Productive infection of Piscirickettsia salmonis in macrophages and monocyte-like cells from rainbow trout, a possible survival strategy
Author
dc.contributor.author
Rojas, Verónica
Author
dc.contributor.author
Galanti Garrone, Norbel
Author
dc.contributor.author
Bols, Niels C.
Author
dc.contributor.author
Marshall, Sergio H.
Admission date
dc.date.accessioned
2019-03-11T12:58:18Z
Available date
dc.date.available
2019-03-11T12:58:18Z
Publication date
dc.date.issued
2009
Cita de ítem
dc.identifier.citation
Journal of Cellular Biochemistry 108:631–637 (2009)
Identifier
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07302312
Identifier
dc.identifier.issn
10974644
Identifier
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10.1002/jcb.22295
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/164867
Abstract
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Piscirickettsia salmonis is the etiologic agent of the salmonid rickettsial septicemia (SRS), an endemic disease which causes significant losses
in salmon production. This intracellular bacterium is normally cultured in salmonid epithelial cell lines inducing characteristic cytopathic
effects (CPEs). In this study we demonstrate that P. salmonis is able to infect, survive, replicate, and propagate in the macrophages/monocytes
cell line RTS11 derived from rainbow trout spleen, without inducing the characteristic CPEs and the host cells showing the same expression
levels as non-infected control cell. On the other hand, bacteria were capable of expressing specific proteins within infected cells. Infected
macrophages cease proliferation and a fraction of them detached from the plate, transform to non-adhesive, monocyte-like cells with
proliferative activity. Productive infection of P. salmonis into salmonid macrophage/monocyte cells in culture provides an excellent model
for the study of host–pathogen interactions, almost unknown in the case of P. salmonis. Our results suggest that the infection of cells from the
salmonid innate immune system without inducing an important cell death response should lead to the persistence of the bacteria and
consequently their dissemination to other tissues, favoring the evasion of the first line of defense against pathogens.