Suppressive effects of the oral administration of Lactobacillus casei on type II collagen-induced arthritis in DBA/1 mice
We investigated the effects of the oral administration of the viable bacterium Lactobacillus casei strain Shirota (LcS), on the development of type II collagen (CII)-induced arthritis (CIA) in DBA/1 mice. Male DBA/1 mice were immunized with an emulsion of 100 μg of CII and complete Freund's adj...
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Veröffentlicht in: | Life sciences (1973) 1998-07, Vol.63 (8), p.635-644 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | We investigated the effects of the oral administration of the viable bacterium
Lactobacillus casei strain Shirota (LcS), on the development of type II collagen (CII)-induced arthritis (CIA) in DBA/1 mice. Male DBA/1 mice were immunized with an emulsion of 100 μg of CII and complete Freund's adjuvant (CFA). The mice were then given orally a suspension of LcS or distilled water (DW) during the experiment. We observed the development of CIA in the mice, and determined the in vivo and
ex vivo CII-specific immune responses in the control and LcS-administered mice. In the control mice, we observed the onset of arthritis at the 27th day after the CII-immunization, and then the severity of CIA developed gradually, In the tested mice, the LcS-trcatment reduced the incidence and the development of CIA and the levels of antibody to CII in serum compared with the control mice. The CII-specific IgG2a and IgG2b antibodies in serum were also down regulated in the tested mice. The administration of this bacterium also inhibited delayed-type hypersensitivity response to CII in DBA/1 mice immunized with CII and CFA. The orally administered-LcS suppressed the CII-specific secretion of interferon-gamma from splenocytes
ex vivo. From these results, we concluded that the oral administration of LcS was able to modify the humoral and cellular immune responses to CII, and these modifications could result in the reduction of the development of CIA in DBA/1 mice. |
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ISSN: | 0024-3205 1879-0631 |
DOI: | 10.1016/S0024-3205(98)00315-4 |