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脂多糖或细胞因子暴露后口腔黏膜水肿。

Edema in oral mucosa after LPS or cytokine exposure.

作者信息

Bletsa A, Nedrebø T, Heyeraas K J, Berggreen E

机构信息

Institute of Biomedicine, Section for Physiology, Faculty of Medicine, University of Bergen, Norway.

出版信息

J Dent Res. 2006 May;85(5):442-6. doi: 10.1177/154405910608500509.

Abstract

Lowering of interstitial fluid pressure (P(if)) is an important factor that explains the rapid edema formation in acute inflammation in loose connective tissues. Lipopolysaccharide (LPS) and the pro-inflammatory cytokines interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) are pathogenetic in gingivitis. To test if these substances induce lowering of P(if) in rat oral mucosa, we measured P(if) with a micropuncture technique. IL-1beta and TNF-alpha caused lowering of P(if), whereas LPS induced an immediate increase in P(if), followed by lowering after 40 min. Measurements of fluid volume distribution showed a significant change in interstitial fluid volume (V(i)) 1.5 hr after LPS exposure as V(i) changed from 0.41 +/- 0.02 to 0.51 +/- 0.03 mL/g wet weight (p < 0.05), confirming edema. These findings show that LPS, IL-1beta, and TNF-alpha induce lowering of P(if) in the rat oral mucosa and contribute to edema formation in LPS-induced gingivitis.

摘要

间质液压力(P(if))的降低是解释疏松结缔组织急性炎症中快速水肿形成的一个重要因素。脂多糖(LPS)以及促炎细胞因子白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)在牙龈炎的发病机制中起作用。为了测试这些物质是否会导致大鼠口腔黏膜中P(if)降低,我们用微穿刺技术测量了P(if)。IL-1β和TNF-α导致P(if)降低,而LPS则导致P(if)立即升高,40分钟后降低。液体体积分布测量显示,LPS暴露1.5小时后,间质液体积(V(i))有显著变化,V(i)从0.41±0.02变为0.51±0.03 mL/g湿重(p<0.05),证实出现水肿。这些发现表明,LPS、IL-1β和TNF-α会导致大鼠口腔黏膜中P(if)降低,并在LPS诱导的牙龈炎中促进水肿形成。

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