Publication: Neutrophil infiltration and oxidant-production
in human atherosclerotic carotid plaques
Authors
Hosokawa, Takatoshi ; Kumon, Yoshitaka ; Kobayashi, Toshihiro ; Enzan, Hideaki ; Nishioka, Yutaka ; Yuri, Kazunari ; Wakiguchi, Hiroshi ; Sugiura, Tetsuro
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Publisher
Murcia: F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
To clarify the clinical implications of
neutrophils in vulnerable plaques we evaluated the
function and activity of infiltrated neutrophils in an
atherosclerotic plaque, focusing on oxidant production.
A histopathological investigation was performed using
carotid arterial samples obtained from seven patients.
The atherosclerotic plaques were examined cytochemically
for naphthol-ASD-chloroacetate esterase
activity and oxidant-production, and immunohistochemically
using N-formyl peptide receptor-like 1
(fPRL1)-, CD66b-, CD68- or p22phox-specific
antibodies. The cytoplasmic fPRL1 intensity value of the
neutrophils in the plaque was estimated using an activity
index.
Naphthol-ASD-chloroacetate esterase activity was
found in cells located in the atherosclerotic plaque,
indicating that the cells were neutrophils. The
cytoplasmic fPRL1 intensity value of the neutrophils in
the plaque decreased to approximately 60% of the
intensity observed in the capillary vessels. Oxidantproduction
was also detected in the plaques, and both
neutrophils and macrophages were observed at the
corresponding oxidant-production sites. p22phox
expression was also located in the same areas in which
oxidant-production was observed in these plaques. We
could not directly evaluate how much ROS generated
from the infiltrated neutrophils contributed the plaque
vulnerability followed by its rupture. However, the
infiltrated neutrophils in the atherosclerotic plaques
morphologically appeared activated and were actively
generating oxidant, implying that neutrophils, together
with macrophages, infiltrate into atherosclerotic plaques
and contribute to plaque vulnerability.
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