The second messenger c-di-AMP is essential for aerobic growth in Staphylococcus aureus; however, many aspects of the c-di-AMP signaling network in S. aureus remain to be elucidated. Josh’s research focuses on uncovering the regulatory role of c-di-AMP in glutamine metabolism, a process crucial for bacterial growth. He has identified a novel regulator, PstA, a PII family protein that modulates the transcription of glutamine synthesis genes. These findings reveal a previously unknown aspect of the nitrogen regulatory circuitry in S. aureus.

Macrophages act as the gatekeepers to detect and resolve bacterial infections. Bacteria phagocytosis by macrophages may lead to intracellular killing, destroying the bacteria by producing antimicrobials including reactive oxygen species (ROS) and nitrogen species (RNS) in the phagosomes. However, S. aureus is resistant to the antimicrobial environment of phagosomes, using these compartments to hide from immune cells and antibiotics. Ultimately, S. aureus will proliferate in the cytoplasm, and cause macrophage death, eventually enabling further bacterial dissemination. The interactions between macrophages and S. aureus directly impact the outcome of the infection. In depth understanding of these host-pathogen interactions could provide insights for future therapeutic developments for MRSA. Omar works on the identification of S. aureus genes that are essential for intracellular growth in macrophages. He has found that the potential cell division protein GpsB is not required for growth in rich medium but is necessary for intracellular growth of S. aureus in macrophages. He later found that GpsB knockout mutant is more susceptible to the ROS produced by macrophages. Omar is currently characterizing the mechanism of GpsB in pathogenesis.

Minh is an undergraduate LSAMP scholar in 2024 who spent the summer working with the Tang Lab. During her time with us, she focused on identifying Staphylococcus aureus genes essential for systemic infection in mice and made remarkable progress in just two months. Minh, you will be greatly missed by all of us.

Qing Tang officially joined Department of Biology at the University of Texas at Arlington as an assitant professor starting in January 2024!

Qing Tang’s publication, titled “Thymidine starvation promotes c-di-AMP-dependent inflammation during pathogenic bacterial infection,” has been selected as a Highlighted Article by Science Signaling.

Abstract: Bacterial stress caused by antibiotics increases a second messenger that directly stimulates host inflammation.

Cell Host & Microbe published a comment article written by Iván C. Acosta and Francis Alonzo III titled “Antibiotic treatment ignites a fire that lasts” and highlighted Qing Tang’s recent research.

Abstract: Tissue damage and persistent inflammation are distinctive features of antibiotic-resistant chronic infections. In this issue of Cell Host & Microbe, Tang et al. demonstrate that anti-folate antibiotics trigger the synthesis of a bacterial second messenger, which induces an exuberant immune response and establishes a paradigm for chronic infection.