New insights into cellular mechanisms during sepsis.
Despite intensive ongoing research efforts, the mortality of patients with sepsis remains unacceptably high. Clinical trials emerging from promising results in animal models have mostly failed to deliver sufficient treatment strategies so far. Many studies investigating the underlying mechanisms of sepsis have focused on deterioration of the humoral and cellular components of the immune system. However, in addition to septic shock, the main cause of death in septic patients is multiorgan failure. So far, not much is known about the effects of a dysregulated immune system as seen in sepsis on parenchymal cells of end organs. Studies on the interaction of the complement system and kidney as well as liver cells resulted in interesting yet still inconclusive data. In this review, we provide new insights into mechanisms during sepsis based on recent findings.
Hoesel
Laszlo M
LM
Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Gao
Hongwei
H
Ward
Peter A
PA
D000818:Animals; D003165:Complement System Proteins / Q000378:metabolism; D006321:Heart / Q000503:physiopathology; D006801:Humans; D032383:Myocytes, Cardiac / Q000276:immunology; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism; D044087:Receptor, Anaphylatoxin C5a / Q000378:metabolism; D018805:Sepsis / Q000276:immunology* / Q000378:metabolism* / Q000503:physiopathology; D018746:Systemic Inflammatory Response Syndrome / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology
D044087:Receptor, Anaphylatoxin C5a; D003165:Complement System Proteins