Abstract
Immune cells and oxidative stress in the endotoxin tolerance mouse model
Highlights
Lipopolysaccharide (LPS) is one of the most potent known inducers of inflammation and exerts its effects via the Toll-like receptor (TLR) 4, which is essential for the recognition of distinct bacterial cell wall components [1,2,3]
Inhibition of TLR signaling by inducible negative regulators, anti-inflammatory cytokines and alterations in the TLR signaling complex has been attributed to the phenomenon of “LPS tolerance” [1]
A murine model of endotoxin tolerance offers an in vivo system for analyzing the regulatory feedback mechanisms involved in cytokine synthesis [5]
Summary
Lipopolysaccharide (LPS) is one of the most potent known inducers of inflammation and exerts its effects via the Toll-like receptor (TLR) 4, which is essential for the recognition of distinct bacterial cell wall components [1,2,3]. The assumption that LPS tolerance is caused by a “generalized” down-regulation of cellular responses and mediator release is not accurate [4,6]. A similar loss of LPS reactivity has been repeatedly reported in circulating leukocytes of septic patients [4,7]. Studies of cellular signaling within leukocytes from septic patients have revealed numerous alterations similar to those observed in endotoxin-tolerant cells [4,7]. The altered responsiveness to LPS of leukocytes from septic patients is not synonymous with LPS tolerance. Tolerance to LPS has been shown to protect against bacterial infections; it is a model of an adequate immune response in contrast to the deadly dysregulation of immune function in sepsis [4]. Monophosphoryl lipid A has been used to produce tolerance and has been shown to protect animals
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Brazilian Journal of Medical and Biological Research
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
