الفهرس 
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Abstract
It is now increasingly clear that human stroke results in multi-organ systemic disease, rather than in solely a brain lesion. While acute stroke patients may survive the initial brain insult, many have subsequent complications over time. Infection is the most common of these complications and the chief cause of morbidity and mortality in the stroke survivor. The role of aberrant systemic immune function in post-stroke infection has only been demonstrated in many clinical studies (Patricia et al., 2007).
This study was carried out on 30 hypertensive atherosclerotic patients (15 patients with acute ischemic stroke and 15 non stroke patients), and 15 totally healthy individuals as a control group. Those patients were selected from Ain Shams University internal medicine inpatient department.
This study was aiming to follow up the changes in cell mediated immunity in acute cerebrovascular stroke in comparison to atherosclerotic patients with no previous vasculo-occlusive disorders.
In conclusion, we found that atherosclerosis is an inflammatory process which is characterized by predominance of Th1 response with increased circulating levels of Th1 cytokines including IFN-gamma. But after acute ischemic brain injury, reversal of Th1/Th2 ratio occurs with decrease in Th1, which leads to immune-depression, protecting brain antigens from recognition by immune cells which helps in neuroprotection after the acute insult. But that immune-depression leads also to increased host liability to infections which restores the Th1 dominance and worsens stroke prognosis.
Finally, we can consider the clinical application of antibiotics in post stroke prophylaxis, and thinking in other modalities of immunomodulation to improve stroke outcome.