Dear Doctor: I read that scientists are close to being able to "turn off" inflammation. What does that mean? And isn't that dangerous, since inflammation is a natural part of the immune system?
Dear Reader: The body's inflammation reaction is a double-edged sword. Most of the time we're grateful for the array of specialized white blood cells that rally to our defense. First to the scene of injury, illness and infection, they're specialists in detecting bacteria, viruses and other harmful organisms. They not only emit chemicals that destroy harmful invaders, they also cart away debris and rally the rest of the immune system to mount a robust response.
That's all great when things are working properly. But sometimes the body's inflammation response goes haywire. The same white blood cells that race to the rescue can be triggered by a case of mistaken identity and attack the body's own tissues. That's what's happening in autoimmune diseases like lupus, Crohn's disease or rheumatoid arthritis.
Certain conditions, like obesity, can rev up the inflammation process as well. That's because fat cells produce a class of small proteins known as cytokines, which are the same biochemicals that our white blood cells produce when they're on the attack. Those cytokines act as a 911 call to a host of other immune system cells, and thus encourage a state of ongoing inflammation. In addition to the autoimmune disorders we mentioned earlier, chronic inflammation has been linked to heart disease and certain cancers. And studies suggest that inflammation may have a hand in some diseases of the central nervous system as well.
All of which brings us back to the recent research that (we suspect) prompted your question. Among the cells that get involved in that initial immune response are white blood cells known as macrophages, which circulate throughout the tissues of the body. Now, a team of scientists from the United States, Ireland and the United Kingdom has identified a metabolic process that's able to get macrophages to stand down.
It turns out that a molecule known as itaconate, which is derived from glucose, acts as an "off" switch for macrophages. In a study published recently in the journal Nature, the researchers reported that the macrophages themselves can be instructed to make itaconate from glucose molecules. The presence of itaconate blocks the cascade of biochemical processes that add up to inflammation.
Specifically, a derivative of itaconate that can move in and out of the walls of our cells can actually decrease the production of cytokines, those small signaling proteins we were talking about earlier. The ability to control how macrophages produce and disperse cytokines would mean that certain types of inflammation could be controlled, or even stopped. The fact that it appears cytokines play a role in pain adds another intriguing layer of possibility to this discovery.
But before we celebrate the end of random inflammation, it's important to understand that at this point, the research has focused on mouse and human cells. The leap between the petri dish and the release of a targeted medication to control inflammation is a huge one.
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