Scientists give new ideas to fight drug-resistant bacteria

: Johns Hopkins University
U.S. scientists now have a better understanding of the biological mechanisms of staphylococcus infections and how mice mobilize their immune systems to fight them. The researchers report the findings in the May 14 issue of the Proceedings of the National Academy of Sciences.
usually causes skin infections, but can also spread throughout the body, leading to invasive infections such as sepsis and the possibility of death.
these Staphylococcus arata bacteria are becoming more resistant to a variety of different antibiotics, making them particularly difficult to treat. In healthy people, the body's natural immune defenses can usually keep bacterial infections in the skin and can be treated effectively with appropriate antibiotics. However, patients with low immune function are often less resistant to bacteria, which makes the latter more invasive and leads to life-threatening infections.
"Although the human immune response against Staphylococcus aelobacter infection is still elusive, as a starting point, we have determined in mice that protective immunity against Staphylococcus ale is driven by specific immune cells called gamma T cells, which move from the lymph nodes to the infected skin at the time of infection, triggering a protective host response. Lloyd S. Miller, associate professor of dermatology at Johns Hopkins University School of Medicine, said.
Miller points out that Staphylococcus ale and other multidring-resistant bacteria are becoming a bigger problem because most antibiotics are no longer resistant to these infections and few new antibiotics have been developed. For Staphylococcus acuity, there are only two or three oral antibiotics left to treat such infections.
Miller and his team are working to understand the specifics of the mouse immune system's fight against Staphylococcus acolytic to study ways to detect the body's immune system, thereby developing alternative immunotherapy that can be used in conjunction with antibiotic treatments, or eliminating the need for antibiotics entirely.
previous study, researchers found that a "cytokine" protein called IL-17 is critical to opening up the host's defense against staphylococcus infections. Until now, however, they didn't know which cells, specifically which type of T cells produced the protein. In addition, there are two types of IL-17, il-17A and IL-17F, but researchers do not know whether one or both are needed to initiate a host response against Staphylococcus acolytic.
, they worked with colleagues at the National Institutes of Health who changed the genetic structure of mice to emit different colors of light depending on the type of IL-17 they made. They then injected Staphylococcus acuity bacteria into the mice's skin and found that the infected skin gave off green and red light. They concluded that both types of IL-17 are involved in the immune response to bacteria.
"We're pretty sure IL-17 is made of T cells, but we don't know if it's T cells that are usually in the skin or T cells that migrate from the lymph nodes to the infected site." Miller said. The researchers wanted to know what would happen if they stopped T cells from leaving the lymph nodes and treated them with FTY720 (Fingomod) in the same luminescent mice. FTY720 is a drug commonly used to treat multiple sclerosis that minimizes inflammatory response by preventing T-cells from moving from the lymph nodes.
researchers did not see the glow after applying FTY720 to mice infected with Staphylococcus aegypti, meaning that the IL-17 seen on the skin at the site of Staphylococcus aegypti infection was made only by T cells migrating from the lymph nodes.
before and after staphylococcus ail in mice, the researchers extracted cells from the site of the infection and from the lymph nodes. Depending on the type of protein found on the surface of each cell, they marked the cells with different colors. The researchers found that in mice that were not infected with Staphylococcus acuity, the number of gamma T cells increased dramatically after the infection of Staphylococcus alip in mice.
then they began to study exactly which cells were increasing. The researchers, in collaboration with colleagues at the University of California, Davis, identified the genetic sequence of all T-cell receptors in the lymph nodes before and after staphylococcus austratic infection in mice. They found that only one type of gamma-T-cell clone amplified the specific T-cell subject.
m not sure if there are exactly the same cell types in the human body, we believe we can find something similar, which means we are on the right track to develop a new T-cell therapy against Staphylococcus aureus," Miller said. "The next step involves examining T-cell reactions in the body to determine if there is a similar mechanism. (Source: China Science Journal Zhao Xixi)
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