Endotoxin-induced uveitis in the rat: Observations on altered vascular permeability, clinical findings, and histology

Cousins, Scott W.; Guss, R. B.; Howes, Edward L.; Rosenbaum, James T.

doi:10.1016/0014-4835(84)90065-4

Cited by 58 publications

(36 citation statements)

References 9 publications

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“…We speculate that the observed reduction in liver radioactivity could be a consequence of three primary causes. First, LPS-induced inflammation increases vascular permeability, which could alter organ blood flow and thus influence the uptake, utilization, and recycling of RA by the liver (7,13). Second, acute inflammation is known to diminish the expression of fatty acid transport protein (FATP) and fatty acid translocase (FAT), both of which are involved in the uptake of long-chain fatty acids from plasma (14,34).…”

Section: Discussionmentioning

confidence: 99%

All-trans-retinoic acid distribution and metabolism in vitamin A-marginal rats

Cifelli¹,

Ross²

2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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Section: Discussionmentioning

confidence: 99%

All-trans-retinoic acid distribution and metabolism in vitamin A-marginal rats

Cifelli¹,

Ross²

2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…prostaglandins, leukotrienes, nitric oxide) are also involved [30][31][32]. The majority of cells infiltrating the anterior segment are polymorphonuclear neutrophils and monocytes [33]. Thalidomide increases the survival rate in rats after high doses of endotoxin (20 mg/kg b.w.…”

Section: Discussionmentioning

confidence: 99%

Thalidomide Inhibits Leukocyte-Endothelium Interaction in Endotoxin-Induced Uveitis

Baatz

Tönessen²,

Prada³

et al. 2001

Ophthalmic Res

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To investigate the effects of thalidomide on leukocyte-endothelium interaction in iris vessels of rats with an endotoxin-induced uveitis (EIU), intravital fluorescence microscopy was used to quantify leukocyte adhesion to the vascular endothelium of iris venules in Lewis rats at 2, 4, 8 and 24 h after induction of EIU. Animals (n = 84) received a single intraperitoneal dose of either thalidomide (80 mg/kg body weight) or prednisolone (10 mg/kg body weight). Both drugs significantly reduced firm adhesion of leukocytes at 4, 8 and 24 h. Thalidomide caused earlier suppression of leukocyte rolling than prednisolone (4 vs. 8 h). TNF-α plasma levels peaked at 2 h and were not significantly reduced in any group compared with controls. Cell count and protein concentration in aqueous humor were significantly reduced by prednisolone and thalidomide at 24 h (p < 0.05). Thalidomide exerts its anti-inflammatory effects by an inhibition of leukocyte-endothelium interaction. Compared with prednisolone, thalidomide shows earlier inhibition of leukocyte rolling, indicating modulation of adhesion molecule expression and/or function.

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“…4,5 Although precise mechanisms remain to be elucidated, cytokines and chemokines, such as vascular endothelial growth factor (VEGF), monocyte chemoattractant protein (MCP)-1, and tumor necrosis factor (TNF)-␣, as well as nitric oxide (NO), released from inflammatory cells and ocular resident cells, including Muller cells and microglia in response to LPS, all contribute to the pathogenesis of EIU. 6 -12 In addition, increased oxidative stress induced by LPS or inflammatory cytokines seems to play a critical role in the regulation of the inflammatory cascade.…”

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confidence: 99%

Arginase Activity Mediates Retinal Inflammation in Endotoxin-Induced Uveitis

Zhang

Baban

Rojas

et al. 2009

The American Journal of Pathology

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Arginase has been reported to reduce nitric oxide bioavailability in cardiovascular disease. However, its specific role in retinopathy has not been studied. In this study, we assessed the role of arginase in a mouse model of endotoxin-induced uveitis induced by lipopolysaccharide (LPS) treatment. Measurement of arginase expression and activity in the retina revealed a significant increase in arginase activity that was associated with increases in both mRNA and protein levels of arginase (Arg)1 but not Arg2. Immunofluorescence and flow cytometry confirmed this increase in Arg1, which was localized to glia and microglia. Arg1 expression and activity were also increased in cultured Muller cells and microglia treated with LPS. To test whether arginase has a role in the development of retinal inflammation, experiments were performed in mice deficient in one copy of the Arg1 gene and both copies of the Arg2 gene or in mice treated with a selective arginase inhibitor. These studies showed that LPS-induced increases in inflammatory protein production, leukostasis, retinal damage, signs of anterior uveitis, and uncoupling of nitric oxide synthase were blocked by either knockdown or inhibition of arginase. Furthermore, the LPS-induced increase in Arg1 expression was abrogated by blocking NADPH oxidase. In conclusion, these studies suggest that LPS-induced retinal inflammation in endotoxin-induced uveitis is mediated by NADPH oxidase-dependent increases in arginase activity.

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Endotoxin-induced uveitis in the rat: Observations on altered vascular permeability, clinical findings, and histology

Cited by 58 publications

References 9 publications

All-trans-retinoic acid distribution and metabolism in vitamin A-marginal rats

All-trans-retinoic acid distribution and metabolism in vitamin A-marginal rats

Thalidomide Inhibits Leukocyte-Endothelium Interaction in Endotoxin-Induced Uveitis

Arginase Activity Mediates Retinal Inflammation in Endotoxin-Induced Uveitis

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