Colette Dissous

Piggy-backing the concept of cancer drugs for schistosomiasis treatment: a tangible perspective?

The fear that schistosomes will become resistant to praziquantel (PZQ) motivates the search for alternatives to treat schistosomiasis. Recent studies of signaling proteins in schistosomes uncovered a way of achieving this goal relatively quickly. It was shown that protein kinases (PKs) control important biological processes in schistosomes. Concurrently, the involvement of mutant forms of PKs was demonstrated in the etiology of cancer. Therefore, different anticancer drugs have been developed to inhibit deregulated PKs. These can also inhibit schistosome PKs, thus blocking parasite development. Recent studies characterizing schistosome PKs are summarized and we discuss the concept of PK inhibitors, including approved cancer drugs, as novel candidate anti-schistosome agents. This is also likely to be of significance for other worm infections.

Stimulation of Schistosoma mansoni miracidia by a 80 kDa glycoprotein from Biomphalaria glabrata

Soluble extracts of Biomphalaria glabrata stimulate in vitro incorporation of methionine in Schistosoma mansoni miracidia. Evidence is presented that a unique 80 kDa glycoprotein representing less than 0.01% of total snail proteins and uniformly distributed in the snail body, is responsible for the observed stimulation. This protein specifically acts on the miracidia and this observation suggests that this glycoprotein influences snail penetration and development of miracidia. However, the presence of molecules stimulating S. mansoni miracidia was also demonstrated in S. mansoni nonpermissive molluscs.

Mediation of T-Helper 17 Responses to Schistosomes by Dendritic Cells but Not Basophils

T-helper (Th) 17 cells that express lineage-specific transcription factor RORC and produce cytokines interleukin 17A (IL-17A), interleukin 17F (IL-17F), and interleukin 22 (IL-22), play a key role in the clearance of both intracellular and extracellular bacteria and fungal infections. However, in the context of certain other infections, such as hepatitis B, chronic toxoplasmic uveitis, encephalitis, and Theiler murine encephalomyelitis, chronic activation of Th17 cells could contribute to tissue damage and immunopathology [1–3]. In line with these observations, Mbow et al [4] recently demonstrated that Th17 cells are associated with pathology in human schistosomiasis. They found elevated Th17 cells in peripheral blood of patients with schistosomiasis as well as in the liver and spleen of Schistosoma mansoni–infected mice. However, considering the essential role of innate immune cells in mediating T-cell responses, questions regarding the identification of innate cells that could promote Th17 responses during Schistosoma infection remain unexplored.