METHODS: A total of 40, one-day-old chickens were fed their basal diet for 42 days and then divided into two groups: SG1 (basal diet) and SG2 (basal diet + 10 g/kg Moringa oleifera leaf powder). Metagenomics analysis was conducted to analyze operational taxonomic units (OTUs), species annotation, and biodiversity. Additionally, 16S rRNA sequencing was performed for molecular characterization of isolated gut bacteria, identified as Enterococcus faecium. The isolated bacteria were tested for essential metabolites, demonstrating antibacterial, antioxidant, and anticancer activities.
RESULTS AND DISCUSSION: The analysis revealed variations in the microbial composition between the control group (SG1) and the M. oleifera-treated group (SG2). SG2 showed a 47% increase in Bacteroides and a 30% decrease in Firmicutes, Proteobacteria, Actinobacteria, and Tenericutes compared to SG1. TM7 bacteria were observed exclusively in the M. oleifera-treated group. These findings suggest that Moringa oleifera leaf powder acts as a modulator that enhances chicken gut microbiota, promoting the colonization of beneficial bacteria. PICRUSt analysis supported these findings, showing increased carbohydrate and lipid metabolism in the M.oleifera-treated gut microbiota.
CONCLUSION: This study indicates that supplementing chicken feed with Moringa oleifera leaf powder as a phytobiotic enhances the gut microbiota in chicken models, potentially improving overall health. The observed changes in bacterial composition, increased presence of Bacteroides, and exclusive presence of TM7 bacteria suggest a positive modulation of microbial balance. The essential metabolites from isolated Enterococcus faecium bacteria further support the potential benefits of Moringa oleifera supplementation.
RESULTS: The amount of total phenolics was estimated to be 70.83 mg Gallic Acid Equivalent (GAE) per gram of dry extract. The antioxidant activity of the L. edodes extract was 39.0% at a concentration of 1 mg/mL and was also concentration dependant, with an EC(50) value of 4.4 mg/mL. Different groups of animals (Wister albino mice) were administered paracetamol (1 g/kg, p.o.). L. edodes extract at a dose of 200 mg/kg was administered to the paracetamol treated mice for seven days. The effects of L. edodes extract on serum transaminases (SGOT, SGPT), alkaline phosphatase (ALP) and bilirubin were measured in the paracetamol-induced hepatotoxic mice. L. edodes extract produced significant (p < 0.05) hepatoprotective effects by decreasing the activity of serum enzymes and bilirubin.
CONCLUSIONS: From these results, it was suggested that L. edodes extract could perhaps protect liver cells from paracetamol-induced liver damage by its antioxidative effect on hepatocytes, hence diminishing or eliminating the harmful effects of toxic metabolites of paracetamol.
RESULTS: Four hundred fifty-three cloacal and farm environment samples were collected from six different commercial chicken farms in Kelantan, Malaysia. E. coli was isolated using standard bacteriological methods, and the isolates were tested for antimicrobial susceptibility using disc diffusion and colistin minimum inhibitory concentration (MIC) by broth microdilution. Multiplex PCR was used to detect mcr genes, and DNA sequencing was used to confirm the resistance genes. Virulence gene detection, phylogroup, and multilocus sequence typing (MLST) were done to further characterize the E. coli isolates. Out of the 425 (94%; 425/453) E. coli isolated from the chicken and farm environment samples, 10.8% (48/425) isolates were carrying one or more colistin-resistance encoding genes. Of the 48 colistin-resistant isolates, 54.2% (26/48) of the mcr positive isolates were genotypically and phenotypically resistant to colistin with MIC of colistin ≥ 4 μg/ml. The most prominent mcr gene detected was mcr-1 (47.9%; 23/48), followed by mcr-8 (18.8%; 9/48), mcr-7 (14.5%; 7/48), mcr-6 (12.5%; 6/48), mcr-4 (2.1%; 1/48), mcr-5 (2.1%; 1/48), and mcr-9 (2.1%; 1/48) genes. One E. coli isolate originating from the fecal sample was found to harbor both mcr-4 and mcr-6 genes and another isolate from the drinking water sample was carrying mcr-1 and mcr-8 genes. The majority of the mcr positive isolates were categorized under phylogroup A followed by phylogroup B1. The most prevalent sequence typing (ST) was ST1771 (n = 4) followed by ST206 (n = 3). 100% of the mcr positive E. coli isolates were multidrug resistant. The most frequently detected virulence genes among mcr positive E. coli isolates were ast (38%; 18/48) followed by iss (23%; 11/48). This is the first research to report the prevalence of mcr-4, mcr-5, mcr-6, mcr-7, and mcr-8 genes in E. coli from broiler chickens and farm environments in Malaysia.
CONCLUSION: Our findings suggest that broiler chickens and broiler farm environments could be reservoirs of colistin-resistant E. coli, posing a risk to public health and food safety.
OBJECTIVE: This study evaluates cytokine expression and T-cells activation in relation to disease non-progression in LTNP.
METHODS: HIV-1 Subtype C infected LTNP (n=20) and progressors (n=15) were enrolled and flowcytometry assays were performed to study HIV-specific CD8 T-cells expressing IL-2, IFN-γ, TNF-α and MIP-1β against gag and env peptides. CD4+ T-cell activation was evaluated by surface expression of HLADR and CD38.
RESULTS: Proportions of cytokines studied did not differ significantly between LTNP and progressors, while contrasting correlations with disease progression markers were observed in LTNP. CD4+ T-cell activation rates were significantly lower in LTNP compared to progressors which indicate the potential role of T-cell activation rates in disease non-progression in LTNP.
CONCLUSION: LTNP and progressors showed similar CD8+ T-cell responses, but final conclusions can be drawn only by comparing multiple immune factors in larger LTNP cohort with HIV-1 infected individuals at various levels of disease progression. A possible role of HIV-1 subtype variation and ethnic differences in addition to host-genetic and viral factors cannot be ruled out.