Treatment of dextran sodium sulfate(DSS) on HeLa cells results to an enhanced susceptibility to Brucella(B.) abortus infection. An increase in the adherence, invasion and intracellular replication of B. abortus was observed in DSS-treated cells. Furthermore, a marked elevation in the intensity of F-actin fluorescence was also observed in DSS-treated cells compared with untreated B. abortus-infected cells. An upregulation of phagocytic signaling proteins by Western blot analysis demonstrated an apparent activation of ERK, p38α and JNK phosphorylation levels in B. abortus-infected DSS-treated cells compared with the control. Colocalization with LAMP-1 proteins was attenuated in DSS-treated cells upon intracellular trafficking of the pathogen compared with control cells. The results of this study demonstrated consistency with other pathogens. The uptake and intracellular replication of B. abortus is hypothesized to be stimulated by various dextran receptors such as C-type lectins that are involved in phagocytosis which can either be direct phagocytic receptors, modulators of the expression of other receptors or as opsonins leading to an enhanced internalization of B. abortus. The complexity of these interactions thus would warrant further investigation into the role of DSS in the pathogenesis of brucellosis. In summary, we conclude that DSS enhanced adhesion, phagocytosis and intracellular replication of B. abortus in epithelial cells which could lead to suppression of the innate immune system in chronic Brucella infection.

Many studies propose that dysfunction of mitochondrial proton-translocating NADH-ubiquinone oxidoreductase (complex I) is associated with neurodegenerative disorders, such as Parkinson's disease and Huntington's disease. Mammalian mitochondrial proton-translocating NADH-quinone oxidoreductase (complex I) consists of at least 46 different subunits. In contrast, the NDI1 gene of Saccharomyces cerevisiae is a single subunit rotenone-insensitive NADH-quinone oxidoreductase that is located on the matrix side of the inner mitochondrial membrane. With a recombinant adeno-associated virus vector carrying the NDI1 gene (rAAV-NDI1) as the gene delivery method, we were able to attain high transduction efficiencies even in the human epithelial cervical cancer cells that are difficult to transfect by lipofection or calcium phosphate precipitation methods. Using a rAAV-NDI1, we demonstrated that the Ndi1 enzyme is successfully expressed in HeLa cells. The expressed Ndi1 enzyme was recognized to be localized in mitochondria by confocal immunofluorescence microscopic analyses and immunoblotting. Using digitonin-permeabilized cells, it was shown that the NADH oxidase activity of the NDI1-transduced HeLa cells were not affected by rotenone which is inhibitor of complex I, but was inhibited by flavone and antimycin A. The NDI1-transduced cells were able to grow in media containing rotenone. In contrast, control cells that did not receive the NDI1 gene failed to survive. In particular, in the NDI1-transduced cells, the yeast enzyme becomes integrated into the human respiratory chain. It is concluded that the NDI1 gene provides a potentially useful tool for gene therapy of mitochondrial diseases caused by complex I deficiency.

세포에 미치는 염화수은(II)과 이온화 방사선의 영향과 수은 처리 전 후 방사선 조사 시 그 상호 작용에 관해 알아보고자 본 연구를 수행하였다. 염화수은(II)의 독성정도를 알아보기 위하여 사람의 자궁암 세포에 농도별로 염화수은(II)을 처리하였다. 세포의 생존율은 3가지 농도(1,0. 1,0. 0.01 μM)모두에서 유의하게 감소하였으며 이미 0.1 μM에서 약 73%의 생존율이 감소하는 것으로 나타났다. 염화수은(II)과 방