Apoptosis as a host defense mechanism in Crassostrea virginica and its modulation by Perkinsus marinus.

Published

Journal Article

Dermo disease caused by the obligatory intracellular protozoan Perkinsus marinus causes extensive oyster mortalities leading to tremendous losses in the oyster industry and damage to estuarine ecosystems. To better understand the mechanisms of the parasite's evasion of the host immune defense system, we have investigated the molecular mechanisms of P.marinus-induced inhibition of apoptosis in oyster cells as a potential parasite's survival strategy. We found that P. marinus modulates apoptosis of oyster immune cells (hemocytes) in a way that may help the parasite to establish infection. We found an increase in apoptosis in the initial stages of infection in vitro and in vivo, consistent with a host response to this intracellular parasite. During infection with highly virulent strains of P. marinus, this was followed by suppression and a return of apoptosis to basal levels 8-24 h post-infection, strongly indicating the parasite-induced inhibition of the immune response. In contrast, during infections with intermediate or low virulence strains of P. marinus, a transient suppression of apoptosis 4-8 h post-infection was followed by sustained elevation of hemocyte apoptosis at later stages, indicating that hemocytes were able to overcome the parasite-induced suppression and successfully combat the infection. Studies of the mechanisms of P. marinus-induced apoptosis indicated that the early post-infection stimulation of apoptosis is caspase-independent. However, this process can be driven (although to a lesser degree) by the killed parasite, suggesting that oyster hemocytes respond to cell surface molecules of P. marinus. Overall, this study provides novel insights into pathogen-induced modulation of apoptosis and its role in parasite virulence and establishment of infections.

Full Text

Duke Authors

Cited Authors

  • Hughes, FM; Foster, B; Grewal, S; Sokolova, IM

Published Date

  • August 2010

Published In

Volume / Issue

  • 29 / 2

Start / End Page

  • 247 - 257

PubMed ID

  • 20371290

Pubmed Central ID

  • 20371290

Electronic International Standard Serial Number (EISSN)

  • 1095-9947

Digital Object Identifier (DOI)

  • 10.1016/j.fsi.2010.03.003

Language

  • eng

Conference Location

  • England