New Treatment For Bacterial Pneumonia Discovered At University Of Virginia


Researchers have discovered a hormone that is accountable for controlling iron metabolism that helps fight off a serious form of bacterial pneumonia. The findings may offer a solution to help in patients recovery.

Scientists at the University of Virginia School of Medicine have found a key hormone crucial for the prevention of pneumonia bacteria spreading throughout the body. The hormone, hepcidin, is formed in the liver and limits the spread of the bacteria by hiding the iron in the blood that the bacteria require to grow and survive.

Stimulating hepcidin production in patients who do not produce it well may help their bodies effectively starve the bacteria to death. That discovery could be lifesaving for these vulnerable patients, especially as pneumonia bacteria grow increasingly antibiotic antibiotic-resistant.

Researcher Borna Mehrad, of UVA’s Division of Pulmonary and Critical Care Medicine stated, “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. Increasingly, the choice of antibiotics to treat these infections is more and more limited, and there are occasions where there just isn’t an antibiotic to treat with, which is a very scary and dangerous situation.”

Mehrad and his team, including colleagues at the University of California, found that mice that had been genetically modified to lack hepcidin were particularly susceptible to bacterial pneumonia. Nearly all of the mice had the pneumonia bacteria spread from the lungs into their bloodstream, ultimately killing them. Mehrad said, “It’s the exact same thing that happens in people. The mice that lacked the hormone weren’t able to hide iron away from the bacteria, and we think that’s why the bacteria did so well in the blood.”

Researcher Kathryn Michels, a graduate student in Mehrad’s lab and the first author of a study (“Hepcidin-mediated iron sequestration protects against bacterial dissemination during pneumonia”), published in JCI Insight”), outlining the findings, noted that many people lack the hormone because of genetic illnesses or liver disease. She said, “It’s quite common. We think this line of research is very relevant to the many people who can’t make this hormone very well and are, clinically, very susceptible to these infections.”

Michels explained that there is already a medication in development that mimics the function of hepcidin and could be used to lower the iron levels in the blood of pneumonia patients who lack hepcidin. That medicine has been developed primarily to treat chronic iron overload, such as is seen in people with hereditary hemochromatosis, but the new research may give it another, life saving application. Mehrad stated, “We think that short-term treatment with this drug should be an effective way of treating these infections. At least in mice, it seems to work extremely well.”


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