Immune modulation and sepsis.
The pathogenesis of sepsis involves not only microbial toxins but also activated host inflammatory mediators. Therefore, besides conventional antibiotic or surgical treatment of infection and supportive intensive therapy, modulating host inflammatory mediators as a conjunctive therapeutic option has been explored in the past decade. Although successful in animal models of sepsis, inhibiting host inflammatory response in human sepsis has failed to improve survival or otherwise show efficacy. Studies are needed which better describe the circumstances under which these therapies may ultimately prove successful.
Karzai
W
W
Department of Anaesthesiology and Intensive Care Therapy, University Hospital of Friedrich Schiller University, Jena, Germany.
Reinhart
K
K
D000276:Adjuvants, Immunologic / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D016207:Cytokines / Q000502:physiology*; D016179:Granulocyte Colony-Stimulating Factor / Q000627:therapeutic use; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology*; D007375:Interleukin-1 / Q000502:physiology; D010972:Platelet Activating Factor / Q000502:physiology; D011993:Recombinant Fusion Proteins / Q000627:therapeutic use; D011994:Recombinant Proteins / Q000627:therapeutic use; D018805:Sepsis / Q000209:etiology / Q000628:therapy*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D000276:Adjuvants, Immunologic; D000911:Antibodies, Monoclonal; D016207:Cytokines; D018836:Inflammation Mediators; D007375:Interleukin-1; D010972:Platelet Activating Factor; D011993:Recombinant Fusion Proteins; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D016179:Granulocyte Colony-Stimulating Factor