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Credit: Paul A. Gulig
Researchers say they’ve determined why patients with hereditary hemochromatosis are so vulnerable to severe illness from Vibrio vulnificus infection.
Patients with hereditary hemochromatosis have a deficiency of the iron-regulating hormone hepcidin and therefore develop excess iron in their blood and tissue, providing prime growth conditions for Vibrio vulnificus.
The researchers also showed that minihepcidin, a medicinal form of the hormone hepcidin that lowers iron levels in blood, could cure the infection by restricting bacterial growth.
The findings appear in Cell Host and Microbe.
“This is the first time that the association of hepcidin deficiency and susceptibility to Vibrio vulnificus infection was tested,” said study author Yonca Bulut, MD, of the David Geffen School of Medicine at UCLA in Los Angeles.
“The dramatic effectiveness of the new treatment, even after the infection was established, was impressive.”
To conduct this study, Dr Bulut and her colleagues compared the fatality of Vibrio vulnificus infection in healthy mice with mice that lacked hepcidin, modeling human hereditary hemochromatosis.
The infection was much more lethal in hepcidin-deficient mice because their bodies could not decrease iron levels in the blood in response to infection, a process mediated by hepcidin in healthy mice.
Giving minihepcidin to hepcidin-deficient mice prevented infection if the hormone was given before Vibrio vulnificus was introduced. And mice given minihepcidin 3 hours after the bacterium was introduced were cured of any infection.
“We found that hepcidin is required for resistance to a Vibrio vulnificus infection,” said study author Joao Arezes, a graduate student from the University of Porto in Portugal.
“The development of the treatment tested in mouse models could reduce the high mortality rate of this disease.”
The next stage of this research is to investigate why Vibrio vulnificus bacteria become so lethal when iron levels are high, and to learn which other microbes respond similarly to excess iron. 
Credit: Paul A. Gulig
Researchers say they’ve determined why patients with hereditary hemochromatosis are so vulnerable to severe illness from Vibrio vulnificus infection.
Patients with hereditary hemochromatosis have a deficiency of the iron-regulating hormone hepcidin and therefore develop excess iron in their blood and tissue, providing prime growth conditions for Vibrio vulnificus.
The researchers also showed that minihepcidin, a medicinal form of the hormone hepcidin that lowers iron levels in blood, could cure the infection by restricting bacterial growth.
The findings appear in Cell Host and Microbe.
“This is the first time that the association of hepcidin deficiency and susceptibility to Vibrio vulnificus infection was tested,” said study author Yonca Bulut, MD, of the David Geffen School of Medicine at UCLA in Los Angeles.
“The dramatic effectiveness of the new treatment, even after the infection was established, was impressive.”
To conduct this study, Dr Bulut and her colleagues compared the fatality of Vibrio vulnificus infection in healthy mice with mice that lacked hepcidin, modeling human hereditary hemochromatosis.
The infection was much more lethal in hepcidin-deficient mice because their bodies could not decrease iron levels in the blood in response to infection, a process mediated by hepcidin in healthy mice.
Giving minihepcidin to hepcidin-deficient mice prevented infection if the hormone was given before Vibrio vulnificus was introduced. And mice given minihepcidin 3 hours after the bacterium was introduced were cured of any infection.
“We found that hepcidin is required for resistance to a Vibrio vulnificus infection,” said study author Joao Arezes, a graduate student from the University of Porto in Portugal.
“The development of the treatment tested in mouse models could reduce the high mortality rate of this disease.”
The next stage of this research is to investigate why Vibrio vulnificus bacteria become so lethal when iron levels are high, and to learn which other microbes respond similarly to excess iron.
Credit: Paul A. Gulig
Researchers say they’ve determined why patients with hereditary hemochromatosis are so vulnerable to severe illness from Vibrio vulnificus infection.
Patients with hereditary hemochromatosis have a deficiency of the iron-regulating hormone hepcidin and therefore develop excess iron in their blood and tissue, providing prime growth conditions for Vibrio vulnificus.
The researchers also showed that minihepcidin, a medicinal form of the hormone hepcidin that lowers iron levels in blood, could cure the infection by restricting bacterial growth.
The findings appear in Cell Host and Microbe.
“This is the first time that the association of hepcidin deficiency and susceptibility to Vibrio vulnificus infection was tested,” said study author Yonca Bulut, MD, of the David Geffen School of Medicine at UCLA in Los Angeles.
“The dramatic effectiveness of the new treatment, even after the infection was established, was impressive.”
To conduct this study, Dr Bulut and her colleagues compared the fatality of Vibrio vulnificus infection in healthy mice with mice that lacked hepcidin, modeling human hereditary hemochromatosis.
The infection was much more lethal in hepcidin-deficient mice because their bodies could not decrease iron levels in the blood in response to infection, a process mediated by hepcidin in healthy mice.
Giving minihepcidin to hepcidin-deficient mice prevented infection if the hormone was given before Vibrio vulnificus was introduced. And mice given minihepcidin 3 hours after the bacterium was introduced were cured of any infection.
“We found that hepcidin is required for resistance to a Vibrio vulnificus infection,” said study author Joao Arezes, a graduate student from the University of Porto in Portugal.
“The development of the treatment tested in mouse models could reduce the high mortality rate of this disease.”
The next stage of this research is to investigate why Vibrio vulnificus bacteria become so lethal when iron levels are high, and to learn which other microbes respond similarly to excess iron.