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首页> 外文期刊>American Journal of Physiology >Immune complexes alter cerebral microvessel permeability: roles of complement and leukocyte adhesion.
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Immune complexes alter cerebral microvessel permeability: roles of complement and leukocyte adhesion.

机译：免疫复合物改变脑微血管通透性：补体和白细胞粘附的作用。

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摘要

Immune complexes (ICs) are potent inflammatory mediators in peripheral tissues. However, very few studies have examined the ability of ICs to induce inflammatory responses in the brain. Therefore, using preformed ICs or the reverse passive Arthus (RPA) model to localize ICs to the pial microvasculature of mice, we aimed to investigate the ability of ICs to induce an inflammatory response in the cerebral (pial) microvasculature. Application of preformed ICs immediately increased pial microvascular permeability, with a minimal change in leukocyte adhesion in pial postcapillary venules. In contrast, initiation of the RPA response in the pial microvasculature induced changes in cerebral microvascular permeability and increased leukocyte adhesion in pial postcapillary venules. The RPA response induced deposition of C3 in perivascular regions adjacent to sites of IC formation. Depletion of C3 abrogated RPA-induced microvascular permeability and leukocyte adhesion, indicating that the complement pathway was critical for this response. Inhibition of leukocyte adhesion via CD18 blockade also reduced IC-induced microvascular permeability. However, this did not require intercellular adhesion molecule-1, inasmuch as blockade of intercellular adhesion molecule-1 did not alter RPA-induced microvascular permeability and adhesion. These findings demonstrate that ICs are capable of rapidly inducing inflammatory responses in the cerebral microvasculature, with the complement pathway and leukocyte recruitment playing critical roles in microvascular dysfunction.
机译：免疫复合物（ICs）是外周组织中有效的炎症介质。但是，很少有研究检查IC诱导大脑炎症反应的能力。因此，使用预先形成的IC或反向被动Arthus（RPA）模型将IC定位于小鼠的皮层微脉管系统，我们旨在研究IC诱导脑（皮）微脉管系统炎症反应的能力。预制IC的应用立即增加了皮层微血管的通透性，使皮层毛细血管后小静脉中白细胞粘附的变化最小。相反，在视网膜微血管中，RPA反应的启动会引起大脑微血管通透性的变化，并增加血浆在毛细血管后小静脉中的白细胞粘附。 RPA反应诱导C3在邻近IC形成部位的血管周围区域沉积。 C3的消耗废除了RPA诱导的微血管通透性和白细胞粘附，表明补体途径对该反应至关重要。通过CD18阻滞抑制白细胞粘附也降低了IC诱导的微血管通透性。但是，这不需要细胞间粘附分子-1，因为对细胞间粘附分子-1的阻断不会改变RPA诱导的微血管通透性和粘附。这些发现表明，IC能够在大脑微脉管系统中快速诱导炎症反应，补体途径和白细胞募集在微血管功能障碍中起关键作用。

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