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.

비록 천연유래물질 중의 하나인 통초가 항산화작용, 항염증작용 및 해열작용과 같은 효능이 있다고 알려져있지 만, 종양에서의 암예방효능에 대한 연구는 보고된 바가 없 다. 본 연구에서는 사람 자궁경부암세포주인 HEP-2세포에서 통초메탄올추출물의 증식억제 효능 및 관련 분자표적을 확인하고자 하였다. 통초메탄올추출물은 세포증식을 유의성있게 억제하고, 세포사멸을 유도하는 것으로 나타났다. 또한, Bid의 발현에 영향을 주어 truncation을 유도하고, 이로 인해 cytochrome c가 마이토콘드리아에서 세포질로 이 동하도록 유도하였지만, Bid 이외의 다른 Bcl-2 family 에는 영향을 주지 못했다. 따라서, 이러한 결과를 종합해 볼 때, 통초메탄올추출물은 자궁경부암에서 암예방효능을 가진 잠재성있는 천연추출물이 될 수 있을 것으로 사료된다.

The experimental manipulation of protooncogenes and their gene products is a valuable research tool for the study of human neoplasia. In this study, the recently identified human cervical cancer protooncogene (HccR-2) was expressed in transgenic mice under the control of the tetracycline regulatory system. The phenotype observed was similar in many respects to human chronic neutrophilic leukemia (CNL). Thus, the HccR-2 transgenic mouse model is important not only for investigating the biological properties of the HccR-2 protooncogene in vivo, but also for analyzing the mechanisms involved in the progression of CNL.

The experimental manipulation of protooncogenes and their gene products is a valuable research tool for the study of human neoplasia. In this study, the recently identified human cervical cancer protooncogene (HccR-2) was expressed in transgenic mice under the control of the tetracycline regulatory system. Mice expressing the HccR-2 transgene showed an altered myeloid development characterized by an increased percentage of mature and band-form neutrophils in the peripheral blood, liver and spleen. This phenotype is similar to human chronic neutrophilic leukemia (CNL) in many ways, which is a rare chronic myeloproliferative disorder (CMD) that presents as a sustained leukocytosis of mature neutrophils with a few or no circulating immature granulocytes, an absence of peripheral blood monocytosis, basophilia, or eosinophilia, and an infiltration of neutrophils into the liver, spleen and kidney. Thus, the HccR-2 transgenic mouse model is imperative not only for investigating the biological properties of the HccR-2 protooncogene in vivo, but also for analyzing the mechanisms involved in the progression of CNL.