Bacteria are everywhere. Some, like the bacteria that live on our skin or in our intestines, keep us healthy and provide us with a variety of useful services. Others, like those that cause pneumonia or invade cuts, can cause serious illness and even death. Fortunately, our bodies have developed many ways of fighting off those damaging invaders and it looks like our fat may have something to do with it.
Our skin is the first line of defense against infection for most of our contact with the world. If an invader can’t get through that layer, it generally can’t make us sick. It’s only when that skin barrier is broken by a cut or crack that we get in trouble. Previously, physicians had thought that once the skin was broken, immune cells circulating in the blood were the next defense. But new research has found that the layer of fat that sits just under the skin, called subcutaneous fat, plays an important role as well.
This layer acts as an energy reserve, helps to pad our body against impacts with the outside world, and helps to insulate our body against the cold. But since it’s also one of the first layers to see invaders once the skin is broken, researchers wondered whether it also responded to infection. To study this, they looked at fat in living mice and at individual human fat cells.
They exposed both these live mice and the human fat cells to Staph aureus, which is the bug behind MRSA infections. They noticed that when fat cells were exposed to these bacteria, they began to grow and multiply. To figure out if this helped protect against infection, the researchers did a genetic analysis to find out which genes were turning on this growth and blocked them in a small group of mice. They found that mice whose fat cells couldn’t multiply in the presence of bacteria were more likely to get skin infections. When the research team investigated further, they found that this happened specifically because fat cells couldn’t expand, not because they were worse at getting the immune system to show up to fight the infection.
To figure out why this growth and expansion of fat might help fight infection, the researchers looked for compounds made by fat cells that might help. They found that the production of a protein called cathelicidin found in mice and human fat got a major boost with this Staph exposure. That protein is an antibacterial that helps to kill invading bacteria. When fat expansion is blocked, fat cells can’t ramp up production of this killer protein and infection happens more easily.
You might think that this means being overweight or obese should also protect you from infection more than those who are slimmer, however the researchers found this wasn’t the case. While obese mice made more cathelicidin, it was at such low levels that it wouldn’t affect bacteria. It was the production with exposure to bacteria that mattered, and both thin and fat mice made enough to attack Staph.
Worryingly, cathelicidin increases the body’s inflammation, which means increased low-level production may be increasing inflammation throughout the body in those who are overweight. Not only that, they found that the fat in those who are overweight and obese is worse at making these antibacterial proteins. The team thinks this might explain why those with excess body fat are actually more likely to get skin infections, not less.