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Review
. 2013:2013:759103.
doi: 10.1155/2013/759103. Epub 2013 Jan 27.

Pivotal roles of monocytes/macrophages in stroke

Tsuyoshi Chiba  1 , Keizo Umegaki
Affiliations
Review

Pivotal roles of monocytes/macrophages in stroke

Tsuyoshi Chiba et al. Mediators Inflamm. 2013.

Abstract

Stroke is an important issue in public health due to its high rates both of morbidity and mortality, and high rate of disability. Hypertension, cardiovascular disease, arterial fibrillation, diabetes mellitus, smoking, and alcohol abuse are all risk factors for stroke. Clinical observations suggest that inflammation is also a direct risk factor for stroke. Patients with stroke have high levels of inflammatory cytokines in plasma, and immune cells, such as macrophages and T-lymphocytes, are noted within stroke lesions. These inflammatory events are considered as a result of stroke. However, recent studies show that plasma levels of inflammatory cytokines or soluble adhesion molecules are high in patients without stroke, and anti-inflammatory therapy is effective at reducing stroke incidence in not only animal models, but in humans as well. Statins have been shown to decrease the stroke incidence via anti-inflammatory effects that are both dependent and independent of their cholesterol-lowering effects. These reports suggest that inflammation might directly affect the onset of stroke. Microglial cells and blood-derived monocytes/macrophages play important roles in inflammation in both onset and aggravation of stroke lesions. We review the recent findings regarding the role of monocytes/macrophages in stroke.

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Figures

Figure 1
Figure 1
Monocytes/macrophages modulate adipose tissue and kidney functions and accelerate stroke. Monocytes/macrophages infiltration into adipose tissue stimulates secretion of leptin and inflammatory cytokines and suppresses secretion of adiponectin, which induce systemic inflammation, endothelial cell dysfunction, and monocytes/macrophages activation. Monocytes/macrophages infiltration into kidney modulates renin-angiotensin system and increase blood pressure, which also induces endothelial cell dysfunction and monocytes/macrophages activation. Endothelial cells express MCP-1 and adhesion molecules, which induce monocytes chemotaxis, adhesion, and migration into subendothelial lesions. Microglial cells and infiltrated monocytes/macrophages in brain induce cerebrovascular damages and cause stroke onset.
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