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

Section 01 - Prosthetics

2 Citations (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.

Original language	English
Journal	Discovery Medicine
Volume	17
Issue number	96
Pages (from-to)	309-12
Number of pages	4
ISSN	1539-6509
Publication status	Published - Jun 2014

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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.

In: Discovery Medicine, Vol. 17, No. 96, 06.2014, p. 309-12.

Research output: Contribution to journal › Journal article › Research › 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, vol. 17, no. 96, pp. 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.",

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AU - Bendtzen, Klaus

AU - Christensen, Ole

AU - Nielsen, Claus Henrik

AU - Holmstrup, Palle

PY - 2014/6

Y1 - 2014/6

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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JF - Discovery medicine

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