Targeted Cancer Therapy May Also Fight Infections

Enzyme blocker shows potential in treating infections such as Ebola virus.

A low dose of a targeted anti-cancer drug can prompt the creation of immune cells that fight bacterial infections such as the Ebola virus, according to a recent study.

Published in the March 30, 2015 edition of PLOS Pathogens, the study suggests the drug imatinib (Gleevec) can prompt bone marrow to produce innate immune cells that aid in the treatment of various infections, or in patients with weakened immune systems. Analysis on the dosing of imatinib for additional clinical applications was provided through research performed in mice and on human bone marrow cells in vitro.

"We think that low doses of imatinib are mimicking 'emergency hematopoiesis,' a normal early response to infection," senior author Daniel Kalman, PhD, said in a press release.

Imatinib blocks tyrosine kinase enzymes that are dysregulated in conditions such as chronic myelogenous leukemia and gastrointestinal stromal tumors, the study noted. The drug was also found to inhibit normal versions of the enzymes found in healthy cells.

Various bacteria and viruses are known to exploit tyrosine kinase enzymes during transit into and out of healthy cells. Prior research indicated that imatinib can reduce cell infection from pathogens that are significantly different from each other, which include tuberculosis bacteria and the Ebola virus.

For the current study, researchers found that imatinib can prompt the immune system to fight a wide variety of bacteria through the stimulation of bone marrow to generate more neutrophils and macrophages, which are vital in resisting bacterial infection.

The drug apparently has the ability to stimulate several white blood cell types that may offer a limit on inflammation as opposed to increasing just neutrophils, which can cause harm, according to the study. Researchers further suggested that imatinib and related drugs may be useful to treat a variety of infections in patients with comprised immune systems, including patients receiving chemotherapy for the treatment of cancer.

"This was surprising because there are reports that imatinib can be immunosuppressive in some patients," Kalman said. "Our data suggest that at sub-clinical doses, imatinib can stimulate bone marrow stem cells to produce several types of myeloid cells, such as neutrophils and macrophages, and trigger their exodus from the bone marrow. However, higher doses appear to inhibit this process."