Signalling pathways and the host-parasite relationship: putative targets for control interventions against schistosomiasis: signalling pathways and future anti-schistosome therapies

Bioessays. 2011 Mar;33(3):203-14. doi: 10.1002/bies.201000077. Epub 2011 Feb 2.

Abstract

A better understanding of how schistosomes exploit host nutrients, neuro-endocrine hormones and signalling pathways for growth, development and maturation may provide new insights for improved interventions in the control of schistosomiasis. This paper describes recent advances in the identification and characterisation of schistosome tyrosine kinase and signalling pathways. It discusses the potential intervention value of insulin signalling, which may play an important role in glucose uptake and carbohydrate metabolism in schistosomes, providing the nutrients essential for parasite growth, development and, notably, female fecundity. Significant progress has also been made in the characterisation of other schistosome growth factor receptors, such as transforming growth factor beta receptor and epidermal growth factor receptor, and in our understanding of their roles in the host-parasite molecular dialogue and parasite development. The use of parasite signal transduction components as novel vaccine or drug targets may prove invaluable in prevention, treatment and control strategies to combat schistosomiasis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • ErbB Receptors / genetics
  • ErbB Receptors / metabolism
  • Female
  • Host-Parasite Interactions*
  • Humans
  • Insulin / genetics
  • Insulin / metabolism*
  • Protein-Tyrosine Kinases / genetics
  • Protein-Tyrosine Kinases / metabolism*
  • Receptor, Insulin / genetics
  • Receptor, Insulin / metabolism
  • Receptors, Transforming Growth Factor beta / genetics
  • Receptors, Transforming Growth Factor beta / metabolism
  • Schistosoma / metabolism*
  • Schistosomiasis / parasitology*
  • Schistosomiasis / therapy*
  • Signal Transduction
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Insulin
  • Receptors, Transforming Growth Factor beta
  • Tumor Necrosis Factor-alpha
  • ErbB Receptors
  • Protein-Tyrosine Kinases
  • Receptor, Insulin