title: Septic encephalopathy: inflammation in man and mouse.
abstract: Septic encephalopathy is a frequent complication of the sepsis syndrome, with no therapies available that can prevent the associated neurological dysfunction in humans. It is caused by a number of processes and networks going awry, the exact cellular and molecular mechanisms of which remain an enigma. Several mediators of inflammation have been assigned a key role in sepsis, including cytokines, chemokines and complement cascade. With the observations that brain dysfunction in a sepsis setting can be alleviated by regulation of the cytokines and complement proteins in various species of animals, optimism is building for a possible therapy of sepsis-damaged brain. This article reviewed the advances in the understanding of the underlying mechanisms causing pathology in SE, with an emphasis on the inflammatory and excitatory mediators such as the cytokines, complement proteins and neurotransmitters, investigating their potential as possible therapeutic targets.
authors.affiliation: Department of Medicine, University of Chicago, Chicago, IL 60637, USA. jalexand@medicine.bsd.uchicago.edu
authors.forename: Alexander
authors.initials: A
authors.lastname: Jacob
authors.forename: James R
authors.initials: JR
authors.lastname: Brorson
authors.forename: Jessy J
authors.initials: JJ
authors.lastname: Alexander
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier; D003165:Complement System Proteins / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004660:Encephalitis / Q000209:etiology* / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D051379:Mice; D018377:Neurotransmitter Agents / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D018805:Sepsis / Q000150:complications* / Q000378:metabolism
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D018377:Neurotransmitter Agents; D009569:Nitric Oxide; D003165:Complement System Proteins