Parecoxib does not suppress thromboxane synthesis in newborn piglets with group B streptococcal sepsis

Nögel, S; Chada, Martin; Schmidt, Ana-Marija; Bosselmann, S; Kandler, Michael Andreas; Schweer, Horst; Watzer, Bernhard; Schneider, Holm; Gessner, André; Rascher, Wolfgang

doi:10.1016/j.prostaglandins.2009.06.003

Cited by 3 publications

(4 citation statements)

References 17 publications

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“…In total, the studies identified for this paper demonstrated that COX inhibition, and genetic COX-2 deletion [12], improved survival in 21 of 29 studies (72.4%) [3, 7, 9, 11, 12, 14, 18–21, 24, 27, 32, 34, 37, 39, 40, 42, 44, 45], caused no change in survival in 7 studies (24.3%) [15, 23, 33, 38, 43, 46, 47], and reduced survival in a single mouse study (3.4%) [35]. …”

Section: Resultsmentioning

confidence: 99%

“…The models of sepsis used in these studies included three mouse CLP studies [46, 53, 60], three rat studies involving the introduction of feces into the peritoneal cavity [49, 57, 61], two rat studies using systemic infection with live E. coli [48, 57], one rat study with systemic infection with live Group B Streptococcus [58], two canine studies with systemic infection with live E. coli [50, 51], three porcine studies with systemic infection with live Group B Streptococcus [47, 56, 59], one mouse study with systemic infection with live Vibrio vulnificus [55], one mouse study using live Group A Streptococcus [54], and one sheep study of infection with live E. coli [48]. …”

Section: Resultsmentioning

confidence: 99%

“…This included one of the two COX-2 knockout mouse studies [54]. Two studies showed no effect on mortality of COX inhibition [46, 47] and two mouse studies revealed increased death in either COX-inhibitor-treated mice [55] or a COX-2 knockout mouse model [53]. …”

Section: Resultsmentioning

confidence: 99%

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Cyclooxygenase Inhibition in Sepsis: Is There Life after Death?

Aronoff

2012

Mediators of Inflammation

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Prostaglandins are important mediators and modulators of the inflammatory response to infection. The prostaglandins participate in the pathogenesis of hemodynamic collapse, organ failure, and overwhelming inflammation that characterize severe sepsis and shock. In light of this, cyclooxygenase (COX) inhibiting pharmacological agents have been extensively studied for their capacity to ameliorate the aberrant physiological and immune responses during severe sepsis. Animal models of sepsis, using the systemic administration of pathogen-associated molecular patterns (PAMPs) or live pathogens, have been used to examine the effectiveness of COX inhibition as a treatment for severe sepsis. These studies have largely shown beneficial effects on mortality. However, human studies have failed to show clinical utility of COX inhibitor treatment in severely septic patients. Why this approach “worked” in animals but not in humans might reflect differences in the controlled nature of animal investigations compared to human studies. This paper contrasts the impact of COX inhibitors on mortality in animal models of sepsis and human studies of sepsis and examines potential reasons for differences between these two settings.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Cyclooxygenase Inhibition in Sepsis: Is There Life after Death?

Aronoff

2012

Mediators of Inflammation

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“…Attention to the dosage regimen may be useful because Nögel and colleagues reported that a single dose of indomethacin administered 2 hr after infusion of GBS in piglets did not prevent death of the animals at 12–16 h, although it did lower the pulmonary artery pressure in the 2 h following administration. 22 Identification of the receptors and pathways which are activated by phosphatidylglycerol and cardiolipin may identify specific targets for therapeutic interventions.…”

Section: Discussionmentioning

confidence: 99%

Group B Streptococcus, phospholipids and pulmonary hypertension

et al. 2011

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Group B streptococcus is the most common cause of bacterial infection in the newborn. Infection in many cases causes persistent pulmonary hypertension which impairs gas exchange in the lung. We purified the bacterial components causing pulmonary hypertension and showed that they are the phospholipids cardiolipin and phosphatidylglycerol. Synthetic cardiolipin or phosphatidylglycerol also induced pulmonary hypertension in lambs. The recognition that bacterial phospholipids may cause pulmonary hypertension in newborns with Group B streptococcal infection opens new avenues for therapeutic intervention and generates hypotheses concerning the etiology of respiratory distress in the newborn and the possible effect of antibiotic therapy.

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Bench-to-bedside review: Neonatal sepsis - redox processes in pathogenesis

Spasojević

Obradović²,

Spasić

2012

Crit Care

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The present review is aimed at elucidating the neonatal 'sepsis redox cycle' - the cascade of inflammatory and redox events involved in the pathogenesis of sepsis in neonates. While adult and neonatal sepses share some common features, there are some substantial differences: higher mortality rates occur in adult sepsis and worse long-term effects are evident in neonatal sepsis survivors. Such epidemiological data may be explained by the lower ability of IL6 and IL8 to activate NF-κB-regulated transcription in neonatal sepsis in comparison to TNF-α, which is involved in the mechanisms of adult sepsis. The activation of NF-κB in neonatal sepsis is further promoted by hydrogen peroxide and results in mitochondrial dysfunction and energy failure as septic neonates experience decreased O2 consumption as well as lower heat production and body temperature in comparison to healthy peers. In neonates, specific organs that are still under development are vulnerable to sepsis-provoked stress, which may lead to brain, lung, and heart injury, as well as vision and hearing impairments. In the light of the processes integrated here, it is clear that therapeutic approaches should also target specific steps in the neonatal 'sepsis redox cycle' in addition to the current therapeutic approach that is mainly focused on pathogen eradication.

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Parecoxib does not suppress thromboxane synthesis in newborn piglets with group B streptococcal sepsis

Cited by 3 publications

References 17 publications

Cyclooxygenase Inhibition in Sepsis: Is There Life after Death?

Cyclooxygenase Inhibition in Sepsis: Is There Life after Death?

Group B Streptococcus, phospholipids and pulmonary hypertension

Bench-to-bedside review: Neonatal sepsis - redox processes in pathogenesis

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