A matrix of cholesterol crystals, but not cholesterol alone, primes human monocytes/macrophages for excessive endotoxin-induced production of tumor necrosis factor-alpha. Role in atherosclerotic inflammation?

Klaus Bendtzen; Ole Christensen; Claus Henrik Nielsen; Palle Holmstrup

A matrix of cholesterol crystals, but not cholesterol alone, primes human monocytes/macrophages for excessive endotoxin-induced production of tumor necrosis factor-alpha. Role in atherosclerotic inflammation?

Klaus Bendtzen, Ole Christensen, Claus Henrik Nielsen, Palle Holmstrup

Sektion 01

2 Citationer (Scopus)

Abstract

When exposed to small amounts of bacterial endotoxin, matrices of cholesterol crystals, but not cholesterol itself, primed human monocytes/macrophages to a highly augmented (>10-fold) production of inflammatory tumor necrosis factor-a. Priming also sensitized the cells, as 10-to 100-fold lower levels of endotoxin were needed for TNF-a production equivalent to that of unprimed cells. The pro-inflammatory effect was selective as endotoxin-induced production of other pro-inflammatory cytokines was unaffected while production of anti-inflammatory interleukin-10 was diminished. These findings suggest that cholesterol matrix formation may play a pathogenic role in atherosclerotic inflammation, and they indicate a mechanism by which bacteria and/or bacterial products may play a role in processes leading to arteriosclerosis.

Originalsprog	Engelsk
Tidsskrift	Discovery Medicine
Vol/bind	17
Udgave nummer	96
Sider (fra-til)	309-12
Antal sider	4
ISSN	1539-6509
Status	Udgivet - jun. 2014

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http://www.discoverymedicine.com/Klaus-Bendtzen/2014/06/a-matrix-of-cholesterol-crystals-primes-monocytes-macrophages-for-excessive-endotoxin-induced-production-of-tumor-necrosis-factor-alpha-role-in-atherosclerotic-inflammation/

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Citationsformater

Bendtzen, K., Christensen, O., Nielsen, C. H., & Holmstrup, P. (2014). A matrix of cholesterol crystals, but not cholesterol alone, primes human monocytes/macrophages for excessive endotoxin-induced production of tumor necrosis factor-alpha. Role in atherosclerotic inflammation? Discovery Medicine, 17(96), 309-12. http://www.discoverymedicine.com/Klaus-Bendtzen/2014/06/a-matrix-of-cholesterol-crystals-primes-monocytes-macrophages-for-excessive-endotoxin-induced-production-of-tumor-necrosis-factor-alpha-role-in-atherosclerotic-inflammation/

A matrix of cholesterol crystals, but not cholesterol alone, primes human monocytes/macrophages for excessive endotoxin-induced production of tumor necrosis factor-alpha. Role in atherosclerotic inflammation? / Bendtzen, Klaus; Christensen, Ole; Nielsen, Claus Henrik et al.
I: Discovery Medicine, Bind 17, Nr. 96, 06.2014, s. 309-12.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

Bendtzen, K, Christensen, O, Nielsen, CH & Holmstrup, P 2014, 'A matrix of cholesterol crystals, but not cholesterol alone, primes human monocytes/macrophages for excessive endotoxin-induced production of tumor necrosis factor-alpha. Role in atherosclerotic inflammation?', Discovery Medicine, bind 17, nr. 96, s. 309-12. <http://www.discoverymedicine.com/Klaus-Bendtzen/2014/06/a-matrix-of-cholesterol-crystals-primes-monocytes-macrophages-for-excessive-endotoxin-induced-production-of-tumor-necrosis-factor-alpha-role-in-atherosclerotic-inflammation/>

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abstract = "When exposed to small amounts of bacterial endotoxin, matrices of cholesterol crystals, but not cholesterol itself, primed human monocytes/macrophages to a highly augmented (>10-fold) production of inflammatory tumor necrosis factor-a. Priming also sensitized the cells, as 10-to 100-fold lower levels of endotoxin were needed for TNF-a production equivalent to that of unprimed cells. The pro-inflammatory effect was selective as endotoxin-induced production of other pro-inflammatory cytokines was unaffected while production of anti-inflammatory interleukin-10 was diminished. These findings suggest that cholesterol matrix formation may play a pathogenic role in atherosclerotic inflammation, and they indicate a mechanism by which bacteria and/or bacterial products may play a role in processes leading to arteriosclerosis.",

author = "Klaus Bendtzen and Ole Christensen and Nielsen, {Claus Henrik} and Palle Holmstrup",

year = "2014",

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AU - Bendtzen, Klaus

AU - Christensen, Ole

AU - Nielsen, Claus Henrik

AU - Holmstrup, Palle

PY - 2014/6

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N2 - When exposed to small amounts of bacterial endotoxin, matrices of cholesterol crystals, but not cholesterol itself, primed human monocytes/macrophages to a highly augmented (>10-fold) production of inflammatory tumor necrosis factor-a. Priming also sensitized the cells, as 10-to 100-fold lower levels of endotoxin were needed for TNF-a production equivalent to that of unprimed cells. The pro-inflammatory effect was selective as endotoxin-induced production of other pro-inflammatory cytokines was unaffected while production of anti-inflammatory interleukin-10 was diminished. These findings suggest that cholesterol matrix formation may play a pathogenic role in atherosclerotic inflammation, and they indicate a mechanism by which bacteria and/or bacterial products may play a role in processes leading to arteriosclerosis.

AB - When exposed to small amounts of bacterial endotoxin, matrices of cholesterol crystals, but not cholesterol itself, primed human monocytes/macrophages to a highly augmented (>10-fold) production of inflammatory tumor necrosis factor-a. Priming also sensitized the cells, as 10-to 100-fold lower levels of endotoxin were needed for TNF-a production equivalent to that of unprimed cells. The pro-inflammatory effect was selective as endotoxin-induced production of other pro-inflammatory cytokines was unaffected while production of anti-inflammatory interleukin-10 was diminished. These findings suggest that cholesterol matrix formation may play a pathogenic role in atherosclerotic inflammation, and they indicate a mechanism by which bacteria and/or bacterial products may play a role in processes leading to arteriosclerosis.

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