Scientists find new way to fight harmful bacteria

Representational image

New Delhi: Researchers have cracked the mystery of how our body quickly prevents an infection from spreading uncontrollably during wound healing, an advance that may lead to new ways to counteract harmful bacteria.

A new study found that fragments of thrombin - a common blood protein found in wounds - can aggregate both bacteria and their toxins; something that was not see in normal blood plasma.

The aggregation takes place quickly in the wound and causes bacteria and toxins not only to gather but also to be "eaten" by the body's inflammatory cells.

"Perhaps we do not need to kill them with antibiotics but simply gather them so that the body can better take care of the infection," said Jitka Petrlova, Professor at Lund University in Sweden.

"This way, the body avoids the spread of the infection. We believe this to be a fundamental mechanism for taking care of both bacteria and their toxins during wound healing," said Petrlova, lead author of the study published in the journal Proceedings of the National Academy of Sciences (PNAS).

"Our discovery links aggregation and amyloid formation to our primary defence against infections - our innate immunity," Petrlova said.

It is well known that various aggregating proteins can cause amyloid disease, in skin or internal organs, such as the brain.

Therefore, a mechanism that is supposed to protect us from infections, can sometimes be over-activated and lead to degenerative diseases, researchers said.

"I have always been fascinated by how nature has effectively created different defence mechanisms, and wound healing provides a rich source of new discoveries," said Artur Schmidtchen, also a Professor at Lund University.

"The ability to effectively heal wounds is of evolutionary significance to our survival," said Schmidtchen.

"Compared to antibiotics, innate immunity has been around for millions of years - and I think we should consider the application of these concepts in an era of increasing antibiotic resistance," he said. 

(With Agency inputs)