Research projects
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Study of the invasion and intracellular traffic of photobacterium damselae subs. piscicida with non-immune cells of the gilthead (sparus aurata)
16th national competition for scientific and technical research
Marine sciences
Research Centre or Institution : Instituto Universitario de Sanidad Animal y Seguridad Alimentaria. Universidad de Las Palmas de Gran Canaria.
Abstract
Photobacterium damselae subsp. piscicida (Phdp) is a causal agent of one of the most important diseases in marine fish farming, pasteurellosis. This pathogen showed its economic importance in Japan, where it caused major losses in the fish farming industry. Although Europe was thought to be free of this disease until years ago, epidemics of the disease started to be detected in several European countries at the start of the 1990s. Pasteurellosis has now become a major problem in fish farming all over the world. In the Canary Islands, it is one of the most common diseases with the greatest economic effect on fish farming. The gilthead bream (Sparus aurata), which is of great economic value, is one of the species of fish most affected by this pathogen. The bacteria is an intracellular pathogen that is able to reside within the phagocyte cells of the gilthead bream. Recent literature has revealed that Phdp is also able to infect the non-phagocyte cells (NPC) of different species of fish. The entry of this pathogen into NPC may be used by this bacteria to escape the immune system or to facilitate its spread through the tissues of fish. This project aims to study in detail the processes of adherence, internalisation, and the intracellular traffic of Phdp in non-phagocyte cells of the gilthead bream, its natural host and the most important in biological and economic terms. It has the following objectives:
- To develop tools for the study of bacteria-cell interactions in the Phdp-gilthead bream model.
- To monitor the intercellular behaviour of Phdp in SAF‑1 cells.
- To study the changes in the genetic expression of cytokines inserted into SAF‑1 cells after infections by Phdp.
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