Barmer, Feb. 24 -- Scientists at Indian Institute of Technology Jodhpur have discovered that a naturally occurring human protein can prevent the formation of dangerous bacterial biofilms, offering a promising new strategy to tackle chronic and hard-to-treat infections. The breakthrough study, published in the prestigious international journal Proceedings of the National Academy of Sciences (PNAS), reveals that the human immune protein beta-2-microglobulin (B2M) can stop bacteria from building biofilms-protective structures that make infections extremely resistant to antibiotics. Biofilms are communities of bacteria that attach to surfaces such as medical implants, catheters, chronic wounds, and tissues. Once formed, these biofilms act as a shield, making bacteria up to 1,000 times more resistant to antibiotics and immune defences. They are a major cause of persistent infections and a key driver of antimicrobial resistance worldwide. The IIT Jodhpur research team found that B2M works in a unique way. Instead of killing bacteria, it blocks the assembly of curli, a structural protein essential for biofilm formation in Escherichia coli. By preventing this early step, the biofilm fails to develop, leaving bacteria more vulnerable and reducing the risk of resistance. Dr. Neha Jain, associate professor, department of bioscience and bioengineering, IIT Jodhpur, and lead author of the study, said, "Biofilms are one of the biggest challenges in treating chronic infections because they protect bacteria from antibiotics and the immune system. Our study shows that beta-2-microglobulin, a naturally occurring human protein, can prevent biofilm formation by selectively blocking curli assembly. Instead of killing bacteria, it weakens their protective structure, reducing the risk of antibiotic resistance and opening new possibilities for future therapies." "By targeting the protective structure of bacteria rather than killing them, we open the door to safer and more sustainable treatment strategies for chronic infections," she said....