title: The role of programmed cell death in Plasmodium-mosquito interactions.
abstract: Many host-parasite interactions are regulated in part by the programmed cell death of host cells or the parasite. Here we review evidence suggesting that programmed cell death occurs during the early stages of the development of the malaria parasite in its vector. Zygotes and ookinetes of Plasmodium berghei have been shown to die by programmed cell death (apoptosis) in the midgut lumen of the vector Anopheles stephensi, or whilst developing in vitro. Several morphological markers, indicative of apoptosis, are described and evidence for the involvement of a biochemical pathway involving cysteine proteases discussed in relationship to other protozoan parasites. Malaria infection induces apoptosis in the cells of two mosquito tissues, the midgut and the follicular epithelium. Observations on cell death in both these tissues are reviewed including the role of caspases as effector molecules and the rescue of resorbing follicles resulting from inhibition of caspases. Putative signal molecules that might induce parasite and vector apoptosis are suggested including nitric oxide, reactive nitrogen intermediates, oxygen radicals and endocrine balances. Finally, we suggest that programmed cell death may play a critical role in regulation of infection by the parasite and the host, and contribute to the success or not of parasite establishment and host survival.
authors.affiliation: Centre for Applied Entomology and Parasitology, School of Life Sciences, Keele University, Staffordshire ST5 5BG, UK. h.hurd@keele.ac.uk
authors.forename: Hilary
authors.initials: H
authors.lastname: Hurd
authors.forename: Victoria
authors.initials: V
authors.lastname: Carter
mesh_terms: D000818:Animals; D017209:Apoptosis; D009033:Culicidae / Q000469:parasitology*; D006790:Host-Parasite Interactions; D007303:Insect Vectors / Q000469:parasitology*; D008288:Malaria / Q000469:parasitology* / Q000635:transmission; D010961:Plasmodium / Q000166:cytology / Q000502:physiology*