Lysozyme and nisin are both antimicrobial proteins effective against gram-positive bacteria. The use of these antimicrobials in combination with chelating agents displays increased effectiveness ag...

Bacterial growth during food transport and storage is a problem that may be addressed with packaging materials that release antimicrobials during food contact. In a series of five experiments, EDTA...

Objective: Sulfate (SO ₄ ²⁻ ) is an abundant component of intestinal mucins and its content is decreased in certain gastrointestinal diseases, including inflammatory bowel disease. In this study, the hyposulfataemic NaS1 sulfate transporter null ( Nas1 ^−/− ) mice were used to investigate the physiological consequences of disturbed sulfate homeostasis on (1) intestinal sulfomucin content and mRNA expression; (2) intestinal permeability and proliferation; (3) dextran sulfate sodium (DSS)-induced colitis; and (4) intestinal barrier function against the bacterial pathogen, Campylobacter jejuni . Methods: Intestinal sulfomucins and sialomucins were detected by high iron diamine staining, permeability was assessed by fluorescein isothiocyanate (FITC)–dextran uptake, and proliferation was assessed by 5-bromodeoxyuridine (BrdU) incorporation. Nas1 ^−/− and wild-type ( Nas1 ^+/+ ) mice received DSS in drinking water, and intestinal damage was assessed by histological, clinical and haematological measurements. Mice were orally inoculated with C jejuni , and intestinal and systemic infection was assessed. Ileal mRNA expression profiles of Nas1 ^−/− and Nas1 ^+/+ mice were determined by cDNA microarrays and validated by quantitative real-time PCR. Results: Nas1 ^−/− mice exhibited reduced intestinal sulfomucin content, enhanced intestinal permeability and DSS-induced colitis, and developed systemic infections when challenged orally with C jejuni . The transcriptional profile of 41 genes was altered in Nas1 ^−/− mice, with the most upregulated gene being pancreatic lipase-related protein 2 and the most downregulated gene being carbonic anhydrase 1 ( Car1 ). Conclusion: Sulfate homeostasis is essential for maintaining a normal intestinal metabolic state, and hyposulfataemia leads to reduced intestinal sulfomucin content, enhanced susceptibility to toxin-induced colitis and impaired intestinal barrier to bacterial infection.

Urolithiasis, a condition in which stones are present in the urinary system, including the kidneys and bladder, is a poorly understood yet common disorder worldwide that leads to significant health care costs, morbidity, and work loss. Acetaminophen-induced liver damage is a major cause of death in patients with acute liver failure. Kidney and urinary stones and liver toxicity are disturbances linked to alterations in oxalate and sulfate homeostasis, respectively. The sulfate anion transporter–1 (Sat1; also known as Slc26a1) mediates epithelial transport of oxalate and sulfate, and its localization in the kidney, liver, and intestine suggests that it may play a role in oxalate and sulfate homeostasis. To determine the physiological roles of Sat1, we created Sat1^–/– mice by gene disruption. These mice exhibited hyperoxaluria with hyperoxalemia, nephrocalcinosis, and calcium oxalate stones in their renal tubules and bladder. Sat1^–/– mice also displayed hypersulfaturia, hyposulfatemia, and enhanced acetaminophen-induced liver toxicity. These data suggest that Sat1 regulates both oxalate and sulfate homeostasis and may be critical to the development of calcium oxalate urolithiasis and hepatotoxicity.

Research in development of antimicrobial packaging applications for further processed meats has become more common with recent outbreaks of contamination of these products. In this present study, lauric acid (8%, wt/wt) and 2.5% pure nisin (4%, wt/wt) were incorporated singly and together into thermally compacted soy films. Biocide-impregnated films were compared to control films containing no biocide for inhibition of Listeria monocytogenes in liquid medium and on turkey bologna surface. L. monocytogenes suspended in 1% peptone medium exposed to control films increased from 106 to 10(9) after 48 h exposure at 22 C. Films with nisin alone suppressed cell numbers 1 log cfu/mL after 2 h but cell numbers increased to 10(8) after 24 and 48 h at 22 C. Films containing lauric acid and nisin completely eliminated detectable cells from a 10(6) culture after 8 h of exposure to the liquid medium (22 C). Refrigerated bologna exposed to control films increased by 0.5 log from 10(6) after 21 d at 4 C. Nisin films reduced cell numbers on turkey bologna from 10(6) to 10(5) after 21 d, as did films containing nisin and lauric acid. Films with lauric acid alone reduced L. monocytogenes culture from 10(6) to < 102 after 48 h and by 1 log on turkey bologna after 21 d.