UNIVERSITY PARK, Pa. — Increased antibiotic use could lead to antibiotics to more problematic infections as bacteria evolve and resist treatment. Answer to this antibiotic resistance Centers for Disease Control and Prevention According to a team led by researchers in Pennsylvania, what is called “one of the world's most urgent public health issues,” could be a drug used for kidney disease.
Antibiotics kill or stop bacteria's growth, but the more they are used, the better bacteria will resist them. The team discovered that the U.S. Food and Drug Administration (FDA)-approved drug Sevelamer, which is prescribed to be prescribed to bind excess phosphorus in the blood of people with chronic kidney disease who are undergoing dialysis, could also bind off-target antibiotics in mice. Antibiotics are labeled “off-target” when they appear in the body away from the site of infection. In this case, the small part is escaped from the bloodstream and excreted into the intestines.
The researchers have published their findings. small. The idea is that Sevelamers can find and bind off-target antibiotics, preventing them from interacting with intestinal bacteria.
“We found that Sevelamer can act as an “anti-antibiotic” by capturing off-target vancomycin and daptomycin (two commonly prescribed antibiotics) in the intestine. Amir SheikiDorothy Foehr Huck and J. Lloyd Huck Early Career Chair in Biomaterials and Regenerative Engineering and Associate Professor of Chemical Engineering.
Vancomycin is often prescribed to treat infections caused by enterococcus present in the intestine, but is present in the intestine, but increases in numbers and spreads to other areas of the body, leading to urinary tract infections, heart infections, cellulitis, and more. However, as bacteria can evolve to resist vancomycin, clinicians will turn to daptomycin as their final treatment to combat infection. According to Sheikhi, these types of infections are particularly common in health care settings where patients have already been undergoing long antibiotic treatment for a primary infection or develop primary infection after medical procedures.
The problem is that bacteria can also evolve and resist daptomycin. He said resistance was born as 5% to 10% of the antibiotics were administered intravenously and reached the gastrointestinal tract. There, non-target antibiotics do not match the number of bacteria that evolve to survive and not be affected by drugs intended to kill them. To address this, researchers are developing ways to capture targeted antibiotics and prevent bacteria from evolving by effectively terminating the drug.
“In place of new antibiotics, the development of antibiotics may potentially protect the efficacy of current antibiotics,” said Sheiki, who is in the Pennsylvania division of biomedical engineering, chemistry and neurosurgery and leads the Institute of Biosoft Materials. b-smalat university.
He explained that as bacteria continue to develop resistance to antibiotics, researchers are turning to researching alternative therapies that go beyond producing stronger antibiotics. One such advancement is the ability to administer drugs that can capture off-target antibiotics in parallel with antibiotics.
The work is constructed in a 2020 Research – Leading Andrew readSenior Vice President of Research, Professor Evan Pugh of Biology and Entomology, and former professor of biotechnology at Everly, and co-author of the current study.
“Antibiotics promote antibiotic resistance,” Reed said. “If antibiotics can be inactivated when they are not needed, antibiotic-resistant drivers can be eliminated. Antibiotics, as a rule, can prevent the intestinal resistance to antibiotics.”
2022, Sheikhi, Read and other collaborators The mechanism was explained Although cholestyramine was used to bind daptomycin, we also found that it was unable to remove vancomycin. So the team turned to another promising candidate, Sevelamer.
In this study, researchers administered vancomycin or saline solution via injection into mice with enterococcal feces, an enterobacterial known to rapidly evolve antibiotic resistance. At the same time, they gave the mice an oral suspension of sevelamer. The researchers then analyzed the genetic content of fecal feces from mice.
“Our findings show that Sevelamer captures low concentrations of daptomycin within minutes and vancomycin within hours,” says Sheiki, who removes both antibiotics, blocks the antibiotic activity of daptomycin in vitro, meaning cellular experiments, and vancomycin in vitro, in vivo, and animal models. “This has put Sevelamer as a more versatile and effective adjunctive therapy to reduce resistance to infections derived from the healthcare environment.”
The findings were conducted in mice, but the researchers said there is direct significance in human medicine.
“To our knowledge, this first demonstrates that FDA-approved drugs can effectively block the emergence of vancomycin-driven resistance in living organisms, and presents a novel and scalable strategy to combat antibiotic resistance in healthcare settings,” Sheeki said. “Sevelamer is already FDA approved, and has an established safety profile and is a strong candidate for clinical applications.”
Sheikhi then said the team plans to conduct clinical trials to assess the efficacy of Sevelamer in human patients receiving vancomycin or daptomycin. They also plan to investigate whether sevelamers may prevent the evolution of resistance to other types of antibiotics excreted in the gastrointestinal tract. The research team invites collaborators with experience in clinical trials to assess antibiotic resistance Please contact them.
Another author of the paper in Pennsylvania is chemical engineering postdoctoral scholar Roya Koshani. Shan Lin Ye received his PhD in Chemical Engineering from Pennsylvania and currently works in industry. Zemin earned a bachelor's degree in chemical engineering from Pennsylvania and currently holds a graduate degree from the University of Pennsylvania. Naveen Narasimhalu also received a bachelor's degree in chemical engineering from Pennsylvania and currently worked for 3M. Landon G. Vom Steeg, postdoctoral scholar in biology and entomology. and Derek G. SimAssociate Professor of Biology and Entomology. Robert J. WoodsAssociate Professor of Internal Medicine – University of Michigan Infectious Diseases, also co-authored this paper. Sheikhi, Sim and Read are also affiliated with the Huck Institutes of the Life Sciences in Pennsylvania, and Vom Steeg is also affiliated with the Geisel School of Medicine at Dartmouth.
Hack Life Science Institute, Pennsylvania through the Patricia and Stephen Benkovic Research Initiative. Early career chairs from Dorothy Fore Huck and J. Lloyd Huck. Agricultural University's Applied Evolution Seed Grant Program. And Biotechnology Chairman Everly supported the study.
