Secret Strategies of Body's 'Iron War' Revealed

When you think "the immune system," you probably think of a scene straight out of Osmoses Jones where hard-on-the-case white blood cells battle with dangerous viral infections. However, professionals know that the body can also try to deprive pathogens of essential irons. Unfortunately, this strategy can backfire, causing anemia. Reversing this self-destructive path is hard work, but recent research with mice has revealed a new way doctors can help their patients.

That's at least according to a study recently published in the journal Blood, which details how experts searched for secret immune system components in mice that can actually "dial down" ferroportin - a protein that helps encourage the exportation of iron throughout the blood stream.

Healthy professionals have long known that most mammals - humans and mice included - can keep iron out of reach of invading microbes by storing it in cells like macrophages. Macrophages traditionally act as recycling agents in the body, taking discarded iron from blood cells and sending it throughout the body. However, when the immune system knows it's under attack, hepcidin, a hormone which regulates iron levels, will rise in concentration. This results in a suppression of ferroportin production. Without enough ferroportin to help export it, iron reserves are then trapped inside the body's macrophages.

Of course, this natural reaction is not trying to sabotage the body's good health. Normally, the body can go much longer without iron than a simple bacteria or virus can. However, if it takes too long for these harmful microbes to be starved, the body will start to suffer too, causing anemia. This is a common problem for chronically ill patients, and doctors frequently find themselves having to reverse the immune system's own self-destructive work.

"Until now, the main approach to develop treatments for anemia of chronic disease was to look for anti-hepcidin therapies," co-lead researcher Matthias Hentze explained in a statement.

However, not all anemic patients boast increased hepcidin levels, indicating that there is another culprit at work.

In their recent study of mice, Hentze and his team found that mammals also boast two molecules, TLR2 and TLR6, that likewise suppress ferroportin. When lab mice were exposed to bacterial infections in particular, these molecules went to work, starting an iron war of their own.

The researchers are now working to find ways to stop that TLR2/TLR6 response when it has gone on too long, hoping to halt anemia in its tracks before it can weaken a chronic patient further.

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