Mediators of inflammation
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Mediators of inflammation · Jan 2013
PD-L1 blockade attenuated sepsis-induced liver injury in a mouse cecal ligation and puncture model.
Liver plays a major role in hypermetabolism and produces acute phase proteins during systemic inflammatory response syndrome and it is of vital importance in host defense and bacteria clearance. Our previous studies indicated that programmed death-1 (PD-1) and its ligand programmed death ligand-1 (PD-L1) are crucial modulators of host immune responses during sepsis. Our current study was designed to investigate the role of PD-L1 in sepsis-induced liver injury by a mouse cecal ligation and puncture (CLP) model. ⋯ Anti-PD-L1 antibody significantly alleviated the morphology of liver injury in CLP mice. Anti-PD-L1 antibody administration decreased ALT and AST release in CLP mice, decreased the levels of tumor necrosis factor (TNF)-α , interleukin (IL)-6, and IL-10 mRNA in liver after sepsis challenge. Thus, anti-PD-L1 antibody might have a therapeutic potential in attenuating liver injury in sepsis.
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Mediators of inflammation · Jan 2013
Relationships of adiponectin with markers of systemic inflammation and insulin resistance in infants undergoing open cardiac surgery.
Insulin resistance and systemic inflammation frequently occur in infants undergoing cardiac surgery with cardiopulmonary bypass, while adiponectin has been demonstrated to have insulin-sensitizing and anti-inflammatory properties in obesity and type 2 diabetes mellitus. In this prospective study, we aimed to investigate the association of adiponectin with insulin resistance and inflammatory mediators in infants undergoing cardiac surgery with cardiopulmonary bypass. ⋯ Although the level of serum adiponectin decreased significantly, there was a significant inverse association of adiponectin with markers of systemic inflammation and insulin resistance in infants undergoing open cardiac surgery.
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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
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.