Inflammatory response during sepsis is incompletely understood due to small sample sizes and variable timing of measurements following the onset of symptoms. This paper from the James Hogg Research Centre and Pulmonary & Critical Care Medicine at Stanford University looks at cytokines and signalling molecules in an attempt to predict clinical outcomes in Sepsis.
The research found a distinct pattern of cytokine levels measured early in the course of sepsis predicts disease outcome. Sub-populations of patients have differing clinical outcomes that can be predicted accurately from small numbers of cytokines. Design of clinical trials and interventions may benefit from consideration of cytokine levels.
The research found a distinct pattern of cytokine levels measured early in the course of sepsis predicts disease outcome. Sub-populations of patients have differing clinical outcomes that can be predicted accurately from small numbers of cytokines. Design of clinical trials and interventions may benefit from consideration of cytokine levels.
Ref: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0079207#ack
This paper from University of Würzburg looks at altered neonatal Toll-like receptor (TLR) function which is hypothesized to contribute to the heightened susceptibility to infection and perpetuated inflammation in term and preterm neonates, clinically evident in neonatal sepsis and increased rates of inflammatory disorders. Current data indicates that basal TLR expression in term neonates equals adult expression patterns, while expression in preterm infants seems to increase, depending on gestational age. Regarding TLR signaling, some studies suggest TLR incompetence in neonates associated with impaired pro-inflammatory responses, others describe neonatal TLR function well developed and allude to its hyper-inflammation tendency.
This paper from University of Würzburg looks at altered neonatal Toll-like receptor (TLR) function which is hypothesized to contribute to the heightened susceptibility to infection and perpetuated inflammation in term and preterm neonates, clinically evident in neonatal sepsis and increased rates of inflammatory disorders. Current data indicates that basal TLR expression in term neonates equals adult expression patterns, while expression in preterm infants seems to increase, depending on gestational age. Regarding TLR signaling, some studies suggest TLR incompetence in neonates associated with impaired pro-inflammatory responses, others describe neonatal TLR function well developed and allude to its hyper-inflammation tendency.
