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Posted on Dec 04, 08:54PM | IANS
Researchers have figured out why iron plays a key role in metabolism and infections, pitting bugs and animals against one another, resolving a 40-year-old debate and opening way to more potent antibiotics.
The collaborative research, led by Phillip Klebba, professor and head of department of biochemistry at Kansas State University, clarifies how micro-organisms colonise animal hosts and how scientists may block them from doing so.
Klebba's team found that E. coli, one of the deadly bugs that cause hosts of gastric infections, must acquire iron from the host to establish a foothold and colonise the gut -- a concept that was often debated by scientists.
E. coli is difficult to get rid of because it has at least eight iron acquisition systems. So when one is blocked, another opens up, journal Public Library of Science ONE, reports.
The study, conducted with with Tyrrell Conway, microarray and bioinformatics researcher from University of Oklahoma, and Salete M. Newton, Kansas research professor of biochemistry, shows how iron acquisition affects the ability of bacteria to colonise animals, which is the first stage of microbial disease.
"This paper establishes that iron uptake in the host is a crucial parameter in bacterial infection of animals," said Klebba, study co-author, according to a Kansas statement.
"For years, it was theorised that iron is a focal point of bacterial pathogenesis (mechanism by which disease is caused) and infectious disease because animals constantly defend the iron in their bodies," Klebba said.
"Animal proteins bind iron and prevent micro-organisms from obtaining it. This is called nutritional immunity, and it is a strategy of the host defence system to minimise bacterial growth. But successful pathogens overcome nutritional immunity and get the iron," Klebba said.
"This is the first time our experiments unambiguously verified the indispensability of iron in infection, because here we created the correct combination of mutations to study the problem," he added.