Bowman-Birk Inhibitor attenuates experimental autoimmune encephalomyelitis by delaying infiltration of inflammatory cells into the CNS.
Bowman-Birk Inhibitor attenuates experimental autoimmune encephalomyelitis by delaying infiltration of inflammatory cells into the CNS.
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DOI：
10.1007/s12026-011-8254-6
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发表时间：
2011-12
影响因子：
4.4
通讯作者：
Rostami A
中科院分区：
文献类型：
--
作者：
Dai H;Ciric B;Zhang GX;Rostami A
Bowman-Birk Inhibitor （BBI）是一种从大豆中提取的丝氨酸蛋白酶抑制剂，具有抗炎特性，能够抑制动物模型中中枢神经系统自身免疫的发展。实验性自身免疫性脑脊髓炎（EAE）是一种广泛应用于多发性硬化症（MS）的动物模型，其特征是血脑屏障被破坏，炎症细胞浸润到中枢神经系统，从而导致病理。在这项研究中，我们观察到，与对照组小鼠相比，bbi治疗的小鼠EAE发作延迟，疾病严重程度降低。bbi处理小鼠的中枢神经系统炎症细胞减少，包括Th1和Th17细胞数量显著减少。在外周，BBI治疗在[免疫后第7天]早期抑制脑源性Th1和Th17反应的发展，而在发病后（第14天）。通过抗原特异性增殖和细胞因子的产生，bbi处理的小鼠有更强的Th反应。这些结果表明，BBI治疗暂时抑制了脑致生反应的发展，但这些反应最终达到正常程度。考虑到BBI处理的小鼠在临床表现为EAE时外周表现出更强的脑源性反应，延迟了疾病的发作，减少了中枢神经系统浸润细胞的数量，BBI可能阻碍了致病性Th1和Th17细胞从淋巴器官的出口，从而延缓了它们向中枢神经系统的迁移。
Bowman–Birk Inhibitor (BBI), a serine protease inhibitor derived from soybeans, has anti-inflammatory properties and is able to suppress the development of central nervous system (CNS) autoimmunity in animal models. Experimental autoimmune encephalomyelitis (EAE), a widely used animal model of multiple sclerosis (MS), is characterized by breakdown of the blood–brain barrier and infiltration of inflammatory cells into the CNS, resulting in pathology. In this study, we observed that BBI-treated mice showed delayed onset of EAE and reduced disease severity compared to control mice. BBI-treated mice had fewer inflammatory cells in the CNS including significantly reduced numbers of Th1 and Th17 cells. In the periphery, BBI treatment suppressed the development of encephalitogenic Th1 and Th17 responses early on [day 7 post-immunization (p.i.)], while after disease onset (day 14 p.i.) BBI-treated mice had stronger Th responses, as determined by antigen-specific proliferation and cytokine production. These results demonstrate that BBI treatment temporarily suppressed the development of encephalitogenic responses, but these responses eventually attained normal magnitude. Given that BBI-treated mice exhibited stronger encephalitogenic responses in the periphery during clinically manifesting EAE, delayed disease onset, and reduced numbers of CNS-infiltrating cells, it appears likely that BBI impedes the exit of pathogenic Th1 and Th17 cells from lymphoid organs, thereby delaying their migration into the CNS.
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DOI：
10.1007/400_2008_17
发表时间：
2010-01-01
期刊：
MOLECULAR BASIS OF MULTIPLE SCLEROSIS: THE IMMUNE SYSTEM
影响因子：
--
作者：
Korn, Thomas;Mitsdoerffer, Meike;Kuchroo, Vijay K.
通讯作者：
Kuchroo, Vijay K.
影响因子：
4.4
作者：
Mekala, DJ;Alli, RS;Geiger, TL
通讯作者：
Geiger, TL
影响因子：
2.7
作者：
ODANI, S;IKENAKA, T
通讯作者：
IKENAKA, T
影响因子：
3.1
作者：
Ware, JH;Wan, XS;Kennedy, AR
通讯作者：
Kennedy, AR
影响因子：
7.1
作者：
Kennedy, AR
通讯作者：
Kennedy, AR