Ricci Susanna, Grandgirard Denis, Wenzel Michael, Braccini Tiziana, Salvatore Paola, Oggioni Marco R, Leib Stephen L, Koedel Uwe
BMC Infect Dis. 2014 Dec 31;14:726. doi: 10.1186/s12879-014-0726-6.
Approximately 7% of survivors from meningococcal meningitis (MM) suffer from neurological sequelae due to brain damage in the course of meningitis. The present study focuses on the role of matrix metalloproteinases (MMPs) in a novel mouse model of MM-induced brain damage.
The model is based on intracisternal infection of BALB/c mice with a serogroup C Neisseria meningitidis strain. Mice were infected with meningococci and randomised for treatment with the MMP inhibitor batimastat (BB-94) or vehicle. Animal survival, brain injury and host-response biomarkers were assessed 48 h after meningococcal challenge.
Mice that received BB-94 presented significantly diminished MMP-9 levels (p < 0.01), intracerebral bleeding (p < 0.01), and blood-brain barrier (BBB) breakdown (p < 0.05) in comparison with untreated animals. In mice suffering from MM, the amount of MMP-9 measured by zymography significantly correlated with both intracerebral haemorrhage (p < 0.01) and BBB disruption (p < 0.05).
MMPs significantly contribute to brain damage associated with experimental MM. Inhibition of MMPs reduces intracranial complications in mice suffering from MM, representing a potential adjuvant strategy in MM post-infection sequelae.
约7%的脑膜炎球菌性脑膜炎(MM)幸存者因脑膜炎病程中的脑损伤而患有神经后遗症。本研究聚焦于基质金属蛋白酶(MMPs)在一种新型MM诱导的脑损伤小鼠模型中的作用。
该模型基于用C群脑膜炎奈瑟菌菌株对BALB/c小鼠进行脑池内感染。小鼠感染脑膜炎球菌后随机分为两组,分别用MMP抑制剂batimastat(BB - 94)或赋形剂进行治疗。在脑膜炎球菌攻击后48小时评估动物存活率、脑损伤和宿主反应生物标志物。
与未治疗的动物相比,接受BB - 94治疗的小鼠MMP - 9水平显著降低(p < 0.01),脑内出血(p < 0.01)和血脑屏障(BBB)破坏(p < 0.05)情况也显著改善。在患有MM的小鼠中,通过酶谱法测得的MMP - 9量与脑内出血(p < 0.01)和BBB破坏(p < 0.05)均显著相关。
MMPs对与实验性MM相关的脑损伤有显著影响。抑制MMPs可减少患有MM的小鼠的颅内并发症,这代表了MM感染后后遗症的一种潜在辅助策略。