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用细菌脂多糖刺激后,单核细胞增生李斯特菌感染小鼠循环中α干扰素、β干扰素和γ干扰素的顺序产生

Sequential production of alpha and beta interferons and gamma interferon in the circulation of Listeria monocytogenes-infected mice after stimulation with bacterial lipopolysaccharide.

作者信息

Nakane A, Minagawa T

出版信息

Microbiol Immunol. 1985;29(7):659-69. doi: 10.1111/j.1348-0421.1985.tb00869.x.

Abstract

Sequential production of interferon (IFN)-alpha/beta and IFN-gamma in the circulation of mice which had been previously infected with viable Listeria monocytogenes was induced by injection of lipopolysaccharide (LPS) derived from Salmonella typhimurium. IFN-alpha/beta production occurred 2 hr after injection of LPS, thereafter IFN-gamma appeared and the maximum titer was demonstrated at 6 hr. At that time, almost all of the IFN was IFN-gamma. IFN-gamma production in response to LPS was observed from the 5th through the 11th day after infection with Listeria, but it was not demonstrated in either mice infected with lower doses of viable Listeria or mice immunized with heat-killed bacteria. IFN-alpha/beta production was not drastically affected by treatment with hydrocortisone, cyclophosphamide, carrageenan, antithymocyte serum, or anti-asialo GM1 antibody, whereas IFN-gamma production was suppressed by administration of all those agents. Noteworthily, IFN-alpha/beta, but not IFN-gamma, was produced even 6 hr after stimulation with LPS in cyclophosphamide- or antithymocyte serum-treated mice. IFN-gamma induction by LPS was markedly suppressed in mice in which IFN-alpha/beta produced by Listeria infection itself had been depleted by treatment with anti-mouse IFN-alpha/beta antibody, but it was not inhibited in mice when IFN-alpha/beta induced not by Listeria infection but by LPS had been depleted by treatment with anti-mouse IFN-alpha/beta antibody.

摘要

给先前感染过活单核细胞增多性李斯特菌的小鼠注射鼠伤寒沙门氏菌来源的脂多糖(LPS)后,可诱导其循环系统中依次产生干扰素(IFN)-α/β和IFN-γ。注射LPS后2小时出现IFN-α/β的产生,此后IFN-γ出现,并在6小时时达到最高滴度。此时,几乎所有的IFN都是IFN-γ。在感染李斯特菌后的第5天至第11天观察到对LPS产生的IFN-γ,但在感染低剂量活李斯特菌的小鼠或用热灭活细菌免疫的小鼠中均未出现。氢化可的松、环磷酰胺、角叉菜胶、抗胸腺细胞血清或抗去唾液酸GM1抗体处理对IFN-α/β的产生没有显著影响,而所有这些试剂的给药均抑制了IFN-γ的产生。值得注意的是,在环磷酰胺或抗胸腺细胞血清处理的小鼠中,即使在LPS刺激6小时后仍产生IFN-α/β,而不产生IFN-γ。在用抗小鼠IFN-α/β抗体处理使李斯特菌感染自身产生 的IFN-α/β耗竭的小鼠中,LPS诱导的IFN-γ明显受到抑制,但在用抗小鼠IFN-α/β抗体处理使非李斯特菌感染而是由LPS诱导的IFN-α/β耗竭的小鼠中,IFN-γ未受到抑制。

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