Pseudomonas aeruginosa and Mycobacterium abscessus are opportunistic pathogens that cause severe infections in hospitals, and their co-infections are increasingly reported. The interspecies interactions between these two bacterial species and their potential impacts on infections are largely unexplored. In this study, we first demonstrated that P. aeruginosa inhibits the growth of M. abscessus by iron chelating via pqs quorum sensing. Next, through proteomic analysis, we discovered that the PQS molecule significantly changed a large amount of protein expression in M. abscessus, including proteins involved in the type VII secretion system and iron homeostasis. Furthermore, we revealed that PQS significantly enhanced the production of bacterial membrane vesicles (MVs) by M. abscessus. Our study suggests that the P. aeruginosa PQS can serve as an interspecies signaling molecule to communicate with Mycobacterium and affect their physiology and virulence.

The association of gut microbiota with lymph node tuberculosis (LNTB) remains unexplored. This study employed metagenomic sequencing and plasma metabolomics analyses to investigate the role of gut microbiota in LNTB patients. Significant alterations in gut microbial diversity were observed in LNTB patients, characterized by a notable reduction in bacterial taxa involved in short-chain fatty acid (SCFA) synthesis, including Ruminococcus, Faecalibacterium, Roseburia, and Blautia, compared to healthy individuals. KEGG pathway analysis further revealed that gut dysbiosis could negatively impact SCFA biosynthesis and metabolism. Plasma metabolomics demonstrated disruptions in metabolites associated with SCFA synthesis and inflammation pathways in the LNTB group. Integrated analysis indicated significant correlations between specific gut microbiota (Blautia, Butyricicoccus, Coprococcus, Ruminococcus, Bacteroides, Clostridium) and plasma metabolites, including α-benzylbutyric acid, acetic acid, and succinic acid. Our findings demonstrate that gut microbiota dysbiosis and related metabolic dysfunction significantly reduce SCFA production in LNTB patients, potentially identifying novel therapeutic targets for LNTB management.