Tumour Necrosis Factor Alpha (TNF‐α) and Interleukin 6 in a Zymosan‐Induced Shock Model

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<jats:p>TNF plays a central role in septic shock induced by endotoxin or Gram‐negative bacteria. Zymosan can elicit a septic shock‐like syndrome in rodents in the absence of endotoxin. TNF and IL‐6 release in mice treated with zymosan was investigated. One hour after intraperitoneal zymosan injection, maximal TNF levels were measured in serum, followed by IL‐6 peak levels 1 h later. Treatment with a monoclonal antibody against TNF lowered zymosan‐induced mortality from 63 to 11.6%, while maximal IL‐6 levels were lowered by about 40%.</jats:p><jats:p>Mechanisms triggering zymosan‐induced cytokine release in murine macrophages were analysed in vitro. Cytokine release was only slightly triggered by uncoated zymosan particles. Thirty‐nine per cent of TNF release by macrophages appeared to be triggered by zymosan‐bound activated complement. Maximal TNT release also required the presence of natural antibodies against zymosan and zymosan‐activated scrum. In contrast, maximal 11–6 release was reached upon stimulation with zymosan‐activated serum only, while the presence of zymosan particles lowered this response.</jats:p><jats:p>We conclude that TNF is a crucial mediator m zymosan‐induced shock. TNF release can be induced by different immunological pathways, without the need for the direct presence of endotoxins. Although IL‐6 release during septic shock is partly dependent on TNF. in vitro trigger mechanisms for IL‐6 and TNF differ remarkably.</jats:p>

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