The Brucella genus is able to cause chronic infection in a wide range of mammals including humans. Oxidative events, lipid peroxidation and inflammatory response against Brucella infection have not yet been well elucidated in vivo. We have investigated oxidative/antioxidative status and nitric oxide production in plasma, brain, liver and spleen during a 60 day period of B. melitensis infection in a rat model. In addition, inducible nitric oxide synthase (iNOS), IL-10, IL-12, IFN-gamma and TNF-alpha mRNA transcriptions were analyzed by semiquantitative reverse transcriptase PCR (RT-PCR) in brain samples. Animals were infected with B. melitensis and sacrificed at 7th, 15th, 30th, 45th and 60th day of post-inoculation. Malondialdehyde (MDA), as an indicator of lipid peroxidation, and nitric oxide (NO) concentrations were significantly increased after Brucella inoculation and began to decline to basal levels from 45th day in plasma, liver and spleen. However, iNOS transcription was not induced during the infection period in brains. In contrast, MDA level was increased in brain during the late phase of infection without any change in NO production. The infection did not alter the antioxidant enzyme activities in the tissues; although significantly increased catalase activity was observed between days 30 and 45 in the liver. Transcription analyses demonstrated that IL-10, IL-12 and IFN-gamma mRNA level were not induced in the brain. Only TNF-alpha mRNA was weakly up-regulated in brain 30 days after pathogen inoculation. The results obtained in this study demonstrate that B. melitensis induces lipid peroxidation and NO production in the liver and spleen in the early days of infection, but that these levels subsequently decline. Moreover, Brucella does not appear to induce antioxidant enzyme activities and inflammation during two months of infection. However, the pathogen does stimulate cerebral lipid peroxidation in the late phase of infection without causing significant inflammation.

译文

布鲁氏菌属能够在包括人类在内的多种哺乳动物中引起慢性感染。体内尚未充分阐明针对布鲁氏菌感染的氧化事件,脂质过氧化作用和炎症反应。我们在大鼠模型中调查了B. melitensis感染60天期间血浆,脑,肝脏和脾脏的氧化/抗氧化状态和一氧化氮的产生。此外,通过半定量逆转录酶PCR(RT-PCR)分析了脑样本中的诱导型一氧化氮合酶(iNOS),IL-10,IL-12,IFN-γ和TNF-αmRNA的转录。在接种后第7、15、30、45和60天,将动物感染了B. melitensis,并处死了动物。布鲁氏菌接种后,丙二醛(MDA)作为脂质过氧化的指标,而一氧化氮(NO)的浓度显着增加,并从第45天开始在血浆,肝脏和脾脏中降至基础水平。但是,iNOS转录在脑部感染期间没有被诱导。相反,在感染后期,大脑中的MDA水平升高,而NO产生没有任何变化。感染并没有改变组织中的抗氧化酶活性。尽管在肝脏第30至45天之间观察到过氧化氢酶活性显着增加。转录分析表明,在大脑中未诱导IL-10,IL-12和IFN-γmRNA的水平。病原菌接种后30天,仅TNF-αmRNA在大脑中微弱上调。在这项研究中获得的结果表明,肉毒梭菌在感染的早期会诱导肝脏和脾脏中脂质过氧化和NO的产生,但是这些水平随后会下降。而且,布鲁氏菌在感染两个月期间似乎没有诱导抗氧化酶活性和炎症。但是,病原体确实会在感染后期刺激脑脂质过氧化,而不会引起明显的炎症。

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