Immune-relevant thrombocytes of common carp undergo parasite-induced nitric oxide-mediated apoptosis.

Dev Comp Immunol

Cell Biology and Immunology Group, Wageningen Institute of Animal Sciences, Wageningen University, PO Box 338, 6700 AH Wageningen, The Netherlands. Electronic address:

Published: June 2015

AI Article Synopsis

  • Common carp thrombocytes are significant, making up 30-40% of blood leukocytes, and are found in large numbers in the spleen, which helps produce them.
  • Research shows that these thrombocytes express many immune-related genes, hinting at their potential role in the fish's immune response.
  • During infections with the parasites Trypanoplasma borreli and Trypanosoma carassii, thrombocytes are greatly reduced in number, particularly during T. borreli infection, suggesting that nitric oxide may play a role in this depletion process.

Article Abstract

Common carp thrombocytes account for 30-40% of peripheral blood leukocytes and are abundant in the healthy animals' spleen, the thrombopoietic organ. We show that, ex vivo, thrombocytes from healthy carp express a large number of immune-relevant genes, among which several cytokines and Toll-like receptors, clearly pointing at immune functions of carp thrombocytes. Few studies have described the role of fish thrombocytes during infection. Carp are natural host to two different but related protozoan parasites, Trypanoplasma borreli and Trypanosoma carassii, which reside in the blood and tissue fluids. We used the two parasites to undertake controlled studies on the role of fish thrombocytes during these infections. In vivo, but only during infection with T. borreli, thrombocytes were massively depleted from the blood and spleen leading to severe thrombocytopenia. Ex vivo, addition of nitric oxide induced a clear and rapid apoptosis of thrombocytes from healthy carp, supporting a role for nitric oxide-mediated control of immune-relevant thrombocytes during infection with T. borreli. The potential advantage for parasites to selectively deplete the host of thrombocytes via nitric oxide-induced apoptosis is discussed.

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Source
http://dx.doi.org/10.1016/j.dci.2015.02.008DOI Listing

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