Staphylococcus aureus is the main cause of skin infections and one of the main causes of nosocomial infections. Approximately 20% of the population is chronically infected with S. aureus, including antibiotic-resistant MRSA (methicillin-resistant S. aureus). Scientists at the University of Chicago recently discovered a key point for the great success of Staphylococcus aureus-the ability to hijack the primary immune defense mechanism of humans and use it to destroy white blood cells. The research was published in the journal Science on November 15. "These bacteria not only use their own weapons to predict each immune defense, but also turn these immune defenses against the host," said Dr. Olaf Schneewind, senior author of the paper, director of the Department of Microbiology at the University of Chicago, and professor of detection ELISA kits. Neutrophils are the first line of defense for human immune response. These white blood cells can trap invaders in neutrophil extracellular traps (NETs), a network of DNA and protein structures. The captured bacteria are subsequently destroyed by macrophages. However, the site of S. aureus infection is often not marked by macrophages, suggesting that this bacterium protects itself against the immune system in some way. To reveal how these bacteria evade the human immune response, Schneewind and his research team screened a series of Staphylococcus aureus. These bacteria have some mutations that shut down some that people think play a role in infection gene. They observed the behavior of these mutant bacteria in living tissue and identified two strains that could not escape the attack of macrophages. When the staphylococcal nuclease (nuc) and adenosine synthase A (adsA) gene mutations in the strain were reversed, the infected site was once again protected from macrophage attack. To find out the mechanism of action, the researchers co-cultured Staphylococcus aureus with neutrophils and macrophages in a laboratory petri dish. In this environment, white blood cells are healthy and able to remove bacteria. But when the researchers added a chemical to stimulate the formation of NET, it triggered the death of macrophages. Recognizing that Staphylococcus aureus produced a toxic product in response to NETs, ​​the study detection ELISA kit team used high-performance liquid chromatography and mass spectrometry to isolate the molecule. They found that Staphylococcus aureus is converting NETs to 2-deoxyadenosine (dAdo), a molecule that is toxic to macrophages. This effectively turns NETs into weapons against the immune system. Schneewind said: “Almost everyone will be infected with some form of Staphylococcus aureus sooner or later. Our research describes for the first time that these bacteria use this mechanism to exclude macrophages from the site of infection. The previously known adaptive immune response suppression mechanism almost guarantees that these organisms can be successfully infected. " Staphylococcus aureus is present on human skin or in the respiratory tract and often causes skin infections in the form of abscesses or boils. These bacteria are usually not very dangerous, and when they enter the bloodstream, they can cause serious problems, leading to diseases such as sepsis and meningitis. Antibiotic-resistant strains, such as methicillin-resistant Staphylococcus aureus (MRSA), are extremely difficult to treat, and have become a problem for the global healthcare system. Schneewind and his research team hope to use their research findings to develop treatments against S. aureus infections. But because both genes and dAdo molecules are closely related to important human physiological mechanisms, Schneewind believes that targeting them in bacteria without compromising human function may be very difficult.
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