Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gram-positive bacteria have become the most common organisms responsible for the development of sepsis. Staphylococcus aureus (S. aureus) is the major gram-positive pathogen in both community-acquired and nosocomial infections. The Mortality associated with nosocomial infections caused by S. aureus may vary but are generally high. In the present study, we found that artesunate (AS) could protect mice against a lethal challenge with heat-killed S. aureus in a dose-dependent manner, and AS in combination with ampicillin sodium-sulbactam sodium (AMPS) could further increase survival of mice challenged with live S. aureus than AMPS alone. This protection was associated with reductions of serum at TNF-alpha level. In in vitro experiments, AS-pretreatment strongly inhibited TNF-alpha release from murine peritoneal macrophage induced by heat-killed S. aureus or peptidoglycan in a dose-dependent manner. AS reduced the Toll like receptor 2 (TLR2) and nucleotide-binding oligomerization domain containing 2 (Nod2) mRNA expressions up-regulated by heat-killed S. aureus and inhibited NF-kappaB activation induced by heat-killed S. aureus. In conclusion, our results demonstrated that AS-mediated protection on septic mice challenged with S. aureus was associated with its reduction on TNF-alpha release via inhibition of TLR2 and Nod2 mRNA expressions and transcription factor NF-kappaB activation.
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PMID:Artesunate protects sepsis model mice challenged with Staphylococcus aureus by decreasing TNF-alpha release via inhibition TLR2 and Nod2 mRNA expressions and transcription factor NF-kappaB activation. 2000 85

Genetic variants of the innate immune system contribute to episodes of spontaneous bacterial peritonitis (SBP) in patients with cirrhosis. We herein report the case of a patient with the homozygous nucleotide-binding oligomerization domain containing 2 (NOD2) frame-shift mutation 1007fs presenting with sepsis and community-acquired SBP by Escherichia coli. Secondary peritonitis, pancreatic ascites and malignant causes were excluded by extensive diagnostic work-up. First-line treatment with ceftriaxone was not successful despite in vitro sensitivity of the isolated strain. Despite prolonged second-line treatment with imipenem/cilastatin and intermittent ascites drainage, the ascitic fluid neutrophil count remained markedly elevated in this patient. In the course of the disease the patient developed pneumonia with identification of the typical hyphae of mucormycosis in the bronchoalveolar lavage and died of sepsis with multi-organ failure. On the basis of this observation, variants of the innate immunity have to be considered in therapy-refractory SBP, even when they are community-acquired and caused by cephalosporin-sensitive Enterobacteriaceae.
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PMID:Homozygous carrier of the NOD2 1007fs frame-shift mutation presenting with refractory community-acquired spontaneous bacterial peritonitis and developing fatal pulmonary mucormycosis: A case report. 2195 74