耐甲氧西林金黃色葡萄球菌（MRSA）是一種抗生素耐藥性細菌，其可以引發致命性的皮膚、血液及外科手術位點的感染及引發肺炎，近日一篇發表在國際雜誌Infection and Immunity上的研究論文中，來自加利福尼亞大學的研究人員通過研究發現，吸煙或可使得MRSA更加“厲害”，相關研究表明當MRSA暴露於煙草中時其會對免疫係統的殺滅作用變得更加具有耐受性。
博士Laura E. Crotty Alexander指出，如今我們已經知道，吸煙會損害人類的呼吸道和免疫細胞，而從相反的方麵來看吸煙反而會使得如今機體的病原菌變得更加具有毒性；研究者表示，他是一名胸肺科醫生，經常看到許多病人抽煙，而且許多患者也患有MRSA感染，於是他想知道是否吸煙會影響到MRSA的毒力，為了檢測研究者的假設，他們利用MRSA感染巨噬細胞，其中一部分細菌可以正常生長，而一部分細菌則可以在香煙煙霧提取物中生長。
研究者發現，當巨噬細胞可以平等攝入兩種細菌群體時，他們往往在殺滅香煙煙霧提取物中生長的MRSA時會比較困難，為了解釋這一原因，研究者檢測了細菌對巨噬細胞的敏感性機製，當細菌處於巨噬細胞中時，煙草暴露的MRSA會在活性氧的幫助下變得難以被殺滅，而活性氧同時也可以幫助巨噬細胞來破壞其內部的微生物。
研究人員表示，煙草暴露的MRSA可在抗菌肽的刺激下變得具有耐受性，而抗菌肽則是機體免疫係統所利用的一係列小分子蛋白，免疫係統可利用其來在細菌細胞上“打洞”並且誘發炎症，這種效應往往是劑量依賴性的，這就意味著煙草提取物暴露的越多，MRSA的耐受性就會越強。
而在實驗室中，利用煙草提取物處理的MRSA往往更擅長於粘附並且入侵人類細胞，在小鼠模型中暴露中的MRSA會很好地生長，並且以高死亡率引發小鼠患肺炎；研究數據顯示，吸煙會通過某種途徑改變機體的細胞壁，進而增強MRSA的耐受性，從而使其可以抵禦抗菌肽及其它製劑的作用。
最後研究者Crotty說道，吸煙者被認為對感染性疾病易感，如今通過本文研究我們也表明，煙草誘導的MRSA耐藥或許是誘發吸煙患者對疾病易感的有一個促成因子。
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.
