Oral supplementation of trans-cinnamaldehyde reduces uropathogenic Escherichia coli colonization in a mouse model.

Urinary tract infections (UTIs) in the United States result in more than 7 million hospital visits per year. Uropathogenic Escherichia coli (UPEC) is responsible for more than 80% of UTIs. Although antibiotics are the drug of choice to control UTIs, their repeated use has resulted in the emergence of antibiotic-resistant UPEC. Thus, there is a need for effective alternate strategies to control UPEC infections. This study investigated the efficacy of trans-cinnamaldehyde (TC), a food-grade molecule present in cinnamon, in reducing UPEC colonization and pathogenesis in the lower UTI. Female C57BL/6 mice (6-8 weeks old) were fed ad libitum with 0, 0·1, 0·2 and 0·4% TC containing mouse chow for 10 days. Following TC supplementation, animals were experimentally infected with UPEC by transurethral catheterization. Mice were euthanized on days 1, 2 and 4 postinfection, and the bladder, urethra and urine were collected for bacterial enumeration. Prophylactic TC supplementation significantly (P ≤ 0·05) reduced UPEC colonization in the urinary bladder and urethra compared to the control. Results indicate that TC could potentially be used as an oral supplement to control UPEC-associated lower UTIs, however, follow-up clinical trials are warranted. SIGNIFICANCE AND IMPACT OF THE STUDY: In this study, we have demonstrated that oral supplementation of trans-cinnamaldehyde (TC) reduced uropathogenic Escherichia coli (UPEC)-associated lower urinary tract infection (UTI) in mice. Specifically, in-feed supplementation of TC significantly decreased UPEC populations in the urethra and bladder, thereby reducing the infectious load. These findings are particularly significant given the increase in incidence and prevalence of antibiotic-resistant UTIs. Our study offers new insights into the potential use of natural antimicrobials including TC, the active ingredient in cinnamon, as a nonantibiotic-based natural dietary intervention in the prophylaxis of lower UTIs.

Caprylic acid reduces Salmonella Enteritidis populations in various segments of digestive tract and internal organs of 3- and 6-week-old broiler chickens, therapeutically.

We investigated the efficacy of feed supplemented with caprylic acid (CA), a natural, 8-carbon fatty acid for reducing Salmonella enterica serovar Enteritidis colonization in commercial broiler chickens. In separate 3- and 6-wk trials, 1-d-old straight-run broiler chicks (n = 70 birds/trial) were assigned to a control group (challenged with Salmonella Enteritidis, no CA) and 2 replicates of 0.7 and 1% CA (n = 14 birds/group). Water and feed were provided ad libitum. On d 1, birds were tested for any inherent Salmonella (n = 2 birds/group). For the 3-wk trial, on d 5, birds were challenged with 8 log(10) cfu of Salmonella Enteritidis of a 4-strain mixture by crop gavage, and after 5 d postchallenge, birds (n = 2 birds/group) were euthanized to ensure Salmonella Enteritidis colonization. Caprylic acid was supplemented the last 5 d before tissue collection (n = 10 birds/group). For the 6-wk trial, on d 25, birds were challenged and confirmed for Salmonella Enteritidis colonization. The birds (n = 10 birds/group) were euthanized for tissue samples after CA supplementation for the last 5 d. Caprylic acid at 0.7 or 1% decreased Salmonella Enteritidis populations in cecum, small intestine, cloaca, liver, and spleen in both 3- and 6-wk trials. Body weight of birds did not differ between the groups (P ≥ 0.05). Further, to elucidate a potential antibacterial mechanism of action of CA, we investigated if CA could reduce Salmonella Enteritidis invasion of an avian epithelial cell line and expression of invasion genes hilA and hilD. The cell invasion study revealed that CA reduced invasive abilities of all Salmonella Enteritidis strains by ~80% (P < 0.05). Gene expression studies indicated that CA downregulated (P < 0.001) Salmonella invasion genes hilA and hilD. These results suggest that supplementation of CA through feed could reduce Salmonella Enteritidis colonization in broiler chicken and potentially reduces the pathogen's ability to invade intestinal epithelial cells by downregulating key invasion genes, hilA and hilD.