The outcome of sepsis and stroke could be improved upon with the use of a new therapeutic model shown in mice. Sepsis is a disease that is estimated to affect over 30 million people per year, according the World Health Organization (WHO). Stroke is experienced by up to 795,000 in the USA per year.
Further damage caused by inflammation can be experienced in both of these conditions. Research is targeted at regulating and interrupting the inflammatory response in attempts to improve effectiveness of treatment. Researchers from Washington State University, Pullman, Washington, USA aimed to demonstrate that with innovative technology the cells that cause inflammation can be the targeted with drug therapy.
The damage response of neutrophils caused them to be the prime target of researchers. Following inflammation, they can act abnormally and unpredictably and overaccumulate in healthy tissue causing further damage. Senior study author Zhenjia Wang, commented on the action of neutrophils: “scientists have started realising that neutrophils, which were always seen as the ‘good guys’ for the key role they play in our immune system, are actually also contributing to the pathology of all kinds of diseases.”
Previous studies have encountered problems with the use of drugs targeted to neutrophils because neutrophils at rest would also be killed by the same drug. The researchers in this present study found that the active cells expressed a greater number of Fc-γ receptors and were able to target the proinflammatory cells with the use of the chemotherapeutic drug, doxorubicin, loaded onto nanoparticles which enter the cells via this receptor. The results showed that survival rates of sepsis and ischemic stroke in mouse models was improved and neurological damage was decreased. Dr Wang reflected on the results of the study, “our experiment found that our doxorubicin albumin nanoparticles can decrease the lifespan of harmful neutrophils in the bloodstream.”