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口服干酪乳杆菌对DBA/1小鼠II型胶原诱导性关节炎的抑制作用。

Suppressive effects of the oral administration of Lactobacillus casei on type II collagen-induced arthritis in DBA/1 mice.

作者信息

Kato I, Endo-Tanaka K, Yokokura T

机构信息

Yakult Central Institute for Microbiological Research, Kunitachi, Tokyo, Japan.

出版信息

Life Sci. 1998;63(8):635-44. doi: 10.1016/s0024-3205(98)00315-4.

Abstract

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 microg 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-treatment 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.

摘要

我们研究了口服活细菌干酪乳杆菌代田株(LcS)对DBA/1小鼠Ⅱ型胶原(CII)诱导的关节炎(CIA)发病的影响。雄性DBA/1小鼠用100微克CII与完全弗氏佐剂(CFA)的乳剂进行免疫。然后在实验期间给小鼠口服LcS悬液或蒸馏水(DW)。我们观察了小鼠CIA的发病情况,并测定了对照小鼠和给予LcS小鼠体内和体外CII特异性免疫反应。在对照小鼠中,我们观察到CII免疫后第27天出现关节炎,然后CIA的严重程度逐渐发展。在受试小鼠中,与对照小鼠相比,LcS治疗降低了CIA的发病率和严重程度以及血清中CII抗体水平。受试小鼠血清中CII特异性IgG2a和IgG2b抗体也下调。给予这种细菌还抑制了用CII和CFA免疫的DBA/1小鼠对CII的迟发型超敏反应。口服LcS在体外抑制了脾细胞中CII特异性干扰素-γ的分泌。从这些结果中,我们得出结论,口服LcS能够改变对CII的体液免疫和细胞免疫反应,并且这些改变可能导致DBA/1小鼠CIA发病的减轻。

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