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저선량 감마선 조사 마우스의 말초면역 세포에 대한 바나듐 함유, 제주 워터의 면역 활성 효과
하단비 ( Dan Bee Ha ),김민주 ( Min Ju Kim ),주해진 ( Hae Jin Joo ),조진희 ( Jin Hee Cho ),빙소진 ( So Jin Bing ),임윤규 ( Yoon Kyu Lim ),현진원 ( Jin Won Hyun ),지영흔 ( Young Heun Jee ) 한국예방수의학회(구 한국수의공중보건학회) 2011 예방수의학회지 Vol.35 No.1
'스콜라' 이용 시 소속기관이 구독 중이 아닌 경우, 오후 4시부터 익일 오전 7시까지 원문보기가 가능합니다.
Vanadium, a dietary micronutrient, has been reported to present interesting biological and pharmacological properties, including superoxide and nitric oxide scavenging effects. Low-dose ionizing radiation (LDR) is known to damage DNA and cause apoptosis of peripheral immunocytes by producing reactive oxygen species (ROS). The aim of this study was to elucidate the capacity of immune activation of Jeju water containing vanadium on immunosuppression caused by LDR. We examined the ROS production, DNA damage, cell apoptosis and proliferation of peripheral immunocytes in irradiated mice drinking different concentrations for 90 days; V0 (vanadium 0㎍/L, control), V1 (vanadium 15~20㎍/ L) and V2 (vanadium 20∼25㎍/L). Compared to V0 control where level of ROS showed tendency to increase, the ROS production was attenuated in peripheral immunocytes of irradiated mice drinking V1 and V2. DNA damage of peripheral immunocytes triggered by LDR significantly increased in mice drinking V0 compared to non-irradiated control, whereas V1 and V2 dramatically induced remission of DNA damage. On the observation of apoptosis of peripheral immunocytes, V1 and V2 showed the potency to reduce the number of apoptotic cells. On the other hand irradiated mice drinking V0 exhibited raised number of apoptotic cells. From the results obtained, we speculated that Jeju water containing vanadium (V1 and V2) has a potential role in decreasing DNA damage and apoptosis of immune cell by inhibiting ROS production. Consistent with this, Jeju water containing vanadium (V1 and V2) exhibits a capacity to enhance cell proliferation of peripheral immunocytes, which is suppressed by LDR as shown in V0 control. Collectively, Jeju water containing vanadium reduced DNA damage and apoptosis and induced the stimulatory potential on immunocytes. Theseresults suggest that Jeju water containing vanadium sustained immune activities under immunosuppression caused by LDR.
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Glatiramer acetate 투여에 의한 자가면역성 뇌척수염 마우스의 중추신경계에서의 NFκB 활성 억제
황인선,하단비,김대승,주해진,지영흔 대한수의학회 2011 大韓獸醫學會誌 Vol.51 No.3
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Glatiramer acetate (GA; Copaxone) has been shown to be effective in preventing and suppressing experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS). It has been recently shown that GA-reactive T cells migrate through the blood-brain barrier, accumulate in the central nervous system (CNS), secrete antiinflammatory cytokines and suppress production of proinflammatory cytokines of EAE and MS. Development of EAE requires coordinated expression of a number of genes involved in the activation and effector functions of inflammatory cells. Activation of inflammatory cells is regulated at the transcriptional level by several families of transcription factors. One of these is the nuclear factor kappa B (NFκB) family which is present in a variety of cell types and involved in the activation of immune-relative genes during inflammatory process. Since it is highly activated at site of inflammation, NFκB activation is also implicated in the pathogenesis of EAE. In this study, we examined whether the inhibition of NFκB activation induced by GA can have suppressive therapeutic effects in EAE mice. We observed the expression of NFκB and phospho-IκB proteins increased in GA-treated EAE mice compared to EAE control groups. The immunoreactivity in inflammatory cells and glial cells of NFκB and phospho-IκB significantly decreased at the GA-treated EAE mice. These results suggest that treatment of GA in EAE inhibits the activation of NFκB and phophorylation of IκB in the CNS. Subsequently, the inhibition of NFκB activation and IκB phosphorylation leads to the anti-inflammatory effects thereby to reduce the progression and severity of EAE.
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C57BL/6 마우스에서 Retroviral 벡터를 이용한 Foxp3 유전자의 도입에 의한 Foxp3 단백의 발현 양상
황인선,하단비,빙소진,전경익,안긴내,김대승,조진희,임재학,임신혁,황규계,지영흔 대한수의학회 2012 大韓獸醫學會誌 Vol.52 No.3
The maintenance of peripheral immune tolerance and prevention of chronic inflammation and autoimmune disease require CD4+CD25+ T cells (regulatory T cells). The transcription factor Foxp3 is essential for the development of functional, regulatory T cells, which plays a prominent role in self-tolerance. Retroviral vectors can confer high level of gene transfer and transgene expression in a variety of cell types. Here we observed that following retroviral vector-mediated gene transfer of Foxp3, transductional Foxp3 expression was increased in the liver, lung, brain, heart, muscle, spinal cord, kidney and spleen. One day after vector administration, high levels of transgene and gene expression were observed in liver and lung. At 2 days after injection, transductional Foxp3 expression level was increased in brain, heart, muscle and spinal cord, but kidney and spleen exhibited a consistent low level. This finding was inconsistent with the increase in both CD4+CD25+ T cell and CD4+Foxp3+ T cell frequencies observed in peripheral immune cells by fluorescence-activated cell-sorting (FACS) analysis. Retroviral vector-mediated gene transfer of Foxp3 did not lead to increased numbers of CD4+CD25+ T cell and CD4+Foxp3+ T cell. These results demonstrate the level and duration of transductional Foxp3 gene expression in various tissues. A better understanding of Foxp3 regulation can be useful in dissecting the cause of regulatory T cells dysfunction in several autoimmune diseases and raise the possibility of enhancing suppressive functions of regulatory T cells for therapeutic purposes.
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