Washington: A new study using systems biology has showed expanded range of possibilities in making the human liver better at killing the malaria parasite.
Although the asymptomatic liver stage of malaria is a crucial part of the parasite's development inside humans, it remains an unexplored black box. Until recently, scientists were convinced that malaria parasites were so adept at taking over liver cells that any attempt by the liver cell to attack the parasite would be futile, However researchers at Seattle BioMed are using systems biology to begin to unravel part of this mystery, with the finding that liver cells infected with malaria parasites are more vulnerable than previously thought, and that existing drugs can be leveraged to force those infected cells to self destruct while leaving the healthy cells intact.
Conventional scientific wisdom regarding the "liver stage" of disease was that the malaria parasites make their host cells exceptionally resistant to death. This meant that bombarding the liver with drugs that cause cells to commit cell suicide, or apoptosis, would destroy healthy liver cells while allowing infected cells to escape unscathed.
Now, new data collected by Alexis Kaushansky, Ph.D., and Stefan Kappe, Ph.D., of Seattle BioMed shift this paradigm.
Kaushansky said that using systems biology, they were able to show the existence of additional pathways that can be used to fight infected cells, demonstrating that their previous research involving p53 was not an isolated case and that we have only begun to scratch the surface of how broad these kinds of host-based therapeutics can be.
Meanwhile, Kappe said that in the study, they looked at an entirely separate pathway, working by an entirely different mechanism, and it still worked to help kill infected cells,
"This gives us hope that there are many other pathways that may also work as drug targets, and we look forward to conducting additional research into other potential pathways that may also hold potential for treating malaria."
The study is published in Cell Death and Disease.