Our body's immune system protects us from skin infections. But, how our immune system responds to this infection depends on a number of things. In a new study that was published in an issue of Science recently says that the researchers at the University of California, San Diego School of Medicines have made a surprising discovery. It reveals that the fat cells below the skin also play the role of protecting us from bacterial infection.
The dermal fat cells are known as adipocytes. In this study carried out by Richard Gallo, MD, PhD, professor and chief of dermatology at UC San Diego School of Medicine, and colleagues, it has discovered that these dermal fat cells produce antimicrobial peptides which help in fending off invading bacteria and other pathogens.
Gallo, the study’s principal investigator said that it was thought that once the skin barrier was broken, the responsibility of protecting us from the infection was on the circulating white blood cells like neutrophils and macrophages. Now, we have discovered that it takes time to recruit these cells at the wound site and till then the fat stem cells produce antimicrobials which protect us.
The way our immune system works is complex; it is multi-tiered and it eventually culminates in the in the arrival of neutrophils and monocytes – specialized cells who fight pathogens. But, since these cells take time to arrive at the wound site, the body needs something else for an immediate response. This work is done by epithelial cells, mast cells and leukocytes that are present at the area of infection.
One of the major causes of skin and soft tissue infections in humans is the bacteria – Staphylococcus aureus. Antibiotic-resistant forms of S. aureus have emerged which pose a significant problem worldwide in clinical medicine. The previous work published by the Gallo lab had made the observation that S. aureus was present in the fat layer of the skin. So, they wanted to find out if the subcutaneous fat played a role in preventing skin infections.
For the study, the experiment mice were exposed to S. aureus by the researcher Ling Zhang, the first author of the paper. Within hours, it was seen that there was a major increase in both the number and size of fat cells at the site of infection. Another important observation was that these fat cells produced high levels of cathelicidin antimicrobial peptide (CAMP) which is an antimicrobial peptide (AMP). These molecules are used by the innate immune response to directly annihilate invasive bacteria, viruses, fungi and other pathogens. Gallo opined that these AMPs are our body's natural first line defense against infection. Even though they are evolutionarily ancient, they are used by all living organisms to protect themselves. But, in humans the presence of AMPs is both beneficial and harmful. Too little CAMP result in frequent infections while too much CAMP can drive autoimmune and other inflammatory diseases in people,
The scientists confirmed their findings by analyzing S. aureus infections in mice. They found that the mice were unable to effectively produce adipocytes. They also noticed that those fat cells did not express sufficient antimicrobial peptides in general and CAMP in particular. Such mice suffered more frequent and severe infections. Further tests were carried out in human that suggested that the immune response is similar in both rodents and humans. It was interesting to note that the obese subjects had more CAMP in their blood than subjects of normal weight.
Gallo said in order to find out the potential clinical applications of the findings, further study will be needed.