The human complement system represents a severe threat for the malaria parasite Plasmodium falciparum. We previously showed that blood stage parasites bind the complement inhibitor factor H to inactivate the complement cascade. Here we investigated the potential role of plasminogen in complement evasion. Plasminogen is a zymogen of the fibrinolysis system that following processing by specific activators converts into the serine protease plasmin.
After being ingested by a female Anopheles mosquito during a bloodmeal on an infected host, and before they can reach the mosquito salivary glands to be transmitted to a new host, Plasmodium parasites must establish an infection of the mosquito midgut in the form of oocysts. To achieve this, they must first survive a series of robust innate immune responses that take place prior to, during, and immediately after ookinete traversal of the midgut epithelium. Understanding how parasites may evade these responses could highlight new ways to block malaria transmission.