The discovery may prove useful to devise new forms of treatments for tuberculosis and many other chronic infections caused by bacteria.
The National Institute of Allergy and Infectious Diseases (NIAID) which is a part of the National Institutes of Health supported this research which was led by Peter Murray, Ph.D., from St. Jude Children's Research Hospital in Memphis and Thomas Wynn, Ph.D., from Laboratory of Parasitic Diseases at NIAID.
Macrophages, meaning "big eater" in Latin, or the white blood cells get rid of the disease-causing bacteria, parasites and all the cell-waste in the body. Macrophages make substances that kill pathogens and free radical nitric oxide (NO) is one of them. NO helps the macrophages to destruct and assimilate the cell-waste.
But the intracellular pathogens, another kind of bacteria present in the body thrive in the cells, with NO having no effect on them. Arginase, an enzyme, tampers with the production of NO depleting its amount in the cells.
Dr. Murray explained that, "The bacteria designed to live inside the cell are highly adapted to their environment. We wanted to determine just how intracellular bacteria were turning on the genes
define that make arginase, thereby controlling the expression of NO and escaping killing by macrophages."
According to the researchers, the intracellular pathogens increase arginase levels to cut down on the quantity of NO released, which helps the pathogens to flourish. People with weak immunity are at risk due to these pathogens.
The study involved mice that were deficit in arginase-producing gene in their macrophages. The mice were infected with Tuberculosis bacteria and it was observed that the mice had high levels of NO and lesser bacteria. Later, arginase knockout mice were infected with an intracellular parasite. The mice deficit in arginase had survived longer than arginase-producing mice.
Dr. Wynn said, "Although NO was named 'molecule of the year' in 1992 by Science Magazine and studied as an important part of the immune response to bacterial infections, arginase, its counterbalance, was widely ignored by the immunologydefine community. This work suggests that targeting arginase may be helpful in treating chronic, intracellular bacterial and parasitic infections."
The researchers are determined to discover the extent of damage arginase can cause and how exactly it affects the immune systemdefine.
The research findings will be published in Nature Immunology's November issue.
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