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ShareScienceDaily (June 25, 2010) — Dr. Einar Eriksson and colleagues at the Karolinska Hosptial, Stockholm, Sweden demonstrate that neutrophils may contribute to atherosclerosis. Their report can be found in the July 2010 issue of The American Journal of Pathology.
Atherosclerosis is a hardening of the arteries due to the build-up of plaques made up of fatty materials such as cholesterol. These plaques may eventually rupture, leading to clots and subsequent arterial narrowing or blockage, which results in insufficient blood supply to tissues and organs.
Although immune cells have been shown to play important roles in the genesis of artherosclerotic plaques, the contribution of neutrophils, the most abundant white blood cell in circulation, remains unclear. Therefore, Rotzius et al examined the role of neutrophils in a mouse model of atherosclerosis. They found that neutrophils accumulate in atherosclerotic lesions, although at lower levels than other white blood cells. Moreover, neutrophils are the predominant immune cells in the high inflammatory shoulder regions of plaques, suggesting that these cells may play a hitherto unappreciated role in the immunological processes of atherogenesis.
Dr. Eriksson's group concludes that "[their] data provide strong evidence for the presence and invasion of significant numbers of neutrophils in atherosclerotic lesions. These findings call for further investigation of the functional importance of neutrophils and their interplay with complex immunological processes in atherogenesis."
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The above story is reprinted from materials provided by American Journal of Pathology, via EurekAlert!, a service of AAAS.
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Journal Reference:
- Rotzius et al. Distinct Infiltration of Neutrophils in Lesion Shoulders in ApoE-/- Mice. American Journal Of Pathology, 2010; DOI: 10.2353/ajpath.2010.090480
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
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