Influence of chylomicron remnants on human monocyte activation in vitro

Bentley, C., Hathaway, N., Widdows, J., Bejta, F., De Pascale, C., Avella, M., Wheeler-Jones, C.P.D., Botham, K.M. and Lawson, C. 2011. Influence of chylomicron remnants on human monocyte activation in vitro. Nutr Metab Cardiovasc Dis.. 21 (11), pp. 871-878. doi:10.1016/j.numecd.2010.02.019

TitleInfluence of chylomicron remnants on human monocyte activation in vitro
AuthorsBentley, C., Hathaway, N., Widdows, J., Bejta, F., De Pascale, C., Avella, M., Wheeler-Jones, C.P.D., Botham, K.M. and Lawson, C.
Abstract

Background and aims

Atherosclerosis is known to be an inflammatory disease and there is increasing evidence that chylomicron remnants (CMR), the lipoproteins which carry dietary fats in the blood, cause macrophage foam cell formation and inflammation. In early atherosclerosis the frequency of activated monocytes in the peripheral circulation is increased, and clearance of CMR from blood may be delayed, however, whether CMR contribute directly to monocyte activation and subsequent egress into the arterial wall has not been established. Here, the contribution of CMR to activation of monocyte pro-inflammatory pathways was assessed using an in vitro model.

Methods and results

Primary human monocytes and CMR-like particles (CRLP) were used to measure several endpoints of monocyte activation. Treatment with CRLP caused rapid and prolonged generation of reactive oxygen species by monocytes. The pro-inflammatory chemokines MCP-1 and IL-8 were secreted in nanogram quantities by the cells in the absence of CRLP. IL-8 secretion was transiently increased after CRLP treatment, and CRLP maintained secretion in the presence of pharmacological inhibitors of IL-8 production. In contrast, exposure to CRLP significantly reduced MCP-1 secretion. Chemotaxis towards MCP-1 was increased in monocytes pre-exposed to CRLP and was reversed by addition of exogenous MCP-1.

Conclusion

Our findings indicate that CRLP activate human monocytes and augment their migration in vitro by reducing cellular MCP-1 expression. Our data support the current hypothesis that CMR contribute to the inflammatory milieu of the arterial wall in early atherosclerosis, and suggest that this may reflect direct interaction with circulating blood monocytes.

KeywordsMonocytes/macrophages; Lipid mediators; Chemokines; Inflammation; Dietary fat
JournalNutr Metab Cardiovasc Dis.
Journal citation21 (11), pp. 871-878
ISSN0939-4753
Year2011
PublisherElsevier
Publisher's version1-s2.0-S0939475310000682-main.pdf
Digital Object Identifier (DOI)doi:10.1016/j.numecd.2010.02.019
Publication dates
Published online31 Jul 2010
Published in printNov 2011
LicenseCC BY 4.0

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