血腦障壁(blood-brain barrier; BBB)被視為腦膜炎的重要病理生理因素，此屏障的損傷會造成白血球浸潤至蜘蛛膜下腔。基質金屬蛋白(matrix metalloproteinases, MMPs)涉及許多中樞神經系統的發炎性疾病，其中MMP-9的過度分解會造成BBB的破壞。本研究結果顯示腦脊髓液(cerebrospinal fluid; CSF)中之MMP-9的酵素活性只在感染廣東住血線蟲誘發嗜伊紅性腦膜炎的小白鼠檢測到此酵素，而未感染組則無法檢測到此酵素。浸潤至CSF中之嗜伊紅性白血球數量與MMP-9活性及CSF之總蛋白濃度明顯相關。相對地，MMP-2出現在所有的CSF檢體，包括未感染的小白鼠，且酵素活性並無改變。此結果顯示MMP-2酵素活性與CSF中之嗜伊紅性白血球數量及CSF之總蛋白濃度並無明顯相關。另外，以MMPs專一的抑制劑GM6001處理後，MMP-9酵素活性及CSF總蛋白濃度皆明顯降低。這些結果顯示MMP-9可能與廣東住血線蟲症引起之BBB損傷有關。
Blood-brain barrier (BBB) breakdown, causing extravasation of leukocytes into subarachnoid space, is regarded as an important pathophysiological event in meningitis. Matrix metalloproteinases (MMPs) are implicated in the pathogenesis of various inflammatory diseases of the central nervous system. Excessive proteolytic activity of MMP-9 can be detrimental, leading to the disruption of the BBB. The present study showed that the activities of MMP-9 in the cerebrospinal fluid (CSF) were significantly increased in mice with eosinophilic meningitis compared with uninfected mice. CSF eosinophilia was significantly correlated with MMP-9 intensity and CSF total protein. In contrast, MMP-2 was presented and remain unchanged in all CSF samples showing that this enzyme was not correlated with CSF eosinophilia and CSF total protein. In addition, MMP-9 enzymatic activity and CSF total protein were significantly increased upon the establishment of infection but subsided due to an inhibition by GM6001, a specific inhibitor for MMPs, These results suggested that MMP-9 proteolytic activity may be associated with BBB disruption in angiostrongyliasis.
