Expression of innate immune complement regulators on brain epithelial cells during human bacterial meningitis.
Expression of innate immune complement regulators on brain epithelial cells during human bacterial meningitis.
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DOI：
10.1186/1742-2094-3-22
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发表时间：
2006-09-02
影响因子：
9.3
通讯作者：
Gasque P
中科院分区：
文献类型：
--
作者：
Canova C;Neal JW;Gasque P
在脑膜炎中，脑脊液含有高水平的先天免疫分子（例如补体），其对于抵御感染性挑战和促进吞噬细胞（中性粒细胞、单核细胞）的浸润是必需的。然而，室管膜层的上皮细胞，成人神经干细胞的一个既定的生态位，或脉络丛可能是非常脆弱的旁观者攻击细胞毒性和细胞溶解补体成分。在这项研究中，我们评估的能力，脑上皮细胞表达膜结合补体调节（即，CD 35，CD 46，CD 55和CD 59）在体外和原位免疫染色的控制和脑膜炎人脑组织切片。室管膜细胞标志物（GFAP、S100、ZO-1、E-cadherin）和补体调节剂的双重免疫荧光实验表明，与CD 46和CD 35的弱染色相比，人室管膜细胞系模型对CD 55、CD 59是强阳性的。在组织中，我们发现CD 55在对照脉络丛和室管膜中弱表达，但在脑膜炎中大量表达。抗CD 59染色的上皮细胞在顶端位置，而增加的CD 59染色仅表现在发炎脉络丛。在对照组织切片中未检测到CD 46和CD 35。相反，在脑膜炎，室管膜，室管膜下和脉络丛上皮细胞的CD 46和CD 35强染色。本研究首次描述了脑室管膜和上皮细胞对先天性补体介导的炎症反应的能力，并可能维持这种能力。
In meningitis, the cerebrospinal fluid contains high levels of innate immune molecules (e.g. complement) which are essential to ward off the infectious challenge and to promote the infiltration of phagocytes (neutrophils, monocytes). However, epithelial cells of either the ependymal layer, one of the established niche for adult neural stem cells, or of the choroid plexus may be extremely vulnerable to bystander attack by cytotoxic and cytolytic complement components. In this study, we assessed the capacity of brain epithelial cells to express membrane-bound complement regulators (ie, CD35, CD46, CD55 and CD59) in vitro and in situ by immunostaining of control and meningitis human brain tissue sections. Double immunofluorescence experiments for ependymal cell markers (GFAP, S100, ZO-1, E-cadherin) and complement regulators indicated that the human ependymal cell line model was strongly positive for CD55, CD59 compared to weak stainings for CD46 and CD35. In tissues, we found that CD55 was weakly expressed in control choroid plexus and ependyma but was abundantly expressed in meningitis. Anti-CD59 stained both epithelia in apical location while increased CD59 staining was solely demonstrated in inflamed choroid plexus. CD46 and CD35 were not detected in control tissue sections. Conversely, in meningitis, the ependyma, subependyma and choroid plexus epithelia were strongly stained for CD46 and CD35. This study delineates for the first time the capacity of brain ependymal and epithelial cells to respond to and possibly sustain the innate complement-mediated inflammatory insult.
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影响因子：
5.4
作者：
Casarsa, C;De Luigi, A;Tedesco, F
通讯作者：
Tedesco, F
影响因子：
6.4
作者：
Lacroix, S;Feinstein, D;Rivest, S
通讯作者：
Rivest, S
影响因子：
56.9
作者：
Johansson, L;Rytkönen, A;Jonsson, AB
通讯作者：
Jonsson, AB
影响因子：
64.8
作者：
Devitt, A;Moffatt, OD;Gregory, CD
通讯作者：
Gregory, CD
影响因子：
4.8
作者：
Laflamme, N;Rivest, S
通讯作者：
Rivest, S