Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland.
Appl Environ Microbiol. 2022 Mar 8;88(5):e0237021. doi: 10.1128/aem.02370-21. Epub 2022 Jan 5.
species are facultative intracellular pathogens that cause a life-threatening pneumonia termed Legionnaires' disease. Legionella pneumophila employs the Lqs-LvbR ( quorum sensing- virulence and biofilm regulator) network to regulate virulence and motility, but its role for growth in media is ill-defined. Here, we report that compared to the L. pneumophila reference strain JR32, a Δ mutant showed a reduced lag phase at 30°C and reached a higher cell density at 45°C, while the Δ, Δ, and Δ mutants showed a longer lag phase and reached a lower cell density. A Δ mutant resumed growth like the parental strain at 30°C but exhibited a substantially reduced cell density at 45°C. Thus, LvbR is an important cell density regulator at elevated temperatures. Environmental and clinical L. pneumophila strains grew in -(2-acetamido)-2-aminoethanesulfonic acid (ACES)-buffered yeast extract (AYE) medium after distinct lag phases with similar rates at 30°C, reached different cell densities at the optimal growth temperature of 40°C, and no longer grew at 50°C. Legionella longbeachae reached a rather low cell density at 40°C and did not grow at and beyond 45°C. Genes encoding components of the Lqs-LvbR network were present in the genomes of the environmental and clinical L. pneumophila isolates, and upon growth at 30°C or 45°C, the P, P, P, and P promoters from strain JR32 were expressed in these strains with distinct patterns. Taken together, our results indicate that the Lqs-LvbR network governs the temperature-dependent growth onset and cell density of the L. pneumophila reference strain JR32 and possibly also of environmental and clinical L. pneumophila isolates. Environmental bacteria of the genus are the causative agents of the severe pneumonia Legionnaires' disease, the incidence of which is on the rise worldwide. Legionella pneumophila and Legionella longbeachae are the clinically most relevant species. The opportunistic pathogens are inhaled through contaminated aerosols and replicate in human lung macrophages with a mechanism similar to that in their natural hosts, free-living amoebae. Given their prevalence in natural and technical water systems, an efficient control of spp. by physical, chemical, or biological means will reduce the incidence of Legionnaires' disease. Here, we show that the quorum sensing (Lqs) system and the pleiotropic transcription factor LvbR govern the temperature-dependent growth onset and cell density of bacterial cultures. Hence, the growth of L. pneumophila in water systems is determined not only by the temperature and nutrient availability but also by quorum sensing, i.e., density- and signaling molecule-dependent gene regulation.
种是兼性细胞内病原体，可引起危及生命的肺炎，称为军团病。铜绿假单胞菌利用 Lqs-LvbR（群体感应-毒力和生物膜调节剂）网络来调节毒力和运动性，但它在培养基中生长的作用尚未明确。在这里，我们报告与铜绿假单胞菌参考株 JR32 相比，Δ突变体在 30°C 时表现出较短的延迟期，在 45°C 时达到更高的细胞密度，而 Δ、Δ和 Δ突变体则表现出较长的延迟期，达到较低的细胞密度。Δ突变体在 30°C 下像亲本菌株一样恢复生长，但在 45°C 下细胞密度显著降低。因此，LvbR 是高温下重要的细胞密度调节剂。环境和临床分离株的铜绿假单胞菌在 -（2-乙酰氨基）-2-氨基乙磺酸（ACES）缓冲的酵母提取物（AYE）培养基中生长，在 30°C 时有明显的延迟期，以相似的速率生长，在最佳生长温度 40°C 时达到不同的细胞密度，在 50°C 时不再生长。嗜肺军团菌在 40°C 时达到相当低的细胞密度，在 45°C 及以上时不再生长。环境和临床分离株的铜绿假单胞菌基因组中存在编码 Lqs-LvbR 网络组件的基因，并且在 30°C 或 45°C 生长时，JR32 株的 P、P、P 和 P 启动子以不同的模式在这些菌株中表达。综上所述，我们的结果表明，Lqs-LvbR 网络控制了铜绿假单胞菌参考株 JR32 和可能的环境和临床分离株的温度依赖性生长起始和细胞密度。 属的环境细菌是严重肺炎军团病的病原体，其发病率在全球范围内呈上升趋势。铜绿假单胞菌和嗜肺军团菌是临床上最相关的物种。这些机会性病原体通过受污染的气溶胶吸入，并通过与它们在自由生活的变形虫中的天然宿主相似的机制在人类肺巨噬细胞中复制。鉴于它们在自然和技术水系统中的普遍性，通过物理、化学或生物手段有效控制 spp. 将降低军团病的发病率。在这里，我们表明，群体感应（Lqs）系统和多效转录因子 LvbR 控制细菌培养物的温度依赖性生长起始和细胞密度。因此，L. pneumophila 在水系统中的生长不仅取决于温度和营养可用性，还取决于群体感应，即密度和信号分子依赖性基因调控。
