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,§,¶,¶
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Department of Anatomy and Cell Biology, University of Marburg, Marburg, Germany;
Department of Microbiology and Immunology, University of Leicester, Leicester, United Kingdom;
Pharmacia & Upjohn SpA, Nerviano Mi, Italy;
§
Melacure Therapeutics AB, Uppsala, Sweden;
¶
Newron Pharmaceuticals Spa, Milan, Italy;
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Medical Research Council, Immunochemistry Unit, Department of Biochemistry, University of Oxford, Oxford, United Kingdom; and
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Institute for Medical Microbiology and Hygiene, Johannes Gutenberg-University of Mainz, Mainz, Germany
Recent evidence suggests that the pathophysiology of neurodegenerative and inflammatory neurological diseases has a neuroimmunological component involving complement, an innate humoral immune defense system. The present study demonstrates the effects of experimentally induced global ischemia on the biosynthesis of C1q, the recognition subcomponent of the classical complement activation pathway, in the CNS. Using semiquantitative in situ hybridization, immunohistochemistry, and confocal laser scanning microscopy, a dramatic and widespread increase of C1q biosynthesis in rat brain microglia (but not in astrocytes or neurons) within 24 h after the ischemic insult was observed. A marked increase of C1q functional activity in cerebrospinal fluid taken 1, 24, and 72 h after the ischemic insult was determined by C1q-dependent hemolytic assay. In the light of the well-established role of complement and complement activation products in the initiation and maintenance of inflammation, the ischemia-induced increase of cerebral C1q biosynthesis and of C1q functional activity in the cerebrospinal fluid implies that the proinflammatory activities of locally produced complement are likely to contribute to the pathophysiology of cerebral ischemia. Pharmacological modulation of complement activation in the brain may be a therapeutic target in the treatment of stroke.
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