Título Gal3 Plays a Deleterious Role in a Mouse Model of Endotoxemia
Autores Fernandez-Martin, Juan Carlos , Espinosa-Oliva, Ana Maria , GARCÍA DOMÍNGUEZ, IRENE, Rosado-Sanchez, Isaac , Pacheco, Yolanda M. , Moyano, Rosario , Monterde, Jose G. , Venero, Jose Luis , de Pablos, Rocio M.
Publicación externa Si
Medio INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Alcance Article
Naturaleza Científica
Cuartil JCR 1
Cuartil SJR 1
Impacto JCR 5.6
Impacto SJR 1.154
Fecha de publicacion 01/02/2022
ISI 000759366900001
DOI 10.3390/ijms23031170
Abstract Lipopolysaccharide (LPS)-induced endotoxemia induces an acute systemic inflammatory response that mimics some important features of sepsis, the disease with the highest mortality rate worldwide. In this work, we have analyzed a murine model of endotoxemia based on a single intraperitoneal injection of 5 mg/kg of LPS. We took advantage of galectin-3 (Gal3) knockout mice and found that the absence of Gal3 decreased the mortality rate oflethal endotoxemia in the first 80 h after the administration of LPS, along with a reduction in the tissular damage in several organs measured by electron microscopy. Using flow cytometry, we demonstrated that, in control conditions, peripheral immune cells, especially monocytes, exhibited high levels of Gal3, which were early depleted in response to LPS injection, thus suggesting Gal3 release under endotoxemia conditions. However, serum levels of Gal3 early decreased in response to LPS challenge (1 h), an indication that Gal3 may be extravasated to peripheral organs. Indeed, analysis of Gal3 in peripheral organs revealed a robust up-regulation of Gal3 36 h after LPS injection. Taken together, these results demonstrate the important role that Gal3 could play in the development of systemic inflammation, a well-established feature of sepsis, thus opening new and promising therapeutic options for these harmful conditions.
Palabras clave endotoxemia; galectin-3; lipopolysaccharide; electron microscopy; sepsis
Miembros de la Universidad Loyola

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