Mediators of inflammation
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Mediators of inflammation · Jan 2013
NF-κB inhibition after cecal ligation and puncture reduces sepsis-associated lung injury without altering bacterial host defense.
Since the NF-κB pathway regulates both inflammation and host defense, it is uncertain whether interventions targeting NF-κB would be beneficial in sepsis. Based on the kinetics of the innate immune response, we postulated that selective NF-κB inhibition during a defined time period after the onset of sepsis would reduce acute lung injury without compromising bacterial host defense. ⋯ Transiently blocking NF-κB activity after the onset of CLP-induced sepsis can effectively reduce acute lung injury in mice without compromising bacterial host defense or survival after CLP.
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Mediators of inflammation · Jan 2013
Heavy ethanol intoxication increases proinflammatory cytokines and aggravates hemorrhagic shock-induced organ damage in rats.
Hemorrhagic shock (HS) following acute alcohol intoxication can increase proinflammatory cytokine production and induce marked immunosuppression. We investigated the effects of ethanol on physiopathology and cytokine levels following HS in acutely alcohol-intoxicated rats. Rats received an intravenous injection of 5 g/kg ethanol over 3 h followed by HS induced by withdrawal of 40% of total blood volume from a femoral arterial catheter over 30 min. ⋯ HS significantly increased HR, blood GOT, GPT, BUN, Cre, LDH, CPK, TNF- α , and IL-6 levels and decreased hemoglobin and MAP in rats. Acute ethanol intoxication further increased serum levels of GOT, GPT, BUN, Cre, LDH, CPK, TNF- α and IL-6 elevation following HS. Acutely intoxicated rats exacerbated the histopathologic changes in the liver, kidneys, and lungs following HS.
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Mediators of inflammation · Jan 2013
Impact of the body mass on complications and outcome in multiple trauma patients: what does the weight weigh?
Obesity is known as an independent risk factor for various morbidities. The influence of an increased body mass index (BMI) on morbidity and mortality in critically injured patients has been investigated with conflicting results. To verify the impact of weight disorders in multiple traumatized patients, 586 patients with an injury severity score >16 points treated at a level I trauma center between 2005 and 2011 were differentiated according to the BMI and analyzed regarding morbidity and outcome. ⋯ In brief, obesity was the highest risk factor for development of a multiple organ dysfunction syndrome (MODS) (OR 4.209, 95%-CI 1.515-11.692) besides injury severity (OR 1.054, 95%-CI 1.020-1.089) and APACHE II score (OR 1.059, 95%-CI 1.001-1.121). In obese patients as compared to those with overweight, normal weight, and underweight, the highest levels of CRP were continuously present while increased systemic IL-6 levels were found until day 4. In conclusion, an altered posttraumatic inflammatory response in obese patients seems to determine the risk for multiple organ failure after severe trauma.
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Mediators of inflammation · Jan 2013
Intoxication by intraperitoneal injection or oral gavage equally potentiates postburn organ damage and inflammation.
The increasing prevalence of binge drinking and its association with trauma necessitate accurate animal models to examine the impact of intoxication on the response and outcome to injuries such as burn. While much research has focused on the effect of alcohol dose and duration on the subsequent inflammatory parameters following burn, little evidence exists on the effect of the route of alcohol administration. We examined the degree to which intoxication before burn injury causes systemic inflammation when ethanol is given by intraperitoneal (i.p.) injection or oral gavage. ⋯ We also found a similar hematologic response and levels of circulating interleukin-6 (IL-6) when either ethanol paradigm achieved intoxication before burn. Furthermore, both i.p. and gavage resulted in similar blood alcohol concentrations at all time points tested. Overall, our data show an equal inflammatory response to burn injury when intoxication is achieved by either i.p. injection or oral gavage, suggesting that findings from studies using either ethanol paradigm are directly comparable.
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Mediators of inflammation · Jan 2013
Protective effects of necrostatin-1 against concanavalin A-induced acute hepatic injury in mice.
Necrostatin-1 (Nec-1) inhibits receptor-interacting protein 1 (RIP1) kinase and programmed necrosis. This study was designed to examine the protective effects and mechanisms of Nec-1 in concanavalin A- (ConA-) induced hepatitis in mice. ⋯ These results demonstrate that Nec-1 prevents ConA-induced liver injury via RIP1-related and autophagy-related pathways.