Putative antihyperpyretic factor induced by LPS in spleen of guinea pigs
Putative antihyperpyretic factor induced by LPS in spleen of guinea pigs
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DOI：
10.1152/ajpregu.00022.2005
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发表时间：
2005-09-01
影响因子：
2.8
通讯作者：
Blatteis, CM
中科院分区：
文献类型：
--
作者：
Feleder, C;Perlik, V;Blatteis, CM
我们以前报道过，发病的LPS诱导的发热，无论其给药途径，在时间上与外观的LPS在肝脏和脾切除术显着增加的发热反应，LPS和摄取的枯否细胞（KC）。为了进一步评估脾在LPS发热产生中的作用，我们结扎脾静脉，并在7天和30天后，监测腹膜内（ip）注射LPS（2 μ g/kg）后6小时内的核心温度变化。KC的发热反应和对LPS的摄取均显著增加。与脾切除术一样，脾静脉结扎（SVL）增加了KC的发热反应和LPS摄取，直到侧支循环形成，这表明脾脏通常可能有助于限制KC摄取LPS的抑制因子，从而影响发热反应。随后，为了验证该因子的存在，我们从用LPS（8 μ g/kg ip）或无热原盐水预处理的豚鼠制备脾提取物，将其均质化并超滤，并将其静脉内注射到用LPS（8 μ g/kg ip）预处理的脾切除（Splex）豚鼠中。结果证实了我们的假设，脾提取物从LPS处理的豚鼠抑制夸大的发热反应和LPS的Splex豚鼠的肝脏摄取，表明存在一个假定的脾抑制因子，证实了脾参与LPS诱导的发热，并建议存在一种新的解热机制。初步数据表明，该因子是一种脂质。
We reported previously that the onset of LPS-induced fever, irrespective of its route of administration, is temporally correlated with the appearance of LPS in the liver and that splenectomy significantly increases both the febrile response to LPS and the uptake of LPS by Kupffer cells ( KC). To further evaluate the role of the spleen in LPS fever production, we ligated the splenic vein and, 7 and 30 days later, monitored the core temperature changes over 6 h after intraperitoneal (ip) injection of LPS ( 2 mu g/kg). Both the febrile response and the uptake of LPS by KC were significantly augmented. Like splenectomy, splenic vein ligation (SVL) increased the febrile response and LPS uptake by KC until the collateral circulation developed, suggesting that the spleen may normally contribute an inhibitory factor that limits KC uptake of LPS and thus affects the febrile response. Subsequently, to verify the presence of this factor, we prepared splenic extracts from guinea pigs pretreated with LPS ( 8 mu g/kg ip) or pyrogen-free saline, homogenized and ultrafiltered them, and injected them intravenously into splenectomized (Splex) guinea pigs pretreated with LPS ( 8 mu g/kg ip). The results confirmed our presumption that the splenic extract from LPS-treated guinea pigs inhibits the exaggerated febrile response and the LPS uptake by the liver of Splex guinea pigs, indicating the presence of a putative splenic inhibitory factor, confirming the participation of the spleen in LPS-induced fever, and suggesting the existence of a novel antihyperpyretic mechanism. Preliminary data indicate that this factor is a lipid.