Lipids from a snail host regulate the multicellular behavior of a predator of parasitic schistosomes

Highlights•Capsaspora forms multicellular aggregates within host snail tissue and snail serum•The snail serum phosphatidylcholine lipid DOPC induces Capsaspora aggregation•Schistosome-infected snails have more DOPC, causing greater Capsaspora aggregation•Chemically regulated aggregation may help Capsaspora survive its host environmentSummaryTransmission of vector-borne diseases can be slowed by symbionts within the secondary hosts that spread disease. Snails spread schistosomiasis, and the snail symbiont Capsaspora owczarzaki kills schistosome larvae. In studying how Capsaspora colonizes its host snail, we discovered that Capsaspora responded to its host by forming multicellular aggregates. We elucidated the chemical cue for aggregation: hemolymph phosphatidylcholines (PCs). Furthermore, we uncovered that Capsaspora cells aggregate to different degrees in sera from different host snails—and these responses correlate with serum concentrations of PCs. Therefore, Capsaspora senses a host factor that can indicate the identity and physiological state of its host. Since cellular aggregation controls microbial motility, feeding, and immune evasion, this response within host tissue may be important for colonization. If so, snail serum PC and Capsaspora aggregation will be molecular and cellular markers to discern which conditions will favor the colonization of snails (and potential exclusion of schistosomes) by Capsaspora.