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BackgroundConsumers are becoming increasingly interested in food containing high concentration of polyunsaturated fatty acids (PUFA). PUFA are considered as functional ingredients to prevent cardiovascular disease. The present study aimed to evaluate the effects of Clostridium butyricum on antioxidant properties, meat quality and fatty acid composition of broilers.MethodsA total of 320 one-day-old Arbor Acres male chicks were randomly assigned to one of five treatments with eight replicates and fed a antibiotic-free basal corn-soybean meal diet (control) or the basal diet supplemented with either 2.5 × 108 (CB1), 5 × 108 (CB2) or 1 × 109 (CB3) cfu of C. butyricum/kg or150 mg of aureomycin/kg (antibiotic) for 42 days.ResultsThe results showed that chicks fed diets supplemented with C. butyricum had higher (P < 0.05) superoxide dismutase activity and lower (P < 0.05) malondialdehyde concentration in liver compared with those in the control group. Broilers had lower (P < 0.05) cholesterol content of serum in either CB2 or CB3 treatment at day 21 and in the C. butyricum-supplemented groups at day 42 than those in the control group. Chicks fed CB3 diet had lower (P < 0.05) percentage of abdominal fat and higher (P < 0.05) breast muscle yield than those in the control and antibiotic groups. The supplementation of C. butyricum increased (P < 0.05) the concentrations of C20:1n-9, C20:2n-6, C20:3n-6, C20:3n-3, C20:4n-6, C20:5n-3, C22:6n-3 and total PUFA as well as ratio of PUFA to saturated fatty acids in breast muscle and the contents of C18:2 t-9, t-12, C20:3n-6, C20:3n-3 and C20:5n-3 in thigh muscle.ConclusionsSupplementation of C. butyricum promotes hepatic antioxidant status, decreases cholesterol content of serum and percentage of abdominal fat, and improves meat quality and fatty acid composition of broiler birds. The results from the present study indicate that the increased PUFA concentrations in meat of broilers fed C. butyricum might be attributable to enhanced antioxidant activity.

The increasing prevalence of antibiotic resistance has created an urgent need for alternative drugs with new mechanisms of action. Antimicrobial peptides (AMPs) are promising candidates that could address the spread of multidrugresistant bacteria, either alone or in combination with conventional antibiotics. We studied the antimicrobial efficacy and bactericidal mechanism of cecropin A2, a 36-residue ␣-helical cationic peptide derived from Aedes aegypti cecropin A, focusing on the common pathogen Pseudomonas aeruginosa. The peptide showed little hemolytic activity and toxicity toward mammalian cells, and the MICs against most clinical P. aeruginosa isolates were 32 to 64 g/ml, and its MICs versus other Gramnegative bacteria were 2 to 32 g/ml. Importantly, cecropin A2 demonstrated synergistic activity against P. aeruginosa when combined with tetracycline, reducing the MICs of both agents by 8-fold. The combination was also effective in vivo in the P. aeruginosa/Galleria mellonella model (P Ͻ 0.001). We found that cecropin A2 bound to P. aeruginosa lipopolysaccharides, permeabilized the membrane, and interacted with the bacterial genomic DNA, thus facilitating the translocation of tetracycline into the cytoplasm. In summary, the combination of cecropin A2 and tetracycline demonstrated synergistic antibacterial activity against P. aeruginosa in vitro and in vivo, offering an alternative approach for the treatment of P. aeruginosa infections.KEYWORDS antimicrobial activity, antimicrobial peptide, cecropin A2, Pseudomonas aeruginosa, tetracycline P seudomonas aeruginosa is a Gram-negative opportunistic bacterial pathogen that causes life-threatening infections with high rates of mortality (1-3). It is associated with nosocomial pneumonia, wound infections, bacteremia, and sepsis among patients with various underlying diseases, including cystic fibrosis, HIV/AIDS, and cancer (4). Antibiotic therapy is challenging in this setting because clinical strains of P. aeruginosa often show extensive intrinsic resistance to a wide range of antimicrobial agents, including tetracyclines, ␤-lactams, aminoglycosides, and fluoroquinolones (5). This intrinsic resistance has generally been attributed to the low membrane permeability of P. aeruginosa, up to 100 times lower than that of Escherichia coli (6). P. aeruginosa can also withstand antibiotics that attack the outer membrane through the efficient deployment of transmembrane efflux pumps, preventing contact between the antibiotics and their intracellular targets (7-11).The ubiquitous and relentless clinical challenge of drug resistance has created a