The bitter taste of infection

The human innate immune response to pathogens is complex, and it has been difficult to establish the contribution of epithelial signaling in the prevention of upper respiratory tract infection. The prevalence of chronic sinusitis in the absence of systemic immune defects indicates that there may be local defects in innate immunity associated with such mucosal infections. In this issue of the JCI, Cohen and colleagues investigate the role of the bitter taste receptors in airway epithelial cells, and find that these are critical to sensing the presence of invading pathogens. The participation of respiratory mucosal epithelial cells in innate immune defense has been increasingly appreciated. Not only do airway cells express the full complement of pattern recognition receptors and corresponding adaptor proteins to signal the recruitment of professional immune cells in response to perceived infection, they also participate directly in pathogen eradication. Mucociliary clearance is activated in response to bacterial components, and bacterial killing is mediated through epithelial production of NO and antimicrobial peptides. Although major defects in ciliary function (e.g., Kartagener syndrome) are clearly associated with increased respiratory infection rates, more subtle epithelial abnormalities that might be important in susceptibility to common conditions such as chronic sinus infection have not been fully characterized. Mutations in cystic fibrosis transmembrane conductance regulator (CFTR) that do not cause cystic fibrosis have been associated with chronic rhinosinusitis, although the specific pathogenetic mechanisms involved have not been determined (1). Given the complexity of the human innate immune response to pathogens, it has been difficult to establish the contribution of epithelial signaling in the prevention of upper respiratory tract infection. Nonetheless, given the large number of patients with chronic sinusitis, in the absence of any clinically apparent systemic immune defect, it seems likely that there must be local defects in innate immunity associated with such mucosal infections. In this issue of the JCI, Cohen and coworkers explore unexpected players in innate immune defense: the bitter taste receptors (2).     

基于感染管理护士为主体的医院感染管理实践

目的探讨基于感染管理护士为主体的医院感染管理实践的效果。方法设立感染管理护士的组织架构,选拔、培训感染管理护士,进一步培训感染管理相关人员,实施全院感染管理并注重持续改进。结果设置感染管理护士后,相关人员手卫生依从率和正确率、感染控制相关知识得分均提高(P0.01),而呼吸机相关肺炎、导管相关血流感染、导尿管相关尿路感染发生率差异无统计学意义(P0.05)。结论基于感染管理护士为主体的医院感染管理实践有助于医院感染管理工作的落实,有效促进多学科合作。     

The cellular basis of bacterial infection

Innate and adaptive immune responses are responsible for the prevention of and recovery from bacterial infections. Fully immunocompetent humans make adaptations to the pathogens within their environment. Bacterial pathogens are capable of responding to immune adaptations to avoid destruction and elimination. Examination of the bacterial mechanisms of evasion has revealed the evolution of many elegant systems capable of thwarting host defenses. Undoubtedly, more mechanisms have yet to be discovered. A major concern as bacteria become more antibiotic resistant is whether human immune adaptation can evolve sufficiently to keep pace with bacterial evolution of evasion mechanisms.     

人工关节假体感染的细菌培养

背景:人工关节感染是关节置换后严重的并发症,可导致置换失败。目的:分析近10年临床应用人工关节假体出现感染的细菌培养情况,以CNKI数据库文献检索和深度分析功能进行学术探讨,旨在丰富相关知识,便于其他检验人员借鉴和参考。设计:文献计量学分析。资料提取:以"人工关节(prosthetic joint),感染(infection),细菌培养(bacterial culture),关节液(synovial fluid,SF),软组织(soft tissue)"为关键词,总结中国各级医务工作者在2001-01/2010-12期间关于人工关节假体感染细菌培养的研究和进展,并分析结果,以文字和图表的形式进行统计和结果分析,描述其分布特征。入选标准:纳入标准:①与人工关节假体感染细菌培养相关的研究文章。排除标准:①与文章目的无关的文献。②重复研究的文献。③试验材料和方法交待不详细或结果存在争议的文章。主要数据判定指标:以出版时间、学科类别、来源期刊、研究机构、发表文献的作者分布以及基金资助情况进行相关分析。结果:从中国各级医务工作者在2001-01/2010-12期间以国内作者及单位为第一作者和第一单位的关于人工关节假体感染细菌培养的文献中,共检索到947篇人工关节假体感染的细菌培养相关文献,文献数量在时间分布上呈总体上升趋势。结论:通过文献计量学方法对人工关节假体感染细菌培养的文献进行分析,可为国内从事人工关节假体研究和临床实施置换的工作者进一步确定科研思路提供有价值的参考。     

骨关节念珠菌感染的治疗

念珠菌骨关节感染少见,常为血源性播散的结果,见于1%~2%的念珠菌血症患者,个别情况亦可由外伤、关节成形术或关节注射直接接种念珠菌所致。念珠菌骨关节感染多见于免疫功能受损人群,如肿瘤、酗酒、肝硬化、早产儿、应用细胞毒药物