Lohia Gaurav Kumar, Riquelme Sebastián A
Department of Pediatrics, Columbia University, New York, NY 10032, USA.
Department of Pediatrics, Columbia University, New York, NY 10032, USA.
Curr Opin Microbiol. 2025 Jun;85:102608. doi: 10.1016/j.mib.2025.102608. Epub 2025 Apr 2.
Opportunistic pathogens like Pseudomonas aeruginosa and Staphylococcus aureus rapidly adapt to the dynamic metabolic landscape of the respiratory mucosa during infection. Host phagocytes recognize these pathogens and trigger metabolic reprogramming, releasing immunometabolites such as succinate and itaconate. P. aeruginosa preferentially consumes succinate as a carbon source to enhance planktonic growth. In response to itaconate-induced membrane stress, it forms protective biofilms, allowing bacterial survival despite host defenses. Additionally, host ketone bodies support microbial communities that are less immunostimulatory and better tolerated by the lung. Similarly, S. aureus responds to itaconate by forming biofilms, aiding colonization in glucose-limited airways. In this milieu, S. aureus consumes proline, linking its survival with the metabolic activity of proline-producing fibroblasts. Here, we will review the competence of both P. aeruginosa and S. aureus to hijack host metabolic pathways, underscoring pathogen metabolic plasticity as an essential strategy to thrive in the human lung.
像铜绿假单胞菌和金黄色葡萄球菌这样的机会性病原体在感染期间会迅速适应呼吸道黏膜动态的代谢环境。宿主吞噬细胞识别这些病原体并触发代谢重编程，释放出琥珀酸和衣康酸等免疫代谢物。铜绿假单胞菌优先消耗琥珀酸作为碳源以增强浮游生长。为应对衣康酸诱导的膜应激，它会形成保护性生物膜，使细菌在宿主防御的情况下仍能存活。此外，宿主酮体支持免疫刺激较弱且肺部耐受性较好的微生物群落。同样，金黄色葡萄球菌通过形成生物膜对衣康酸作出反应，有助于在葡萄糖受限的气道中定殖。在这种环境中，金黄色葡萄球菌消耗脯氨酸，将其存活与产生脯氨酸的成纤维细胞的代谢活动联系起来。在此，我们将综述铜绿假单胞菌和金黄色葡萄球菌劫持宿主代谢途径的能力，强调病原体代谢可塑性是在人类肺部生存的关键策略。
