Antibacterial activity of pepsin-digested lactoferrin on foodborne pathogens in buffered broth systems and ultra-high temperature milk with EDTA.

AIMS: To evaluate the antimicrobial activity in peptone yeast extract glucose (PYG) broth and ultra-high temperature (UHT) milk of bovine lactoferrin hydrolysate (LFH) with pepsin against the foodborne pathogens Salmonella Stanley, Escherichia coli, Listeria monocytogenes and Staphylococcus aureus. METHODS AND RESULTS: The LFH was suspended in PYG and the minimum inhibitory concentration for each pathogen determined. The LFH was also suspended in UHT milk adjusted to pH 4 or 7, samples incubated at 4 or 35 degrees C and the change in bacterial cell population determined. Experiments in UHT milk were conducted using L. monocytogenes and E. coli O157:H7. At pH 4 LFH reduced the population of E. coli O157:H7 and L. monocytogenes by approx. 2 log; however, only E. coli O157:H7 was inhibited in samples adjusted to pH 7. The addition of EDTA (10 mg ml(-1)) to UHT milk supplemented with LFH did not markedly influence the growth of E. coli O157:H7 or L. monocytogenes. CONCLUSIONS: The results suggest that, under low pH and refrigeration conditions, LFH can limit the growth or reduce the population of pathogenic bacteria in a dairy product. SIGNIFICANCE AND IMPACT OF THE STUDY: Natural preservatives that are active against Gram-negative and Gram-positive bacteria are desirable to the food industry. This study demonstrates that LFH is effective in a complex food system. Moreover, the LFH used was not purified, making its use by industry more attractive.

[Casual influence of the stimulation of macrophage production by proteose-peptone, in the experimental infection of mice by Plasmodium berghei]. / Estudo sobre eventual influência do estímulo para produção de macrófagos, por meio da proteose-peptona, na infecção experimental de camundongos pelo Plasmodium berghei.

Proteose-peptone is a known powerful stimulator of macrophages. This stimulation was studied in an experimental malaria infection model, using Plasmodium berghei in mice. Parasitemia and mortality did not change in stimulated animals, and macrophage mobilization, contrary to other published papers, was not effective to increase either parasite levels in the blood or mortality.

Analysis of protective mechanisms against infection by Serratia marcescens.

The present paper is concerned with an experimental study of effects of some agents on parameters pertinent to host resistance to infection of Serratia marcescens (S. marcescens) which was isolated from a patient. The results obtained are the following: In the control mice injected intravenously with S. marcescens, most of the bacteria were trapped in the liver, spleen and lung, the so-called reticuloendothelial system (RES), and the number of bacteria decreased gradually with time. In the kidney, the bacterial count did not decrease because of the existence of few macrophages in this organ. In the animals treated with X-irradiation and cyclophosphamide, the mortality rate increased, and the number of S. marcescens in the organs increased significantly with time. These observations were irreversible in the X-irradiated group, but were reversible in the cyclophosphamide-treated group, depending on the challenge dose. In the mice treated with carrageenan, which functions as a macrophage blocker, the mortality rate did not increase significantly, but there was a delay before the bacteria were eliminated from the liver indicating that the bacteria were not killed in the early phase. After intraperitoneal administration of proteose peptone, polymorphonuclear cells (PMNs) and macrophages accumulated in the peritoneal cavity on the 1st day and 4th day. When S. marcescens was injected intraperitoneally to these 2 groups. The 50% lethal dose (LD50) did not increase significantly in each group. After intraperitoneal inoculation of S. marcescens in a dose equal to 1.5 LD50 in normal mice, the elimination of bacteria from the peritoneal cavity was very rapid in the mice pretreated with proteose peptone.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential expression of macrophage effector functions: bactericidal versus tumoricidal activities.

Macrophage populations may be induced to express tumoricidal or bactericidal activities following exposure to certain stimuli. An understanding of the differences in the stimulatory mechanisms and in the characteristics of the macrophages they affect will be facilitated by comparing functional activities of various macrophage populations. The experiments described here were conducted to determine whether injection of a single stimulus necessarily drives cells to express both tumoricidal and bactericidal activities or whether selected reagents can drive cells to express one activity without expressing the other. The data show that a single population of mouse or hamster peritoneal exudate cells obtained following injection of proteose peptone is bactericidal for Listeria monocytogenes and for E. coli, but is not tumoricidal for TCMK-1, Ad2HE3, or mKS-A TU-5 target cells. In contrast, peritoneal exudate cells collected after injection of Bacillus Calmette Guerin (BCG) organisms are always highly tumoricidal, and either show no effect on Listeria monocytogenes or E. coli, or are at best bacteriostatic. Data indicate that the effector cells in these assays are macrophages, that the dissociation of tumoricidal and bactericidal activity occurs over a wide dose range, and that the tumoricidal capabilities are not artifacts of the assay system. These results suggest that a given macrophage population may preferentially express tumoricidal or bactericidal activities depending on the stimulus used.

Macrophage processing of antigen for induction of tumor immunity.

Previous studies have indicated, that, after in vitro incubation of antigen with macrophages, the "processed" antigen preferentially induces cell-mediated immunity. To investigate this phenomenon with tumor antigens, mycobacteria-stimulated macrophages were incubated with irradiated syngeneic EMT6 tumor cells for varying lengths of time and injected into normal mice. On subsequent challenge with EMT6, there was a significant increase in protection in mice immunized with macrophage-processed tumor antigen over control animals. Mineral oil-stimulated macrophages were also capable of processing irradiated EMT6, but macrophages induced by thioglycollate or proteose peptone were not. Freeze-thawed mycobacteria-stimulated macrophages were nearly as effective as viable macrophages in processing tumor antigen, but heat-treated macrophages lost this capacity. The immunity generated was specific and could be passively transferred by immune cells but not by immune serum. The results indicate that incubation of tumor antigen with appropriately activated macrophages leads to the enhanced induction of immunity to the tumor. Macrophage enzymes may degrade tumor antigens to fragments with few antigenic determinants that preferentially induce cell-mediated immunity.

An inhibitor of cell proliferation released by cultures of macrophages.

Culture fluids from mouse peritoneal exudate cells inhibited [(3)H]thymidine incorporation by, and proliferation of, EL-4 leukemia cells, 3T3 cells, and mitogen-stimulated spleen lymphocytes. Inhibited EL-4 leukemia cells recovered their normal proliferative capacity when washed and incubated in normal medium. The inhibitory activity resided in a low-molecular-weight substance that could be absorbed by incubation with the tumor cells. This substance was dialyzable and resistant to tryptic digestion and phosphodiesterase treatment. The mononuclear phagocytes in the peritoneal exudate seemed to be the source of the inhibitor. The inhibitory material was found in the same amounts in exudates of normal mice or mice injected with peptone or infected with Listeria monocytogenes; spleen cells adherent to plastic released the inhibitor but in lesser amount. We suggest that this inhibitor may contribute to the deleterious effects found when various cells, including neoplastic ones, are cultured in the presence of macrophages.