for histomorphology, antioxidant, secretory immunoglobulin A (sIgA) content, apoptosis, gene and protein expression analysis; cecal contents were also collected for microbiota analysis based on 16S rDNA sequencing.ResultsDietary EPS promoted the average daily gain (ADG) of broilers during 3-4 weeks of HS (P < 0.05). At the end of HS on broilers, the activity of total superoxide dismutase (T-SOD), glutathione S-transferase (GST), and the content of sIgA in jejunum were improved by EPS supplementation (P < 0.05). Besides, dietary EPS reduced the epithelial cell apoptosis of jejunum and ileum in heat-stressed broilers (P < 0.05). Addition of EPS in HS group broilers' diet upregulated the relative mRNA expression of Occludin, ZO-1, γ-GCLc and IL-10 of the jejunum (P < 0.05), whereas downregulated the relative mRNA expression of NF-κB p65, TNF-α and IL-1β of the jejunum (P < 0.05). Dietary EPS increased the protein expression of Occludin and ZO-1, whereas it reduced the protein expression of NF-κB p65 and MLCK (P < 0.01) and tended to decrease the protein expression of TNF-α (P = 0.094) in heat-stressed broilers. Furthermore, the proportions of Bacteroides and Oscillospira among the three groups were positively associated with jejunal apoptosis and pro-inflammatory cytokine expression (P < 0.05) and negatively correlated with jejunal Occludin level (P < 0.05). However, the proportions of Lactobacillus, Barnesiella, Subdoligranulum, Megasphaera, Collinsella, and Blautia among the three groups were positively related to ADG (P < 0.05).ConclusionsEPS can be used as a feed additive in yellow-feathered broilers. It effectively improves growth performance and alleviates HS-induced intestinal injury by relieving inflammatory damage and improving the tight junction proteins expression. These beneficial effects may be related to inhibiting NF-κB/MLCK signaling pathway activation and regulation of cecal microbiota.
Project description:The increasing trend of global warming has affected the livestock industry through the heat stress, especially in poultry. Therefore, a better understanding of the mechanisms of heat stress in poultry would be helpful for maintaining the poultry production. Three groups were designed to determine early heat stress effects during chronic heat stress: CC, raised at a comfortable temperature; CH, chronic heat exposure at 35 °C for 21-35 days continuously; and HH, early heat exposure at 40 °C for 24 h at 5 days old with 35 °C temperature for 21-35 days continuously. In this study, proteome analysis was carried out to identify differentially expressed proteins in the liver tissue of broilers under chronic and early heat exposure. There were eight differentially expressed proteins from early heat stress during chronic heat exposure, which were related to actin metabolism. According to KEGG (Kyoto encyclopedia of genes and genomes) analysis, the proteins involved in carbohydrate metabolism were expressed to promote the metabolism of carbohydrates under chronic heat stress. Early heat reduced the heat stress-induced expression changes of select proteins. Our study has shown that early heat exposure suggests that the liver of broilers has various physiological mechanisms for regulating homeostasis to aid heat resistance.
Project description:This study evaluated the effects of vitamin E (Vit E) and selenium (Se) supplementation on mRNA abundance of antioxidant, immune response, and tight junction genes, as well as taxonomic and functional profiles of ileal microbiota of broilers exposed to daily 4-h elevated temperature during d 28 to 35. A total of 640-day-old Cobb male broiler chicks were randomly allocated to 32 floor pens in a 2 × 2 factorial arrangement that included ambient temperature (thermoneutral [TN] or heat stress [HS]) and dietary treatments (basal diet or Vit E + Se). Vit E and organic Se were added to the basal diet at the rate of 250 mg/kg and 1 mg/kg, respectively. Liver and jejunum tissue samples were taken on d 27 (1 bird/pen), d 28 and d 35 (2 birds/pen) from birds for qPCR analysis. Data were subjected to a 2-way ANOVA using the GLM procedure of JMP. Ileal contents were taken on d 27 and d 35 for microbial profiling. Microbiota data were analyzed in QIIME 2 and significance between treatments identified linear discriminant analysis effect size (LEfSe, P < 0.05). Dietary Vit E/Se significantly downregulated the mRNA levels of HSPs in liver and jejunal tissues of the HS-challenged birds both on d 28 and d 35. Moreover, mRNA abundance of TLR2, TNFα, IFNγ, IL-1β, IL-10, and iNOS in the liver were significantly downregulated in birds fed the Vit E/Se diet on d 35. However, dietary treatment had no significant impact on oxidative stress, immunity, and gut integrity related genes analyzed in jejunal tissues on d 28 and d 35, except downregulation of IFNγ on d 35 (P = 0.052). LEfSe analysis revealed that Lachnospiraceae FE2018 and Ruminococcaceae NK4A214 groups was enriched in the Vit E/Se birds on d 35. Moreover, PICRUSt analysis predicted significant functional differences among the treatment groups. In conclusion, dietary supplementation of Vit E/Se mitigated the negative effects of HS potentially via improving antioxidant status, regulating cytokine responses and modifying ileal microbiota and its function.
Project description:Heat stress is one of the most prevalent issues in poultry production that reduces performance, robustness, and economic gains. Previous studies have demonstrated that native chickens are more tolerant of heat than commercial breeds. However, the underlying mechanisms of the heat tolerance observed in native chicken breeds remain unelucidated. Therefore, we performed a phenotypical, physiological, liver transcriptome comparative analysis and WGCNA in response to heat stress in one native (Beijing You, BY) and one commercial (Guang Ming, GM) chicken breed. The objective of this study was to evaluate the heat tolerance and identify the potential driver and hub genes related to heat stress in these two genetically distinct chicken breeds. In brief, 80 BY and 60 GM, 21 days old chickens were submitted to a heat stress experiment for 5 days (33 °C, 8 h/day). Each breed was divided into experimental groups of control (Ctl) and heat stress (HS). The results showed that BY chickens were less affected by heat stress and displayed reduced DEGs than GM chickens, 365 DEGs and 382 DEGs, respectively. The transcriptome analysis showed that BY chickens exhibited enriched pathways related to metabolism activity, meanwhile GM chickens' pathways were related to inflammatory reactions. CPT1A and ANGPTL4 for BY chickens, and HSP90B1 and HSPA5 for GM chickens were identified as potential candidate genes associated with HS. The WGCNA revealed TLR7, AR, BAG3 genes as hub genes, which could play an important role in HS. The results generated in this study provide valuable resources for studying liver transcriptome in response to heat stress in native and commercial chicken lines.