title: TLR signaling pathway in patients with sepsis.
abstract: The pathogenesis of sepsis involves complex interaction between the host and the infecting microorganism. Bacterial recognition and signaling are essential functions of the cells of innate immune systems and drive a coordinated immune response. One of the more intriguing aspects of sepsis is the fact that the protective and damaging host response are part of the same process, that is, the inflammatory response that is aimed to control the infectious process also underscores many of the pathophysiological events of sepsis. The discovery of Toll-like receptors (TLRs) in humans, and the early recognition of TLR-4 as the receptor that signals LPS bioactivity were major breakthroughs not only in the field of sepsis but also in immunology as a whole. In this article, we aimed to review TLR expression and signaling in the context of sepsis. The results obtained by our group show that TLR and other cellular surface receptors may be differently regulated on mononuclear cells and neutrophils, and that they are dynamically modulated across the stages of sepsis. Toll-like receptor signaling gene expression in mononuclear cells is decreased in more severe forms of the disease. In contrast, up-regulated genes are seen along the clinical spectrum of sepsis in neutrophils.
authors.forename: Reinaldo
authors.initials: R
authors.lastname: Salomão
authors.forename: Paulo Sérgio
authors.initials: PS
authors.lastname: Martins
authors.forename: Milena Karina Colo
authors.initials: MK
authors.lastname: Brunialti
authors.forename: Maria da Luz
authors.initials: Mda L
authors.lastname: Fernandes
authors.forename: Leandro S W
authors.initials: LS
authors.lastname: Martos
authors.forename: Marialice Erdelyi
authors.initials: ME
authors.lastname: Mendes
authors.forename: Natália E
authors.initials: NE
authors.lastname: Gomes
authors.forename: Otelo
authors.initials: O
authors.lastname: Rigato
mesh_terms: D002462:Cell Membrane / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D007249:Inflammation; D008070:Lipopolysaccharides / Q000378:metabolism; D008954:Models, Biological; D009000:Monocytes / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D018805:Sepsis / Q000097:blood / Q000276:immunology* / Q000378:metabolism*; D012772:Shock, Septic / Q000097:blood / Q000276:immunology* / Q000378:metabolism*; D015398:Signal Transduction; D051197:Toll-Like Receptor 4 / Q000276:immunology / Q000378:metabolism; D051193:Toll-Like Receptors / Q000378:metabolism*
chemical_list: D008070:Lipopolysaccharides; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors