Heat stress has been considered as a critical risk factor for decreasing performance and causing oxidative stress in broilers. The tryptophan (TRP) derivative 5-hydroxytryptophan has been reported to protect membrane fluidity in broilers suffering from oxidative stress. Therefore, this experiment was conducted to investigate the effects of dietary TRP supplementation on antioxidant status and mitochondrial function-related genes expressions in broilers exposed to acute heat stress (34 ± 1°C, 24 h). Female Arbor Acres broilers (19-d-old, n = 180) were randomly assigned to 1 of 3 treatments. Broilers were fed a basal diet and in the thermoneutral conditions (TN, 23 ± 1°C) was considered as the TN group. Broilers were fed a basal diet and exposed to acute heat stress (HS, 34 ± 1°C) was regarded as the HS group. Broilers were fed a basal diet supplemented with 0.18% L-tryptophan and under HS conditions was treated as the HS + TRP groups. Heat stress led to increased malondialdehyde (MDA) concentration (P < 0.05), while it elevated catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and total antioxidant capacity activities (T-AOC) (P < 0.05) compared with the TN group. Nevertheless, compared with the HS group, TRP supplementation increased SOD activity (P < 0.05). The effects of acute heat stress were associated with increased mRNA abundance for redox-related genes (P < 0.05), and reduced mRNA levels for mitochondrial function-related genes (P < 0.05). Notably, the effects of acute heat stress on mitochondrial function-related genes expressions were reversed by TRP treatment. Collectively, dietary 0.18% TRP supplementation beneficially protects against acute heat stress-induced oxidation stress and mitochondrial dysfunction by regulating antioxidant states and increasing mitochondrial function-related genes expressions in broilers.
BackgroundThe dysbiosis of respiratory microbiota plays an important role in asthma development. However, there is limited information on the changes in the respiratory microbiota and how these affect the host during the progression from acute allergic inflammation to airway remodeling in asthma.ObjectiveAn ovalbumin (OVA)-induced mouse model of chronic asthma was established to explore the dynamic changes in the respiratory microbiota in the different stages of asthma and their association with chronic asthma progression.MethodsHematoxylin and eosin (H&E), periodic acid-schiff (PAS), and Masson staining were performed to observe the pathological changes in the lung tissues of asthmatic mice. The respiratory microbiota was analyzed using 16S rRNA gene sequencing followed by taxonomical analysis. The cytokine levels in bronchoalveolar lavage fluid (BALF) specimens were measured. The matrix metallopeptidase 9 (MMP-9) and vascular endothelial growth factor (VEGF-A) expression levels in lung tissues were measured to detect airway remodeling in OVA-challenged mice.ResultsAcute allergic inflammation was the major manifestation at weeks 1 and 2 after OVA atomization stimulation, whereas at week 6 after the stimulation, airway remodeling was the most prominent observation. In the acute inflammatory stage, Pseudomonas was more abundant, whereas Staphylococcus and Cupriavidus were more abundant at the airway remodeling stage. The microbial compositions of the upper and lower respiratory tracts were similar. However, the dominant respiratory microbiota in the acute inflammatory and airway remodeling phases were different. Metagenomic functional prediction showed that the pathways significantly upregulated in the acute inflammatory phase and airway remodeling phase were different. The cytokine levels in BALF and the expression patterns of proteins associated with airway remodeling in the lung tissue were consistent with the metagenomic function results.ConclusionThe dynamic changes in respiratory microbiota are closely associated with the progression of chronic asthma. Metagenomic functional prediction indicated the changes associated with acute allergic inflammation and airway remodeling.
The present study was conducted to investigate the effects of tryptophan supplementation on the rectal temperature, hormone, and cytokine levels in broilers subjected to acute heat stress. A total of 300 female Arbor Acres broilers were randomly allocated to ve dietary treatment groups with 6 replicates per treatment group and 10 birds per replicate. Broilers raised under thermoneutral (TN) conditions (22 ± 1°C) were fed a basal diet, and other broilers exposed to acute heat stress (34 ± 1°C) for 24 h were fed basal diets supplemented with 0%, 0.09%, 0.18%, and 0.27% tryptophan. Results indicated that acute heat stress increased the rectal temperature (P < 0.05), enhanced the concentrations of corticosterone, dopamine, adrenaline, adrenocorticotrophic hormone, and corticotropin-releasing hormone in serum (P < 0.05), and elevated the levels of serum tryptophan hydroxylase 1, tryptophan 2, 3-dioxygenase, and indoleamine 2, 3dioxygenase, and kynurenate (P < 0.05), as compared with the TN group. Meanwhile, acute heat stress increased the levels of serum tryptophan, hypothalamic tryptophan, 5-hydroxytryptophan, and interleukin-22 (P < 0.05) relative to the TN group. However, dietary tryptophan supplementation decreased the rectal temperature, reduce the levels of hormones associated with heat stress, and promoted the immune functions of heat-stressed broilers. Moreover, dietary supplemented with 0.18% tryptophan was evaluated to be the optimal level in broilers reared under acute heat stress.
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