TREM-1 in sepsis

It has been long been recognised that sepsis is characterised by a dysregulated host response to microbial components, such as lipopolysaccharide (in the case of gram-negative bacteria) and peptidoglycan or extracellular toxins (from gram-positive bacteria). Neutrophils and monocyte/macrophages exposed to lipopolysaccharide, for instance, are activated and release proinflammatory cytokines, such as tumour-necrosis factor (TNF) α and interleukin-1β. Excessive production of these cytokines is widely believed to contribute to the multiorgan failure that is seen in septic patients. 1 Sriskandan S Cohen J The pathogenesis of septic shock. J Infect. 1995; 30: 201-206 Summary Full Text PDF PubMed Scopus (41) Google Scholar , 2 Dinarello CA Proinflammatory and anti-inflammatory cytokines as mediators in the pathogenesis of septic shock. Chest. 1997; 112: 321S-329S Summary Full Text Full Text PDF PubMed Scopus (414) Google Scholar However, until recently little was known of the mechanism that linked bacteria on the outside of the cell with transcription of genes for cytokines in the cell nucleus. Triggering receptor expressed on myeloid cells (TREM)-1 is the most recent of a series of discoveries that have begun to open this particular black box.