Antibiotics are a wonder of medicine, but many microorganisms have acquired the ability to resist and tolerate these treatments. Scientists at St. Jude Children’s Research Hospital have revealed how it works. pneumococcus Adapts to antibiotic exposure and immune pressure. Their findings revealed that changes in RNA regulation allow bacteria to enter a state of antibiotic resistance. The results provide a deeper understanding of how pathogens tolerate treatment and may inform strategies to improve the effectiveness of existing antibiotics. The survey results are announced today. Cell hosts and microorganisms.
Bacterial infections remain a significant clinical challenge for children with cancer and other immunocompromised diseases, as immunosuppression can make infections more difficult to control and increase the risk of serious complications. pneumococcusis a leading cause of serious bacterial infections worldwide and is especially dangerous for these patients, who can cause serious illnesses such as pneumonia, bloodstream infections, and meningitis. Antibiotics are essential for the prevention and treatment of these infections, but some bacteria can survive exposure to antibiotics through mechanisms such as antibiotic resistance and resistance.
The ability to target bacterial populations that are resistant to antibiotic treatment is extremely important. We discovered new strategies for how bacteria respond to antibiotics and provided new insights into how persistent infections develop. These insights may guide strategies to improve antibiotic efficacy. ”
Dr. Jason Roche, Corresponding Author, St. Jude Host-Microbe Interactions Division
Host pressure overcomes resistance and drives bacterial survival strategies
How to use infection models to track pneumococcus Although they evolved within the host, researchers found that they are formed by pressure from the host environment and immune system. pneumococcus evolution. This evolution has promoted adaptations that allow bacteria to withstand antibiotic exposure while maintaining viability, rather than acquiring resistance mutations that can compromise fitness during infection.
Single-cell analysis revealed that this resistance strategy involves a bet-hedging response in which bacterial populations adopt different survival states in response to antibiotic stress. While many bacterial cells undergo cell death after antibiotic exposure, some bacterial cells temporarily enter a state of antibiotic resistance, slowing normal cellular activity and reducing the damage caused by treatment.
The researchers found that this response is driven by changes in RNA regulation, including mutations in RNA. thatgenes involved in RNA degradation. The resistant cells avoided the cell damage normally caused by antibiotics and entered a protective hypoactive state, allowing them to withstand treatment and resume proliferation as soon as the antibiotic was removed.
“This is essentially a population-based survival strategy,” Roche says. “If all cells responded to antibiotics in the same way, the population would be less likely to survive. Instead, we found that while most cells died, a small number of cells temporarily tolerated antibiotic exposure and promoted repopulation after treatment ended.”
These findings highlight the importance of understanding how bacteria survive exposure to antibiotics. This knowledge is important for designing novel antibiotics and improving their performance.
“I think this really opens our eyes to the fact that bacteria have many more strategies for evading antibiotics than we currently realize,” Roche said. “Antibiotic treatments can fail even in the absence of traditional resistance. This reveals the importance of resistance mechanisms in allowing bacteria to survive, and this will guide new strategies to improve antibiotic effectiveness.”
sauce:
St. Jude Children’s Research Hospital
Reference magazines:
Nishimoto, AT, others. (2026). RNA quality control enables antibiotic resistance. Cell hosts and microorganisms. DOI: 10.1016/j.chom.2026.06.019. https://www.cell.com/cell-host-microbe/fulltext/S1931-3128(26)00279-9
