Subcutaneous fat cells are the keys to fighting skin infections, according to a new study set to be published in the Jan. 2, 2015 issue of "Science."
Researchers at the University of California, San Diego School of Medicine claim that fat cells can protect us from bacteria, according to the university via NewsWise.
Dr. Richard Gallo, professor and chief of dermatology at the school, has found that dermal fat cells, also known as adipocytes, produce antimicrobial peptides.
Gallo is the study's lead investigator and worked with co-authors Tissa Hata, from the University of California, San Diego School of Medicine, Christian F. Guerrero-Juarez, Paul Ramos and Maksim V. Plikus, from University of California, Irvine and Sagar P. Bapat, The Salk Institute for Biological Studies.
"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," Gallo said. "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. It was not known that adipocytes could produce antimicrobials, let alone that they make almost as much as a neutrophil."
When skin is broken, it takes time for white blood cells to arrive, so the body needs an immediate responder, or responders, like epithelial cells, mast cells and leukocytes. Then, neutrophils and monocytes can sweep in and finish the clean up.
Skin infections, like Staphylococcus or the resistant strain MRSA, are common problems in health care settings. Gallo's lab had looked into Staphylococcus aureus in fat cells during previous studies, so researchers looked less-deep in the fat just below the skin.
The first author of the previous study, Ling Zhang, infected mice with Staphylococcus aureus. Within hours, Zhang observed an increase in size and number of fat cells that produced an antimicrobial peptide (AMP) called cathelicidin antimicrobial peptide (CAMP).
"AMPs are our natural first line defense against infection," Gallo said. "They are evolutionarily ancient and used by all living organisms to protect themselves."
"However, in humans it is becoming increasingly clear that the presence of AMPs can be a double-edged sword, particularly for CAMP," Gallo continued. "Too little CAMP and people experience frequent infections. The best example is atopic eczema (a type of recurring, itchy skin disorder). These patients can experience frequent Staph and viral infections. But too much CAMP is also bad. Evidence suggests excess CAMP can drive autoimmune and other inflammatory diseases like lupus, psoriasis and rosacea."
Obese subjects were found to have higher CAMP levels than peers of normal weight.
Defective AMP production by mature adipocytes can occur due to obesity or insulin resistance, resulting in greater susceptibility to infection, but too much cathelicidin may provoke an unhealthy inflammatory response, according to Newswise.
"The key is that we now know this part of the immune response puzzle. It opens fantastic new options for study. For example, 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," Gallo said.
The National Institutes of Health, The Atopic Dermatitis Research Network, the Edward Mallinckrodt Jr. Foundation, the Dermatology Foundation, the National Science Foundation and the California Institute for Regenerative Medicine partially funded the recent study.
