Department of Biology, Indiana University-Purdue University Indianapolis, Indianapolis, USA.
J Bacteriol. 2022 Jan 18;204(1):e0039821. doi: 10.1128/JB.00398-21. Epub 2021 Oct 11.
Stenotrophomonas maltophilia has recently arisen as a prominent nosocomial pathogen because of its high antimicrobial resistance and ability to cause chronic respiratory infections. Often the infections are worsened by biofilm formation which enhances antibiotic tolerance. We have previously found that mutation of the gene, encoding the glycolytic enzyme phosphoglycerate mutase, impacts the formation of this biofilm on biotic and abiotic surfaces at early time points. This finding, indicating an association between carbon source and biofilm formation, led us to hypothesize that metabolism would influence S. maltophilia biofilm formation and planktonic growth. In the present study, we tested the impact of various growth substrates on biofilm levels and growth kinetics to determine metabolic requirements for these processes. We found that S. maltophilia wild type preferred amino acids versus glucose for planktonic and biofilm growth and that deletion inhibited growth in amino acids. Furthermore, supplementation of the Δ strain by glucose or ribose phenotypically complemented growth defects. These results suggest that S. maltophilia shuttles amino acid carbon through gluconeogenesis to an undefined metabolic pathway supporting planktonic and biofilm growth. Further evaluation of these metabolic pathways might reveal novel metabolic activities of this pathogen. Stenotrophomonas maltophilia is a prominent opportunistic pathogen that often forms biofilms during infection. However, the molecular mechanisms of virulence and biofilm formation are poorly understood. The glycolytic enzyme phosphoglycerate mutase appears to play a role in biofilm formation, and we used a mutant in its gene () to probe the metabolic circuitry potentially involved in biofilm development. The results of our study indicate that S. maltophilia displays unique metabolic activities, which could be exploited for inhibiting growth and biofilm formation of this pathogen.
嗜麦芽寡养单胞菌最近作为一种重要的医院获得性病原体出现，因为它具有高度的抗药性和引起慢性呼吸道感染的能力。生物膜的形成往往会使感染恶化，从而增强抗生素的耐受性。我们之前发现，编码糖酵解酶磷酸甘油酸变位酶的基因的突变，会影响生物和非生物表面上的生物膜在早期的形成。这一发现表明碳源与生物膜形成之间存在关联，这使我们假设代谢会影响嗜麦芽寡养单胞菌生物膜的形成和浮游生物的生长。在本研究中，我们测试了各种生长底物对生物膜水平和生长动力学的影响，以确定这些过程的代谢需求。我们发现，嗜麦芽寡养单胞菌野生型更喜欢氨基酸而不是葡萄糖用于浮游生物和生物膜的生长，并且缺失抑制了氨基酸的生长。此外，葡萄糖或核糖对Δ 菌株的补充表型上补充了生长缺陷。这些结果表明，嗜麦芽寡养单胞菌通过糖异生将氨基酸的碳穿梭到支持浮游生物和生物膜生长的未定义代谢途径中。对这些代谢途径的进一步评估可能会揭示该病原体的新的代谢活性。
