Inflammasome-mediated glucose limitation induces antibiotic tolerance in Staphylococcus aureus

Interactions with the host immune system alters S. aureus response to therapeutic antibiotics. We find that S. aureus α-toxin, a pore-forming toxin, interacts with macrophages to alter the microenvironment of the pathogen and influence its susceptibility to antibiotics. α-toxin-mediated activation of the NLRP3 inflammasome induces antibiotic tolerance through increased glycolysis in the host cells, resulting in glucose limitation and ATP depletion in S. aureus. Additionally, inhibition of NLRP3 activation improves antibiotic efficacy in vitro and in vivo. Our findings identify interactions between S. aureus and the host that result in metabolic crosstalk that can determine the outcome of antimicrobial therapy. This data contains GraphPad Prism files containing data from the main and supplemental figures of J.E.Beam. et al., 2023.

与宿主免疫系统的相互作用改变了金黄色葡萄球菌对治疗性抗生素的响应。研究发现，金黄色葡萄球菌α毒素，一种形成孔的毒素，与巨噬细胞相互作用，改变病原体的微环境并影响其对抗生素的敏感性。α毒素介导的NLRP3炎症小体的激活通过增加宿主细胞的糖酵解，导致葡萄糖限制和金黄色葡萄球菌中ATP耗竭，从而诱导抗生素耐受。此外，抑制NLRP3激活在体外和体内提高了抗生素的疗效。我们的发现揭示了金黄色葡萄球菌与宿主之间的相互作用，这种相互作用导致代谢性串扰，可能决定抗菌治疗的结果。该数据集包含GraphPad Prism文件，其中包含J.E.Beam等，2023年的主要和补充图中的数据。