A hormone responsible for controlling iron metabolism was found to be critical for preventing pneumonia bacteria from spreading throughout the body by a team of researchers at the University of Virginia (UVA) School of Medicine.
The hormone is called hepcidin, and is produced in the liver. Hepcidin can limit the spread of the bacteria by hiding iron in the blood – bacteria needs iron to thrive in the human body.
The findings were published in the journal JCI Insight in an article titled “Hepcidin-mediated iron sequestration protects against bacterial dissemination during pneumonia.”
Triggering hepcidin production in patients with a dysfunctional iron production, like those with liver disease or iron overload, could help their bodies starve the bacteria to death without the need of using antibiotics. This could save the lives of vulnerable patients, especially those with bacterial pneumonia who have increased 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,” Borna Mehrad, senior author of the study, said in a UVA news story. “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.”
The research team also found that mice with genetic modifications that caused dysfunctional production of hepcidin were highly susceptible to bacterial pneumonia – almost all mice had the bacteria spread from the lungs into the bloodstream, a process that proved deadly.
“It’s the exact same thing that happens in people,” Mehrad explained. “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.”
Kathryin Michels, first author of the study, added that the reason why so many people lack hepcidin might be because of genetic factors or liver diseases.
“It’s quite common,” Michels said. “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 added that a drug is being developed to mimic the function of hepcidin, and it could be used to lower iron levels in the blood. The drug is being developed to treat chronic iron overload, but these findings could add another potentially lifesaving purpose to its development.
“We think that short-term treatment with this drug should be an effective way of treating these [pneumonia] infections,” Mehrad said. “At least in mice, it seems to work extremely well.”
