By IANS,
Washington : Like humans, bacteria need iron to survive, a discovery that can open up new and more effective ways to target diseases like tuberculosis.
Some bacteria are equipped with a gene that enables them to harvest iron from their environment or human host in a unique and energy efficient manner, said Robert Doyle, a Syracuse University assistant professor, who led the research team.
“Iron is the single most important micronutrient bacteria need to survive,” Doyle said. “Understanding how these bacteria thrive within us is a critical element of learning how to defeat them.
“It’s amazing that the bacteria could learn to extract iron from their environment in this way. We went into these experiments with no idea that this mechanism existed. But then, bacteria have to be creative to survive in some very hostile environments; and they’ve had maybe 3.5 billion years to figure it out.”
Doyle’s research group studied Streptomyces coelicolor, a gram-positive bacteria that is closely related to the bacteria that causes tuberculosis.
Streptomyces is abundant in soil and in decaying vegetation, but does not affect humans. The TB bacteria and Streptomyces are both part of a family of bacteria called Actinomycetes.
Actinomycetes need lots of iron to wage chemical warfare on their enemies; however, iron is not easily accessible in the environments in which the bacteria live, such as the human body or the soil.
Doyle and his research team wondered if the compound iron-citrate could be a source of iron for the bacteria. In a series of experiments that took place over two years, researchers observed that Streptomyces could ingest iron-citrate, metabolise the iron, and use the citrate as a free source of energy.
Other experiments demonstrated that the bacteria ignored citrate when it was not bonded to iron; likewise, the bacteria ignored citrate when it was bonded to other metals, such as magnesium, nickel and cobalt.
The next task was to uncover the mechanism that triggered the bacteria to ingest iron-citrate. Computer modelling predicted that a single Streptomyces gene enabled the bacteria to identify and ingest iron-citrate.
Researchers isolated the gene and added it to E. coli bacteria (which is not an Actinomycete bacteria). They found that the mutant E. coli bacteria could also ingest iron-citrate. Without the gene, E. coli could not gain access to the iron.
The Streptomyces gene enables the bacteria to passively diffuse iron-citrate across the cell membrane, which means that the bacteria do not spend additional energy to ingest the iron.
Once in the cell, the bacteria metabolise the iron and, as an added bonus, use the citrate as an energy source. Doyle’s team is the first to identify this mechanism in a bacteria belonging to the Actinomycete family.
The research is scheduled for publication in August issue of Journal of Bacteriology.