吸烟或可使得超级细菌更加“无敌”

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  耐甲氧西林金黄色葡萄球菌（MRSA）是一种抗生素耐药性细菌，其可以引发致命性的皮肤、血液及外科手术位点的感染及引发肺炎，近日一篇发表在国际杂志Infection and Immunity上的研究论文中，来自加利福尼亚大学的研究人员通过研究发现，吸烟或可使得MRSA更加“厉害”，相关研究表明当MRSA暴露于烟草中时其会对免疫系统的杀灭作用变得更加具有耐受性。

  博士Laura E. Crotty Alexander指出，如今我们已经知道，吸烟会损害人类的呼吸道和免疫细胞，而从相反的方面来看吸烟反而会使得如今机体的病原菌变得更加具有毒性；研究者表示，他是一名胸肺科医生，经常看到许多病人抽烟，而且许多患者也患有MRSA感染，于是他想知道是否吸烟会影响到MRSA的毒力，为了检测研究者的假设，他们利用MRSA感染巨噬细胞，其中一部分细菌可以正常生长，而一部分细菌则可以在香烟烟雾提取物中生长。

研究者发现，当巨噬细胞可以平等摄入两种细菌群体时，他们往往在杀灭香烟烟雾提取物中生长的MRSA时会比较困难，为了解释这一原因，研究者检测了细菌对巨噬细胞的敏感性机制，当细菌处于巨噬细胞中时，烟草暴露的MRSA会在活性氧的帮助下变得难以被杀灭，而活性氧同时也可以帮助巨噬细胞来破坏其内部的微生物。

研究人员表示，烟草暴露的MRSA可在抗菌肽的刺激下变得具有耐受性，而抗菌肽则是机体免疫系统所利用的一系列小分子蛋白，免疫系统可利用其来在细菌细胞上“打洞”并且诱发炎症，这种效应往往是剂量依赖性的，这就意味着烟草提取物暴露的越多，MRSA的耐受性就会越强。

而在实验室中，利用烟草提取物处理的MRSA往往更擅长于粘附并且入侵人类细胞，在小鼠模型中暴露中的MRSA会很好地生长，并且以高死亡率引发小鼠患肺炎；研究数据显示，吸烟会通过某种途径改变机体的细胞壁，进而增强MRSA的耐受性，从而使其可以抵御抗菌肽及其它制剂的作用。

最后研究者Crotty说道，吸烟者被认为对感染性疾病易感，如今通过本文研究我们也表明，烟草诱导的MRSA耐药或许是诱发吸烟患者对疾病易感的有一个促成因子。

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Analysis of the Effects of Cigarette Smoke on Staphylococcal Virulence Phenotypes

Elisa K. McEacherna,b, John H. Hwanga,b, Katherine M. Sladewskia,b, Shari Nicatiaa,b,c, Carola Dewitza,b,d, Denzil P. Mathewa, Victor Nizete,f and Laura E. Crotty Alexander#,a,b

Cigarette smoking is the leading preventable cause of death, disease and disability worldwide. It is well studied that cigarette smoke provokes inflammatory activation and impairs antimicrobial functions of human immune cells. Here we explore whether cigarette smoke likewise affects the virulence properties of an important human pathogen, Staphylococcus aureus (S. aureus), and in particular, methicillin-resistant S. aureus (MRSA), one of the leading causes of invasive bacterial infections. MRSA colonizes the nasopharynx and is thus exposed to inhalants including cigarette smoke. MRSA exposed to cigarette smoke extract (CSE) were more resistant to macrophage killing (4-fold higher survival, p<0.0001). CSE-MRSA demonstrated reduced susceptibility to cell lysis (1.78-fold, p=0.032) and antimicrobial peptide (AMP) killing (MIC 8 μM vs 4 μM LL-37). CSE modified the surface charge of MRSA in a dose-dependent fashion, impairing the binding of particles with charge similar to AMPs by 90% (p<0.0001). These changes persisted for 24 h post-exposure, suggesting heritable modifications. CSE exposure increased hydrophobicity by 55% (p<0.0001), which complemented findings of increased MRSA adherence and invasion of epithelial cells. CSE induced up-regulation of mprF, consistent with increased MRSA AMP resistance. S. aureus without mprF had no change in surface charge upon exposure to CSE. In vivo, CSE-MRSA pneumonia induced higher mouse mortality (40% vs. 10%) and increased bacterial burden at 8 and 20 hours post-infection compared to control MRSA infected mice (p<0.01). We conclude that cigarette smoke-induced immune resistance phenotypes in MRSA may be an additional factor contributing to susceptibility to infectious disease in cigarette smokers.