Humans have iron in their blood just like hundreds of other organisms; iron is an essential component in many proteins, and almost all organisms need iron in some form. Unfortunately, bacteria need iron to survive just as much as humans do, and the competition for iron in the blood becomes a matter of life or death in an age where bacteria are becoming increasingly resistant to existing antibiotics.
All kinds of bacteria causing infections “feed” off of the free iron ions in the bloodstream, including bacteria causing pneumonia. However, a hormone exclusively synthesized by the liver, hepcidin, has the unique ability of “hiding” iron from bacteria, limiting their spread throughout the human body.
Hepcidin is responsible for controlling iron metabolism: absorption, recycling, and utilization, and scientists from the University of Virginia (UVA) are quickly realizing that because of its unique role, hepcidin could be used to overcome many of the roadblocks put in place by bacterial resistance to antibiotics. "The rate at which these organisms become resistant to antibiotics is far faster than the rate at which we come up with new antibiotics. It's a race, and they're winning it," explained UVA’s Borna Mehrad, MBBS. Doctors are concerned in their anticipation for the day when there are no effective antibiotics left to treat a patient with bacterial pneumonia.
The power of hepcidin could be particularly life-saving for liver disease patients or people with genetic diseases like hereditary hemochromatosis who are especially vulnerable to bacterial pneumonia and other infections due to their lack of adequate hepcidin. In hereditary hemochromatosis, the body absorbs too much iron from the diet; excess iron stored in tissues and organs like the skin, heart, liver, pancreas, and joints; excess iron damages these tissues and organs, causing fatigue, joint pain, abdominal pain, and loss of sex drive.
Mehrad and a team of researchers from UVA tested hepcidin’s potential in mice studies, where the mice were genetically altered to lack hepcidin. As expected, these mice were extremely susceptible to infection when exposed to bacterial pneumonia; the connection between lacking hepcidin and being prone to infection is expected to be mirrored in humans.
There exists, in fact, a drug that closely resembles hepcidin; it decreases the iron levels in the blood. While being careful to avoid anemia, this drug could be applied to temporarily treat bacterial pneumonia in patients with liver disease or another hepcidin-limiting condition. Soon, another version of the drug could be developed based on the UVA research to increase hepcidin in the blood to treat bacterial infections.
The present study was published in the journal JCI Insight.
Sources: The Clinical Biochemist Reviews, Genetics Home Reference, American Lung Association, JCI Insight, University of Virginia Health System