Ramirez Violette I, Wray Robin, Blount Paul, King Maria D
Department of Biological and Agricultural Engineering, Texas A&M University, College Station, TX 77845, USA.
Department of Physiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Microorganisms. 2023 Sep 5;11(9):2236. doi: 10.3390/microorganisms11092236.
Understanding how bacteria respond to ventilated environments is a crucial concept, especially when considering accurate airflow modeling and detection limits. To properly design facilities for aseptic conditions, we must minimize the parameters for pathogenic bacteria to thrive. Identifying how pathogenic bacteria continue to survive, particularly due to their multi-drug resistance characteristics, is necessary for designing sterile environments and minimizing pathogen exposure. A conserved characteristic among bacterial organisms is their ability to maintain intracellular homeostasis for survival and growth in hostile environments. Mechanosensitive (MS) channels are one of the characteristics that guide this phenomenon. Interestingly, during extreme stress, bacteria will forgo favorable homeostasis to execute fast-acting survival strategies. Physiological sensors, such as MS channels, that trigger this survival mechanism are not clearly understood, leaving a gap in how bacteria translate physical stress to an intracellular response. In this paper, we study the role of mechanosensitive ion channels that are potentially triggered by aerosolization. We hypothesize that change in antimicrobial uptake is affected by aerosolization stress. Bacteria regulate their defense mechanisms against antimicrobials, which leads to varying susceptibility. Based on this information we hypothesize that aerosolization stress affects the antimicrobial resistance defense mechanisms of (). We analyzed the culturability of knockout strains with different numbers of mechanosensitive channels and compared antibiotic susceptibility under stressed and unstressed airflow conditions. As a result of this study, we can identify how the defensive mechanisms of resistant bacteria are triggered for their survival in built environments. By changing ventilation airflow velocity and observing the change in antibiotic responses, we show how pathogenic bacteria respond to ventilated environments via mechanosensitive ion channels.
了解细菌如何对通风环境做出反应是一个至关重要的概念，尤其是在考虑精确的气流建模和检测限的时候。为了正确设计无菌条件下的设施，我们必须尽量减少致病细菌得以繁殖的参数。确定致病细菌如何持续存活，特别是由于它们的多重耐药特性，对于设计无菌环境和尽量减少病原体暴露是必要的。细菌生物体的一个保守特征是它们在恶劣环境中维持细胞内稳态以实现生存和生长的能力。机械敏感（MS）通道是引导这一现象的特征之一。有趣的是，在极端压力下，细菌会放弃有利的稳态以执行快速起效的生存策略。触发这种生存机制的生理传感器，如MS通道，目前还没有被清楚地理解，这在细菌如何将物理压力转化为细胞内反应方面留下了空白。在本文中，我们研究了可能由雾化触发的机械敏感离子通道的作用。我们假设抗菌药物摄取的变化受雾化压力影响。细菌调节它们对抗菌药物的防御机制，这导致了不同的敏感性。基于这些信息，我们假设雾化压力会影响（）的抗耐药性防御机制。我们分析了具有不同数量机械敏感通道的基因敲除菌株的可培养性，并比较了在有压力和无压力气流条件下的抗生素敏感性。作为这项研究的结果，我们可以确定耐药细菌的防御机制是如何在建筑环境中被触发以实现其生存的。通过改变通风气流速度并观察抗生素反应的变化，我们展示了致病细菌如何通过机械敏感离子通道对通风环境做出反应。
