Prior burn insult induces lethal acute lung injury in endotoxemic mice: effects of cytokine inhibition

Abstract

oki Aikawa. Prior burn insult induces lethal acute lung injury in endotoxemic mice: effects of cytokine inhibition. Am

Effect of Aspiration Pneumonia-Induced Sepsis on Post-Burn Cardiac Inflammation and Function in Mice

“…Infectious challenge seven days after burn injury exaggerated the myocyte cytokine responses seen with sepsis in the absence of burn injury and exacerbated the myocardial contraction and relaxation deficits compared with that seen in sepsis alone. These data are consistent with previous reports that an initial burn insult compromises immune responses, worsening organ dysfunction following a second insult [24,25]. These murine data also are consistent with our previous finding that burn complicated by sepsis in a rat model exaggerated cardiopulmonary dysfunction over that seen in burn injury alone [12][13][14] and support previous reports that a second insult, such as sepsis, that occurs after major trauma promotes multiple organ failure and increases mortality [24,26,27].…”

Suppression of MAPK and NF-κB Pathways by Limonene Contributes to Attenuation of Lipopolysaccharide-Induced Inflammatory Responses in Acute Lung Injury

“…Both TNF-α and IL-6 induce adhesion molecule expression in vascular endothelial cells, resulting in recruitment of leukocytes into the inflammatory site [32]. Since cytokines have been considered as therapeutic targets for LPS-induced ALI, many treatments have had inhibitory effects on the gene expression of cytokines in the lung [33]. Therefore, TNF-α, IL-1β, and IL-6 served as predictive markers for ALI severity.…”

Naringin attenuates acute lung injury in LPS-treated mice by inhibiting NF-κB pathway

“…ALI patients had high BALF TNF-α levels and the level was significantly higher in non-survivors than survivors [37]. Cytokines have been considered as therapeutic targets for LPS-induced ALI and many treatments have had inhibitory effects on the gene expression of cytokines in the lung (i.e., glucocorticoids) [38]. LPS triggers monocytes and macrophages to produce several inflammatory cytokines and mediators as well as biological mediators involved in the control of pathogens.…”