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机构地区:[1]武汉大学同仁医院(武汉市第三医院),湖北武汉430060
出 处:《现代预防医学》2018年第2期364-367,共4页Modern Preventive Medicine
摘 要:目的从细胞水平探讨青霉素耐药对抗生素治疗肺炎链球菌(Streptococcupneumoniae,SP)感染BEAS-2B细胞疗效的影响。方法通过体外次抑菌浓度的青霉素诱导SP标准株ATCC 49619获得耐青霉素肺炎链球菌(Penicillin Resistant Streptococcus Pneumoniae,PRSP),再用其感染BEAS-2B细胞构建PRSP感染细胞模型作为实验组,同时用SP感染BEAS-2B细胞构建的SP感染细胞模型作为对照组。使用不同抗生素干预治疗以上构建的感染细胞模型,最后检测其细胞毒性以及促炎症因子IL-6的表达。结果实验组相比于对照组,其细胞毒性减弱(P<0.05),且IL-6表达水平也有所降低(P<0.05)。抗生素干预治疗后,感染细胞模型的细胞毒性得到了抑制,且其IL-6水平下降,差异具有统计学意义(P<0.05),抗生素对实验组细胞毒性的抑制水平以及IL-6的降低水平都低于对照组(P<0.05)。结论虽然PRSP在拥有耐药性的同时毒力也有所减弱,但其仍然减弱了抗生素治疗肺炎链球菌感染细胞模型的疗效。Objective The aim of this study was to investigate the effects of penicillin resistance on the efficacy of antibiotics in the treatment of Streptococcus pneumoniae (SP) infected BEAS-2B cells at the cellular level. Methods The standard SP was induced with the sub-inhibitory concentrations incremental method to obtain the penicillin resistant Streptococcus pneumoniae (PRSP). The BEAS-2B cells were infected with PRSP to construct cell model as the experimental group. At the same time, the constructed cell model infected with SP was used as the control group. Cell models were treated by different antibiotics and the cytotoxicity and the expression level of IL-6 were analyzed. Results The cytotoxicity of experimental group was higher than the control group (P〈0.05), and the expression level of IL-6 of experimental group was lower (P〈0.05). After antibiotic treatment, the cytotoxicity of infected cell model was inhibited, while the expression level of IL-6 was decreased (P〈0.05). However, the level of cytotoxicity and the IL-6 in experimental group were lower than those in the control group (P〈0.05). Conclusion Although the PRSP had stronger resistance and weaker virulence, it still impaired the efficacy of antibiotic therapy for the cell model infected with SP.
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