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Plos One : Galectin-3 Functions as an Alarmin ; Pathogenic Role for Sepsis Development in Murine Respiratory Tularemia, Volume 8

By Alves-filho, Carlos, Jose

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Book Id: WPLBN0003948820
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Reproduction Date: 2015

Title: Plos One : Galectin-3 Functions as an Alarmin ; Pathogenic Role for Sepsis Development in Murine Respiratory Tularemia, Volume 8  
Author: Alves-filho, Carlos, Jose
Volume: Volume 8
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection (Contemporary)
Historic
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Publisher: Plos

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Alves-Filho, C. J. (n.d.). Plos One : Galectin-3 Functions as an Alarmin ; Pathogenic Role for Sepsis Development in Murine Respiratory Tularemia, Volume 8. Retrieved from http://netlibrary.net/


Description
Description : Sepsis is a complex immune disorder with a mortality rate of 20–50% and currently has no therapeutic interventions. It is thus critical to identify and characterize molecules/factors responsible for its development. We have recently shown that pulmonary infection with Francisella results in sepsis development. As extensive cell death is a prominent feature of sepsis, we hypothesized that host endogenous molecules called alarmins released from dead or dying host cells cause a hyperinflammatory response culminating in sepsis development. In the current study we investigated the role of galectin- 3, a mammalian b-galactoside binding lectin, as an alarmin in sepsis development during F. novicida infection. We observed an upregulated expression and extracellular release of galectin-3 in the lungs of mice undergoing lethal pulmonary infection with virulent strain of F. novicida but not in those infected with a non-lethal, attenuated strain of the bacteria. In comparison with their wild-type C57Bl/6 counterparts, F. novicida infected galectin-3 deficient (galectin-32/2) mice demonstrated significantly reduced leukocyte infiltration, particularly neutrophils in their lungs. They also exhibited a marked decrease in inflammatory cytokines, vascular injury markers, and neutrophil-associated inflammatory mediators. Concomitantly, in-vitro pre-treatment of primary neutrophils and macrophages with recombinant galectin-3 augmented F. novicida-induced activation of these cells. Correlating with the reduced inflammatory response, F. novicida infected galectin- 32/2 mice exhibited improved lung architecture with reduced cell death and improved survival over wild-type mice, despite similar bacterial burden. Collectively, these findings suggest that galectin-3 functions as an alarmin by augmenting the inflammatory response in sepsis development during pulmonary F. novicida infection.

 

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