Chuck Bednar for redOrbit.com – Your Universe Online
Fat cells located beneath a person’s skin could help protect them from bacterial infections, according to a new study published Thursday in the journal Science.
In the study, Dr. Richard Gallo, a professor and chief of dermatology at the University of California, San Diego School of Medicine, and his colleagues report that they had discovered a previously unknown function of these dermal fat cells, also known as adipocytes: they produce antimicrobial peptides that help combat bacteria and other types of pathogens.
“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,” explained Gallo. “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. That was totally unexpected,” he added. “It was not known that adipocytes could produce antimicrobials, let alone that they make almost as much as a neutrophil.”
A person’s body launches a complex, multi-tiered defense against microbial infection, the authors said. Several different types of cells are involved, and the process ends with the arrival of specialized cells known as neutrophils and monocytes that target and destroy pathogens.
Before any of that can happen, a more immediate response is required – one that can counter the ability of pathogens to rapidly increase their numbers, however. That task is typically performed by epithelial cells, mast cells and leukocytes residing in the area of infection.
Previous research conducted in Gallo’s lab detected Staphylococcus aureus, a common type of bacteria and a major source of skin infection on humans, in the fat layer of the skin. Antibiotic-resistant forms of this bacterial have become a significant health issue throughout the world, so the study authors looked to see what role adipocytes played in preventing skin infections.
First author Dr. Ling Zhang exposed mice to S. aureus, and just a few hours later, she detected a significant increase in both the number and size of fat cells present at the infection sites. The cells were also found to be producing high levels of cathelicidin antimicrobial peptide (CAMP), a substance used by a creature’s immune system to directly kill harmful pathogens.
Gallo called antimicrobial peptides such as CAMP “our natural first line defense against infection. They are… used by all living organisms to protect themselves.” He noted that too little CAMP caused people to “experience frequent infections,” but too much of the substance “Can drive autoimmune and other inflammatory diseases like lupus, psoriasis and rosacea.”
He and his colleagues confirmed their findings by analyzing S. aureus infections in rodents that were either unable to effectively produce adipocytes, or whose fat cells did not have express an adequate amount of antimicrobial peptides. In every case, they said, the mice suffered more frequent and severe skin infections.
Their research also revealed that human adipocytes also produce cathelicidin, suggesting that their immune response is similar to that of the mice, and that obese people were found to have more CAMP in their blood than their normal weight counterparts. Gallo said that the potential clinical applications of these findings will require additional research.
“We now know this part of the immune response puzzle. It opens fantastic new options for study,” he said. “Current drugs designed for use in diabetics might be beneficial to other people who need to boost this aspect of immunity. Conversely, these findings may help researchers understand disease associations with obesity and develop new strategies to optimize care.”
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