The objective of this study was to determine the in vitro antimicrobial activity of several organic acids and their derivatives against Gram-positive (G+) and Gram-negative (G−) bacteria. Butyric acid, valeric acid, monopropionin, monobutyrin, valerate glycerides, monolaurin, sodium formate, and ProPhorce—a mixture of sodium formate and formic acid (40:60 w/v)—were tested at 8 to 16 concentrations from 10 to 50,000 mg/L. The tested bacteria included G− bacteria (Escherichia coli, Salmonella enterica Typhimurium, and Campylobacter jejuni) and G+ bacteria (Enterococcus faecalis, Clostridium perfringens, Streptococcus pneumoniae, and Streptococcus suis). Antimicrobial activity was expressed as minimum inhibitory concentration (MIC) of tested compounds that prevented growth of tested bacteria in treated culture broth. The MICs of butyric acid, valeric acid, and ProPhorce varied among bacterial strains with the lowest MIC of 500–1000 mg/L on two strains of Campylobacter. Sodium formate at highest tested concentrations (20,000 mg/L) did not inhibit the growth of Escherichia coli, Salmonella Typhimurium, and Enterococcus faecalis, but sodium formate inhibited the growth of other tested bacteria with MIC values from 2000 to 18,800 mg/L. The MIC values of valerate glycerides, monolaurin, and monobutyrin ranged from 2500 to 15,000 mg/L in the majority of bacterial strains. Monopropionin did not inhibit the growth of all tested bacteria, with the exception that the MIC of monopropionin was 11,300 mg/L on Clostridia perfringens. Monolaurin strongly inhibited G+ bacteria, with the MIC value of 10 mg/L against Streptococcus pneumoniae. The MIC tests indicated that organic acids and their derivatives exhibit promising antimicrobial effects in vitro against G− and G+ bacteria that are resistant to antimicrobial drugs. The acid forms had stronger in vitro antimicrobial activities than ester forms, except that the medium chain fatty acid ester monolaurin exhibited strong inhibitory effects on G+ bacteria.

The objectives of the study were to test the biological activities of peppermint and spearmint oils via (i) measuring in vitro anti-inflammatory effects with porcine alveolar macrophages (PAMs), (ii) determining the barrier integrity of IPEC-J2 by analyzing transepithelial electrical resistance (TEER), (iii) testing their antioxidant activities, and (iv) investigating the antimicrobial activity against enterotoxigenic Escherichia coli (ETEC) F18+. Briefly, (i) macrophages were seeded at 10⁶ cells/mL and treated (24 h) with mint oils and lipopolysaccharide (LPS). The treatments were 2 (0 or 1 μg/mL of LPS) × 5 (0, 25, 50, 100, 200 µg/mL of mint oils). The supernatants were collected for TNF-α and IL-1β measurement by ELISA; (ii) IPEC-J2 cells were seeded at 5 × 10⁵ cells/mL and treated with mint oils (0, 25, 50, 100, and 200 μg/mL). TEER (Ωcm²) was measured at 0, 24, 48, and 72 h; (iii) the antioxidant activity was assessed (0, 1, 50, 100, 200, 500, and 600 mg/mL) using the 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging and reducing power assays; (iv) overnight-grown ETEC F18+ were quantified (CFU/mL) after supplementing with peppermint and spearmint oils (0, 1.44, 2.87, 5.75, 11.50, and 23.00 mg/mL). All data were analyzed using the MIXED procedure. Both mint oils significantly inhibited (p < 0.05) IL-1β and TNF-α secretion from LPS-stimulated PAMs. Mint oil treatments did not affect TEER in IPEC-J2. Spearmint and peppermint oils exhibited (p < 0.05) strong antioxidant activities in DPPH and reducing power assays. Both mint oils also dose-dependently inhibited (p < 0.05) the growth of ETEC F18+ in vitro. The results of the study indicated that both mint oils are great candidate feed additives due to their in vitro anti-inflammatory, antioxidant, and antimicrobial effects. Further research is needed to evaluate their efficacy in vivo.

Background: There is a great demand for antibiotic alternatives to maintain animal health and productivity. The objective of this experiment was to determine the efficacy of dietary supplementation of a blood group A6 type 1 antigen oligosaccharides-based polymer (Coligo) on growth performance, diarrhea severity, intestinal health, and systemic immunity of weaned pigs experimentally infected with an enterotoxigenic Escherichia coli (ETEC), when compared with antibiotics. Results: Pigs in antibiotic carbadox or Coligo treatment groups had greater (P < 0.05) body weight on d 5 or d 11 post-inoculation (PI) than pigs in the control group, respectively. Supplementation of antibiotics or Coligo enhanced (P < 0.05) feed efficiency from d 0 to 5 PI and reduced (P < 0.05) frequency of diarrhea throughout the experiment, compared with pigs in the control group. Supplementation of antibiotics reduced (P < 0.05) fecal β-hemolytic coliforms on d 2, 5, and 8 PI. Pigs in antibiotics or Coligo groups had reduced (P < 0.05) neutrophil counts and serum haptoglobin concentration compared to pigs in the control group on d 2 and 5 PI. Pigs in Coligo had reduced (P < 0.05) total coliforms in mesenteric lymph nodes on d 5 and 11 PI, whereas pigs in antibiotics or Coligo groups had reduced (P < 0.05) total coliforms in spleen on d 11 PI compared with pigs in the control group. On d 5 PI, pigs in the Coligo group had greater (P < 0.05) gene expression of ZO1 in jejunal mucosa, but less (P < 0.05) mRNA expression of IL1B, IL6, and TNF in ileal mucosa, in comparison with pigs in the control group. Supplementation of antibiotics enhanced (P < 0.05) the gene expression of OCLN in jejunal mucosa but decreased (P < 0.05) IL1B and IL6 gene expression in ileal mucosa, compared with the control. On d 11 PI, supplementation of antibiotics or Coligo up-regulated (P < 0.05) gene expression of CLDN1 in jejunal mucosa, but Coligo reduced (P < 0.05) IL6 gene expression in ileal mucosa compared to pigs in the control group. Conclusions: Supplementation of Coligo improved growth performance, alleviated diarrhea severity, and enhanced gut health in weaned pigs infected with ETEC F18 in a manner similar to in-feed antibiotics.

The authors wish to make the following corrections to this paper published in Molecules