Interleukin-1beta-induced growth enhancement of Staphylococcus aureus occurs in biofilm but not planktonic cultures.
Interleukin-1beta-induced growth enhancement of Staphylococcus aureus occurs in biofilm but not planktonic cultures.
复制标题
白细胞介素-1β 诱导的金黄色葡萄球菌生长增强发生在生物膜中，但不在浮游培养物中。
作者：
Renee A McLaughlin;A. Hoogewerf
金黄色葡萄球菌会引起顽固性感染并形成耐药生物膜。生物膜对宿主防御的抵抗机制可能包括基因表达的变化，从而赋予对化学介质的反应性。在早期的研究中，新鲜的临床分离株对炎症细胞因子有反应，但在多次体外传代后反应性消失[Meduri 等人，2017]。细胞因子 IL-1β、IL-6 和 TNF-α 增强细菌的体外生长。 Am J Respir Crit Care Med 1999；160：961-7]。由于生物膜更类似于体内生长并且与顽固性感染有关，因此我们假设生物膜而不是浮游细胞会对细胞因子做出反应。在金黄色葡萄球菌 ATCC 12600 中通过乙醇诱导生物膜。用 2 ng/mL 白细胞介素 1β (IL-1β) 处理 6 小时的生物膜所含细胞数量是未处理生物膜的 2.5 倍，但浮游培养物中没有出现生长增强。通过流式细胞术测定，IL-β 与 63.1% 的生物膜细胞结合，但仅与 11.2% 的浮游细胞结合。我们的结果提供了生物膜和浮游细菌对化学介质的不同反应的证据，并表明生物膜细菌可能通过响应激活的宿主防御细胞释放的炎症介质而更快地生长来逃避宿主防御。
Staphylococcus aureus causes recalcitrant infections and forms resistant biofilms. Mechanisms of biofilm resistance to host defenses may include changes in gene expression that confer responsiveness to chemical mediators. In earlier studies fresh clinical isolates responded to inflammatory cytokines, but responsiveness was lost after multiple in vitro passages [Meduri et al. Cytokines IL-1beta, IL-6, and TNF-alpha enhance the In vitro growth of bacteria. Am J Respir Crit Care Med 1999;160:961-7]. Since biofilms more closely resemble in vivo growth and are implicated in recalcitrant infections, we hypothesized that biofilms, but not planktonic cells, would respond to cytokines. Biofilms were induced by ethanol in S. aureus ATCC 12600. Biofilms treated with 2 ng/mL interleukin-1beta (IL-1beta) for 6 h contained 2.5-fold more cells than untreated biofilms, but no growth-enhancement occurred in planktonic cultures. As determined by flow cytometry, IL-beta bound to 63.1% of biofilm cells, but only 11.2% of planktonic cells. Our results provide evidence of a differential response of biofilm and planktonic bacteria to chemical mediators, and suggest that biofilm bacteria may evade host defenses by growing more rapidly in response to the inflammatory mediators released by activated host defense cells.