"It was thought that once the skin barrier was broken, it was entirely the responsibility of circulating (white) blood cells like neutrophils and macrophages to protect us from getting sepsis," said principal investigator Richard Gallo, professor at University of California, San Diego School of Medicine.

"But it takes time to recruit these cells (to the wound site). We now show that the fat stem cells are responsible for protecting us," Gallo added.

It was not known that adipocytes could produce antimicrobials, let alone that they make almost as much as a neutrophil, Gallo said.

For the study, the researchers exposed mice to Staphylococcus aureus, a common bacterium and major cause of skin and soft tissue infections in humans.

They detected a major increase in both the number and size of fat cells at the site of infection within hours.

Besides, these fat cells produced high levels of an antimicrobial peptide (AMP) called cathelicidin antimicrobial peptide or CAMP.

AMPs are molecules used by the innate immune response to directly kill invasive bacteria, viruses, fungi and other pathogens.

"AMPs are our natural first line defence against infection," Gallo said.

The study appeared in the journal Science.

Latest News from Lifestyle News Desk