[Posttraumatic pyogenic and granulomatous encephalitis. An animal experimental contribution on inflammation (author's transl)].

W Schachenmayr
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Abstract

The present studies were performed to elucidate the factors responsible for the relative resistance of the brain to bacterial infections. As a model, group A streptococci were used to produce an experimental brain infection in mice. Attention was focussed on the activity of brain macrophages, the function of which to date is poorly understood. The primary purpose of the experiments was to compare the types of inflammation elicited in the brain by the injection of either killed or living group A streptococci. As a result, two fundamentally different types of encephalitis were observed histologically. A granulomatous inflammation was induced by killed streptococci; when deposited in the brain by intracerebral injection, these were phagocytosed by invading mononuclear macrophages and polymorphonuclear granulocytes during the first day p.i. There was no necrosis of brain tissue excepting the stab wound at the site of injection. The number of granulocytes in the inflammatory infiltrates decreased during the first week p.i. whereas, during the same period, the number of macrophages forming granuloma-like cell accummulations increased. At the beginning of the third week a fading of the granulomatous encephalitis was observed. In contrast, living streptococci produced a pyogenic inflammation of the meninges as well as of the grey and white matter in the region of the stab wound combined with extended tissue necrosis surrounding deposits of bacteria. This pyogenic infection progressed until the end of the first week, forming a brain abscess. A phlegmonous spreading of the pyogenic inflammation predominantly in the white matter and pyocephalus internus was also observed. In contrast to the increase of mononuclear macrophages in the border zone of the abscesses, the granulocytic inflammation decreased. During the second and third weeks p.i. granulation tissue consisting of proliferating connective tissue cells, macrophages and lymphocytes replaced pyogenic necrosis. A secondary purpose was to determine the fate of living and killed streptococci within the pyogenic and granulomatous encephalitis. In these studies immunohistologic, electron microscopic, bacteriologic and serologic methods were employed in addition to the techniques already mentioned. In the majority of the experimental animals streptococci were killed by granulocytes within the first week after injection of the living bacteria. At this time, most of the streptococci were contained within granulocytes and macrophages located to the periphery of the brain abscesses. Corresponding to the granulomatous encephalitis produced by injection of killed streptococci it was possible to detect persistent cell wall material in macrophages by immunohistology. By electronmicroscopy streptococci and their cell walls were found within the phagocytic vacuoles of macrophages. During the course of degradation the group-specific cell wall carbohydrate was enzymatically converted into the group A-variant specific structure...

创伤后化脓性和肉芽肿性脑炎。对炎症的动物实验贡献[作者简介]。
目前的研究是为了阐明大脑对细菌感染的相对抗性的因素。以a组链球菌为模型,制造小鼠实验性脑感染。注意力集中在脑巨噬细胞的活动上,其功能迄今为止知之甚少。实验的主要目的是比较注射死A组链球菌和活A组链球菌在大脑中引起的炎症类型。结果,在组织学上观察到两种根本不同类型的脑炎。杀死链球菌诱导肉芽肿性炎症;经脑内注射沉积于脑内后,第一天即被侵入的单核巨噬细胞和多形核粒细胞吞噬。除注射部位的刀伤外,脑组织未见坏死。炎性浸润中的粒细胞数量在第一周内减少,而在同一时期,形成肉芽肿样细胞积聚的巨噬细胞数量增加。第三周初观察到肉芽肿性脑炎消退。相比之下,活的链球菌在刺伤区域的脑膜以及灰质和白质中产生化脓性炎症,并在细菌沉积物周围产生广泛的组织坏死。这种化脓性感染一直持续到第一周结束,形成脑脓肿。化脓性炎症主要在白质和内白头部可见痰性扩散。与脓肿边界区单核巨噬细胞增多相反,粒细胞炎症减少。在第二和第三周,由增殖的结缔组织细胞、巨噬细胞和淋巴细胞组成的p.i.肉芽组织取代化脓性坏死。第二个目的是确定化脓性和肉芽肿性脑炎中存活和死亡链球菌的命运。在这些研究中,除了上述技术外,还采用了免疫组织学、电镜、细菌学和血清学方法。在大多数实验动物中,链球菌在注射活菌后的第一周内被粒细胞杀死。此时,大多数链球菌被包含在位于脑脓肿周围的粒细胞和巨噬细胞中。与注射灭活链球菌引起的肉芽肿性脑炎相对应,免疫组织学可以在巨噬细胞中检测到持久的细胞壁物质。电镜观察巨噬细胞吞噬空泡内可见链球菌及其细胞壁。在降解过程中,组特异性细胞壁碳水化合物被酶转化为a组变异特异性结构。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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