Instituto Nacional de Ciência e Tecnologia Translacional em Medicina, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil.
J Neuroimmunol. 2010 Apr 15;221(1-2):42-5. doi: 10.1016/j.jneuroim.2010.02.009. Epub 2010 Mar 3.
Bacterial meningitis caused by Streptococcus pneumoniae is associated with a significant mortality rate and persisting neurologic sequelae, including sensory-motor deficits, seizures, and impairment of learning and memory. The presence of proliferating bacteria within the subarachnoid and ventricular space compartments triggers an intense inflammatory host response at killing the invading microorganism. Proinflammatory mediators released in the process, including tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1beta, and IL-6, were shown to contribute to the development of brain injury in bacterial meningitis. Thus, the aim of this study was to verify the levels of the TNF-alpha, IL-1beta, IL-6, and CINC-1 in the rat brain after pneumococcal meningitis. The animals underwent a magna cistern tap receiving either 10 microL of sterile saline as a placebo or an equivalent volume of a S. pneumoniae suspension at the concentration of 5x10(9) cfu/mL. The placebo group was killed immediately after the induction and the meningitis group at 0, 6, 12, 24, 48, and 96h after induction. The brains were removed followed by the isolation of the hippocampus and prefrontal cortex for determining TNF-alpha, IL-1beta, IL-6, and CINC-1 levels. In the hippocampus we found increased levels of the TNF-alpha only at 6h (p<0.01; F=3.777); CINC-1 levels increased at 6 and 24h (p<0.001; p<0.05; F=15.05); and IL-6 and IL-1beta levels were not altered. In the prefrontal cortex, the TNF-alpha levels were found to be increased only at 6h (p<0.05; F=4.921); IL-6 (p<0.05; F=11.69) and IL-1beta (p<0.001; F=132.0) levels were found to be increased only at 24h after meningitis induction; and CINC-1 levels were found to be increased at 6, 12, and 24h (p<0.01; p<0.01; p<0.01; F=16.86) after meningitis induction. Our data suggest that cytokine/chemokine levels can be putative biomarkers of brain damage in the first hours of the pneumococcal meningitis.
肺炎链球菌引起的细菌性脑膜炎与较高的死亡率和持续的神经后遗症相关，包括感觉运动缺陷、癫痫发作和学习记忆损伤。在蛛网膜下腔和脑室腔室中增殖的细菌会引发强烈的炎症反应，以杀死入侵的微生物。在这个过程中释放的促炎介质，包括肿瘤坏死因子-α (TNF-α)、白细胞介素 (IL)-1β 和 IL-6，被证明有助于细菌性脑膜炎的脑损伤的发展。因此，本研究旨在验证肺炎球菌性脑膜炎后大鼠脑中 TNF-α、IL-1β、IL-6 和 CINC-1 的水平。动物接受了脑池穿刺，接受了 10 μL 无菌生理盐水（作为安慰剂）或相当于 5x10(9)cfu/mL 肺炎链球菌混悬液的等体积药物。安慰剂组在诱导后立即处死，脑膜炎组在诱导后 0、6、12、24、48 和 96 小时处死。取出大脑，分离海马体和前额皮质，以确定 TNF-α、IL-1β、IL-6 和 CINC-1 的水平。在海马体中，我们仅在 6 小时发现 TNF-α 水平升高（p<0.01；F=3.777）；CINC-1 水平在 6 和 24 小时升高（p<0.001；p<0.05；F=15.05）；而 IL-6 和 IL-1β 水平没有改变。在前额皮质中，仅在 6 小时发现 TNF-α 水平升高（p<0.05；F=4.921）；IL-6（p<0.05；F=11.69）和 IL-1β（p<0.001；F=132.0）水平仅在脑膜炎诱导后 24 小时升高；而 CINC-1 水平在脑膜炎诱导后 6、12 和 24 小时升高（p<0.01；p<0.01；p<0.01；F=16.86）。我们的数据表明，细胞因子/趋化因子水平可能是肺炎球菌性脑膜炎最初几个小时脑损伤的潜在生物标志物。
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