Dietary therapy with Lactobacillus GG, bovine colostrum or bovine immune colostrum in patients with juvenile chronic arthritis: evaluation of effect on gut defence mechanisms
- PMID: 17638132
- DOI: 10.1007/s10787-997-0001-1
Dietary therapy with Lactobacillus GG, bovine colostrum or bovine immune colostrum in patients with juvenile chronic arthritis: evaluation of effect on gut defence mechanisms
Abstract
The effect of dietary therapy with a human Lactobacillus strain GG (ATCC 53103), bovine colostrum, or bovine immune colostrum with specific antibodies against anaerobic intestinal bacteria on gut defence mechanisms were studied in juvenile chronic arthritis. Thirty patients with juvenile chronic arthritis were randomly allocated to receive a freeze-dried powder of Lactobacillus GG, or bovine colostrum, or bovine immune colostrum, for a two-week period. Immunologic and non-immunologic gut defence mechanisms were indirectly investigated in blood and faecal samples. In patients receiving Lactobacillus GG, the median (interquartile range) frequency of immunoglobulin-secreting cells, determined by enzyme-linked immunospot assay, increased in the IgA class from 1840 (690-2530) to 3480 (1030-13 170)/10(6) cells; p=0.02. Likewise the median (interquartile range) frequency of specific antibody-secreting cells against dietary antigens increased during the Lactobacillus GG therapy in the IgM class from 3.8 (1.4-5.0) to 11.2 (5.0-30.0)/10(6) cells; p=0.02. In addition, Lactobacillus GG therapy decreased the median (interquartile range) activity of faecal urease, which has been associated with mucosal tissue damage, from 40.3 (21.7-54.3) to 28.6 (24.5-49.4) nmol. min(-1) (mg protein)(-1); p=0.10, while, in patients receiving bovine colostrum, faecal urease activity increased (from 42.2 to 80.6; p=0.04). All findings were transient. We suggest that gut defence mechanisms are disturbed in juvenile chronic arthritis and we further suggest that orally administered Lactobacillus GG has a potential to reinforce the mucosal barrier mechanisms in juvenile chronic arthritis.
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