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Pivotal roles of monocytes/macrophages in stroke
Tsuyoshi Chiba1, Keizo Umegaki
1Information Center, National Institute of Health and Nutrition, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8636, Japan. tyschiba@nih.go.jp
Insights
Inflammation, particularly involving monocytes and macrophages, may directly contribute to stroke onset and severity. Anti-inflammatory therapies show promise in reducing stroke incidence, suggesting a causal role for inflammation.
Area of Science:
- Neuroscience
- Immunology
- Public Health
Background:
- Stroke is a leading cause of disability and mortality worldwide.
- Established risk factors include hypertension, diabetes, smoking, and cardiovascular disease.
- Emerging evidence suggests inflammation plays a direct role in stroke pathogenesis.
Purpose of the Study:
- To review recent findings on the role of monocytes and macrophages in stroke.
- To explore the contribution of inflammation to stroke onset and progression.
Main Methods:
- Review of recent scientific literature on inflammation and stroke.
- Analysis of studies investigating immune cell involvement in stroke lesions.
- Examination of data on inflammatory markers and anti-inflammatory therapies in stroke patients and models.
Main Results:
- Elevated inflammatory cytokines and immune cells (macrophages, T-lymphocytes) are observed in stroke patients.
- High levels of inflammatory markers are present even in individuals without stroke.
- Anti-inflammatory therapies, including statins, reduce stroke incidence through both cholesterol-dependent and independent mechanisms.
Conclusions:
- Inflammation, mediated by microglial cells and blood-derived monocytes/macrophages, is implicated in both the initiation and exacerbation of stroke.
- These findings suggest inflammation is a direct risk factor for stroke, not merely a consequence.
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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