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Artículo

Macrophages and Galectin 3 Control Bacterial Burden in Acute and Subacute Murine Leptospirosis That Determines Chronic Kidney Fibrosis

Ferrer, Maria FlorenciaIcon ; Scharrig Fernandez, Maria EmiliaIcon ; Charó, Nancy LorenaIcon ; Rípodas, Ana L.; Drut, Ricardo; Carrera Silva, Eugenio AntonioIcon ; Nagel, Ariel GastónIcon ; Nally, Jarlath E.; Montes de Oca, Daniela PaulaIcon ; Schattner, Mirta AnaIcon ; Gomez, Ricardo MartinIcon
Fecha de publicación: 10/2018
Editorial: Frontiers Research Foundation
Revista: Frontiers in cellular and infection microbiology
ISSN: 2235-2988
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Biología Celular, Microbiología

Resumen

Previous studies have suggested that macrophages may contribute to acute Leptospira dissemination, as well as having a major role in kidney fibrosis. Our aim was to characterize the role of macrophages and galectin 3 (Gal-3) on the survival, clinical course, bacterial burden, interstitial nephritis, and chronic kidney fibrosis in Leptospira interrogans serovar Copenhageni (LIC)-induced experimental murine leptospirosis. C57BL/6J mice depleted of macrophages by liposome-encapsulated clodronate treatment and infected with LIC presented a higher bacterial burden, had reduced subacute nephritis and enhanced chronic kidney fibrosis relative to untreated, infected mice. Moreover, LIC infection in mice whose Gal-3 was disrupted (Lgals3-/-) had a higher bacterial burden and enhanced subacute nephritis and chronic kidney fibrosis when compared to C57BL/6J wild-type mice. Chronic fibrosis did not correlate with higher transcription levels of TGF-β1 or IL-13 in the kidneys. Kidney fibrosis was found in chronically infected rats as well as in wild infected rats. On the other hand, human fibroblast cultures exhibited enhanced differentiation to myofibroblasts after treatment with LIC. Our results demonstrate that macrophages and Gal-3 play a critical role in controlling the LIC burden but has a minor role in subsequent fibrosis. Instead, kidney fibrosis was better correlated with bacterial burden. Taken together, our results do not support a role for macrophages to disseminate leptospires during acute infection, nor in chronic kidney fibrosis.
Palabras clave: FIBROSIS , GALECTIN 3 , LEPTOSPIRA , MACROPHAGES , PATHOGENESIS
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info:eu-repo/semantics/openAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution 2.5 Unported (CC BY 2.5)
Identificadores
URI: http://hdl.handle.net/11336/96468
URL: https://www.frontiersin.org/article/10.3389/fcimb.2018.00384/full
DOI: http://dx.doi.org/10.3389/fcimb.2018.00384
Colecciones
Articulos(IBBM)
Articulos de INST.DE BIOTECNOLOGIA Y BIOLOGIA MOLECULAR
Articulos(IEGEBA)
Articulos de INSTITUTO DE ECOLOGIA, GENETICA Y EVOLUCION DE BS. AS
Articulos(IMEX)
Articulos de INST.DE MEDICINA EXPERIMENTAL
Articulos(SEDE CENTRAL)
Articulos de SEDE CENTRAL
Citación
Ferrer, Maria Florencia; Scharrig Fernandez, Maria Emilia; Charó, Nancy Lorena; Rípodas, Ana L.; Drut, Ricardo; et al.; Macrophages and Galectin 3 Control Bacterial Burden in Acute and Subacute Murine Leptospirosis That Determines Chronic Kidney Fibrosis; Frontiers Research Foundation; Frontiers in cellular and infection microbiology; 8; 384; 10-2018; 1-15
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