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The complement cascade in mammalian blood can damage the alimentary tract of haematophagous arthropods. As such, these animals have evolved their own repertoire of complement-inactivating factors, which are inadvertently exploited by blood-borne pathogens to escape complement lysis. Unlike the bloodstream stages, the procyclic (insect) stage of  Trypanosoma brucei  is highly susceptible to complement killing, which is puzzling considering that a tsetse takes a bloodmeal every 2–4 days. In this study, we identified four tsetse ( Glossina morsitans morsitans ) serine protease inhibitors (serpins) from a midgut expressed sequence tag (EST) library ( GmmSRPN3 ,  GmmSRPN5 ,  GmmSRPN9  and  GmmSRPN10 ) and investigated their role in modulating the establishment of a  T. brucei  infection in the midgut. Although not having evolved in a common blood-feeding ancestor, all four serpins have an active site sharing remarkable homology with the human complement C1-inhibitor serpin, SerpinG1. RNAi knockdown of individual  GmmSRPN9  and  GmmSRPN10  genes resulted in a significant decreased rate of infection by procyclic form  T. brucei . Furthermore, recombinant  GmmSRPN10  was both able to inhibit the activity of human complement-cascade serine proteases, C1s and Factor D, and to protect the  in vitro  killing of procyclic trypanosomes when incubated with complement-activated human serum. Thus, the secretion of serpins, which may be part of a bloodmeal complement inactivation system in tsetse, is used by procyclic trypanosomes to evade an influx of fresh trypanolytic complement with each bloodmeal. This highlights another facet of the complicated relationship between  T. brucei  and its tsetse vector, where the parasite takes advantage of tsetse physiology to further its chances of propagation and transmission.

Tsetse GmmSRPN10 Has Anti-complement Activity and Is Important for Successful Establishment of Trypanosome Infections in the Fly Midgut