Few would call 2020 their favorite year. Both politically and in public health, it has been a stressful time in the U.S. and globally. Researchers are now concerned the massive changes in behavior and fighting of pathogens on a global scale might lead to another surprise—superbugs.

Antibiotics are an important kind of drug in society. They help save countless lives and treat a wide variety of infections, from mild urinary tract infections to life threatening sepsis. Antibiotic resistance is a different kind of concern with no way to stop it completely. In the U.S., more people will die from infectious diseases because of antibiotic resistance than from cancer.

COVID-19 situation is undoubtedly putting the public at risk for increasing resistance to antibiotics. It's more important now than ever for science to develop alternative treatments. Today, Scientists around the globe are fighting a deadly plague. One laboratory at the University of Colorado at Boulder is working to develop novel weapons to fight another plague with similar sinister tendency.

The launch of one of their new discoveries was published in an article on Friday in PLOS Pathogens. The article describes a chemical compound that functions with the host's innate immune response to push past cellular barriers which enable bacteria to withstand antibiotics. The authors suggest that, like their other recent results, the findings may lead to a new arsenal to tackle the next great public health threat.

"Salmonella Bacteria"by NIAID is licensed under CC BY 2.0

"If we don't solve the problem of finding new antibiotics or somehow making old antibiotics work again, we are going to see sharply increasing deaths from bacterial infections we thought we had beaten decades ago," said study co-author Corrella S. Detweiler. "This study offers a totally new approach and could point the way toward new drugs that work better and have fewer side effects."

The team identified a small molecule, JD1, that kills Salmonella enterica serovar Typhimurium in macrophages. JD1 doesn't kill bacteria in standard culture media. It only inhibits their growth. Using cellular indicators and super resolution microscopy, we found that JD1 damages bacterial membranes by increasing fluidity, disrupting barrier function, and causing membrane distortions.

According to laboratory and rodent experiments, JD1 reduces survival and extent of excretion of Gram-negative bacteria called Salmonella enterica by 95%.

The research underpins a promise for "small molecule antibiotics" to access the bacterial cell wall. Research suggests that this new molecule will be able to block resistance to existing antibiotics.

Cover Photo: "Mycobacterium tuberculosis Bacteria, the Cause of TB"by NIAID is licensed under CC BY 2.0