SUMMARYInteraction of macrophages with bacteria is a stimulus for production of cytokines such as IL-10 and IL-12. IL-12 stimulates T cell and natural killer (NK) cell cytotoxicity and interferon-gamma (IFN-g) production. IL-10 opposes the T cell-stimulating action of IL-12, decreases the release of proinflammatory cytokines from macrophages, and stimulates B cells. We have studied the capacity of human intestinal isolates from the three Lactobacillus species dominating on the human gastrointestinal mucosa, L. plantarum, L. rhamnosus and L. paracasei ssp. paracasei, to induce production of IL-10 and IL-12 from human blood mononuclear cells, or monocytes. Whole killed lactobacilli were potent stimulators of IL-12 over a wide range of bacterial concentrations. Lactobacillus paracasei gave the highest levels of IL-12 (1·5 ng/ml in response to 5 × 10 6 bacteria/ml), roughly 10 times more than obtained by stimulation with L. rhamnosus or L. plantarum. Escherichia coli induced on average < 50 pg/ml of IL-12 regardless of the bacterial concentration used. The secretion of free p40 subunit IL-12 followed the same pattern as the secretion of p70 (bioactive IL-12) with regard to the efficiency of different bacteria as stimulators. Escherichia coli was the most efficient trigger of IL-10 production, inducing 0·5 ng/ml IL-10 after stimulation with 5 × 10 6 bacteria/ml. Lactobacillus rhamnosus induced the highest levels of IL-10 among the lactobacilli (0·5 ng/ml) compared with 0·1 ng/ml evoked by L. plantarum or L. paracasei, but 10 times more bacteria were required for optimal stimulation than with E. coli. When neutralizing anti-IL-10 antibodies were added to the cultures, the IL-12-inducing capacity of L. rhamnosus was increased markedly, while that of E. coli remained low. The results show that mucosa-associated lactobacilli can be potent stimulators of IL-12, and thus potentially of cell-mediated immunity, if they pass over the gut epithelial barrier and interact with cells of the gut immune system.

In this study, we investigated the anti-inflammatory effects of orally administered human lactoferrin (hLF) and two peptides, based on the bactericidal region of hLF (HLD1 and HLD2), on the course of experimental colitis. Acute colitis was induced in C57Bl/6 mice by giving 5% dextran sulphate (DX) in the drinking water. The mice were killed after 2 or 7 days of DX exposure. The animals were given hLF or the peptides orally twice a day (2 mg/dose/mouse) during the DX exposure. In the control animals, the hLF or the peptides were replaced by bovine serum albumin or water.The appearance of occult blood in the faeces and macroscopic rectal bleeding were significantly delayed and partly reduced in the hLF-treated animals compared with the control animals. The shortening of the colon, a pathological effect of DX exposure, was significantly less pronounced in the hLF-treated group compared with the control group. Also, the interleukin-1b (IL-1b) levels in the blood were significantly diminished in this group after 2 days of DX exposure. A significantly lower crypt score was observed in the distal part of the colon in the hLF-treated group compared with the control group. Also, significantly reduced numbers of CD4 cells, F4/80-positive macrophages and tumour necrosis factor-a-producing cells were detected by immunohistochemistry in the distal colon of the hLF-treated animals compared with the control animals after 7 days of DX exposure. A reduction was also observed concerning the IL-10-producing cells in the middle colonic submucosa. The HLD1 and HLD2 treatment, which was carried out for 2 days, only gave results almost identical to those of hLF, concerning clinical parameters after the 2 days of DX exposure. An even stronger effect was observed for HLD2, regarding decreased occult blood in the faeces and colon length.Our results show that perorally given hLF mediates anti-inflammatory effects on the DX-induced acute colitis, and further suggest that the bactericidal region of the hLF molecule may be involved in these activities.

B221, which is a medical food, can be used to significantly improve the condition of children with acute, as well as prolonged diarrhoea caused by a broad range of undefined pathogens.

Aim: The aim of the study was to try to induce anti‐secretory factor (AF) in human milk and possibly prevent mastitis. Methods: Forty mothers who had normal deliveries and healthy full‐term infants were randomly divided into two groups, 3–7 days postpartum. The experimental group received a food inducing AF. The control group received the same type of food, without AF‐inducing properties. Milk was tested for AF after the mothers had eaten the cereals for 4–5 wk. AF was determined by intravenous injection of milk samples into rats measuring their capacity to prevent secretion into a gut loop of the rat injected with cholera toxin. Results: The median levels of AF differed between the experimental (n= 12) and control groups (n= 16): 1.1 (0.7–1.25) units vs 0.1 (0.0–0.25) units, Z =–4.492, p > 0.0001 (11 mothers dropped out and one milk sample is missing from one of the control mothers). The frequency of mastitis in the experimental compared with the control group was reduced (p= 0.0086, permutation test). The median AF levels in mothers with or without mastitis differed; 0.0 (0.0–0.1) vs 0.5 (0.2–1.1), Z =–2.399, p= 0.017. Conclusion: We suggest a specially treated cereal induces AF in human milk and protects against clinically manifested mastitis.

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