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1.
Poult Sci ; 103(6): 103695, 2024 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-38626693

RESUMEN

This research assessed the impacts of dietary nano-propolis liposomes (NPRL) inclusion on the growth, blood biochemical components, immune function, and oxidative status of broilers exposed to cyclic heat stress (HS). Birds were fed with a basal diet supplemented with various levels of NPRL at 0 (HS), 100 (NPRL100), 250 (NPRL250) and 400 (NPRL400) mg/kg diets. Diets supplemented with NPRL significantly improved the growth indices and feed utilization, hemoglobin and red blood cells (P < 0.01). White blood cells, lymphocytes and monocytes were significantly decreased by NPRL inclusion (P < 0.001). Dietary supplementation of 250 or 400 mg of NPRL /kg reduced the pathogenic bacteria counts (Salmonella, E. coli and Enterococci) (P < 0.01). The birds fed diets with NPRL (400 mg/kg diet) significantly downregulated the mRNA IFNγ gene (p < 0.001), while both groups (NPRL100 and NPRL250) had similar results (P > 0.05). The iNOS gene was significantly decreased by the dietary NPRL inclusion in a dose-dependent manner. Birds in NRPL groups had inferior levels of the mRNA of interleukin-4 and tumor necrosis factor genes. The lysosome activity was significantly reduced by dietary 250 or 400 mg of NPRL inclusion (P < 0.001). Birds in NPRL250 and NPRL100 had greater IgG (P < 0.05) than the other groups. Regarding oxidative-related biomarkers, dietary NPRL inclusion decreased myeloperoxidase and malondialdehyde levels significantly compared to those with the HS group (P < 0.001). Broilers in the NPRL400 group had the lowest levels of total bilirubin and gamma-glutamyl transferase. NPRL250 had the lowest values of urea compared with other groups (P < 0.001). Dietary NPRL inclusion improved the broiler's hepatic and intestinal architecture exposed to cyclic heat stress. These results indicate that employing NPRL in the diets of stressed broilers can enhance heat resistance by enhancing blood metabolites and immunity, reducing inflammation and oxidative stress.


Asunto(s)
Alimentación Animal , Pollos , Dieta , Suplementos Dietéticos , Liposomas , Animales , Pollos/fisiología , Pollos/crecimiento & desarrollo , Alimentación Animal/análisis , Liposomas/administración & dosificación , Liposomas/química , Dieta/veterinaria , Suplementos Dietéticos/análisis , Masculino , Distribución Aleatoria , Respuesta al Choque Térmico/efectos de los fármacos , Nanopartículas/administración & dosificación , Nanopartículas/química , Relación Dosis-Respuesta a Droga , Enfermedades de las Aves de Corral/prevención & control , Trastornos de Estrés por Calor/veterinaria
2.
Poult Sci ; 103(1): 103218, 2024 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-37980733

RESUMEN

Heat stress (HS) is still the essential environmental agent influencing the poultry industry. Research on HS in poultry has progressively acquired growing interest because of increased attention to climate alteration. Poultry can survive at certain zone of environmental temperatures, so it could be considered homoeothermic. In poultry, the normal body temperature is essential to enhance the internal environment for growth, which is achieved by normal environmental temperature. Recently, many studies have revealed that HS could cause mitochondrial dysfunction in broilers by inducing redox dysfunction, increasing uncoupling protein, boosting lipid and protein oxidation, and oxidative stress. Moreover, HS diminished the energy suppliers supported by mitochondria activity. A novel strategy for combating the negative influences of HS via boosting the mitochondria function through enrichment of the diets with mitochondria enhancers was also described in this review. Finally, the current review highlights the mitochondria dysfunction induced by HS in broilers and attempts to boost mitochondria functionality by enriching mitochondria enhancers to broiler diets.


Asunto(s)
Pollos , Aves de Corral , Animales , Estrés Oxidativo , Respuesta al Choque Térmico , Mitocondrias/metabolismo
3.
Front Microbiol ; 14: 1135806, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-37089535

RESUMEN

Non-typhoidal Salmonella is the tremendously predominant source of acquired foodborne infection in humans, causing salmonellosis which is a global threat to the healthcare system. This threat is even worse when it is combined with the incidence of multidrug-resistant Salmonella strains. Bacteriophage therapy has been proposed as a promising potential candidate to control a diversity of foodborne infective bacteria. The objective of this study designed to isolate and characterize lytic phages infecting zoonotic multi-drug resistant and strong biofilm producer Salmonella enterica serovar Enteritidis EG.SmE1 and then apply the isolated phage/s as a biocontrol agent against infections in ready-to-eat food articles including milk, water, apple juice, and chicken breasts. One lytic phage (LPSent1) was selected based on its robust and stable lytic activity. Phage LPSent1 belonged to the genus Jerseyvirus within the Jerseyvirinae subfamily. The lysis time of phage LPSent1 was 60 min with a latent period of 30 min and each infected cell burst about 112 plaque-forming units. Phage LPSent1 showed a narrow host range. Furthermore, the LPSent1 genome did not encode any virulence or lysogenic genes. In addition, phage LPSent1 had wide pH tolerance, prolonged thermal stability, and was stable in food articles lacking its susceptible host for 48 h. In vitro applications of phage LPSent1 inhibited free planktonic cells and biofilms of Salmonella Enteritidis EG.SmE1 with a lower occurrence to form phage-resistant bacterial mutants which suggests promising applications on food articles. Application of phage LPSent1 at multiplicities of infections of 100 or 1000 showed significant inhibition in the bacterial count of Salmonella Enteritidis EG.SmE1 by 5 log10/sample in milk, water, apple juice, and chicken breasts at either 4°C or 25°C. Accordingly, taken together these findings establish phage LPSent1 as an effective, promising candidate for the biocontrol of MDR Salmonella Enteritidis in ready-to-eat food.

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