Essential role for IL-6 in postresuscitation inflammation in hemorrhagic shock

Zhi Hong Meng, Kevin Dyer, Timothy R. Billiar, David J. Tweardy*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

114 Scopus citations


Interleukin-6 (IL-6) is produced within multiple tissues and can be readily detected in the circulation in resuscitated hemorrhagic shock (HS). Instillation of IL-6 into lungs of normal rats induces polymorphonuclear neutrophilic granulocyte (PMN) infiltration and lung damage, while infusion of IL-6 into the systemic circulation of rats during resuscitation from HS reduces PMN recruitment and lung injury. The current study was designed to determine whether or not IL-6 makes an essential contribution to postresuscitation inflammation and which of the two effects of IL-6, its local proinflammatory effect or its systemic anti-inflammatory effect, is dominant in HS. Wild-type and IL-6-deficient mice were subjected to HS followed by resuscitation and death 4 h later. IL-6-deficient mice subjected to HS did not demonstrate any features of postresuscitation inflammation observed in wild-type mice, including increased PMN infiltration into the lungs, increased alveolar cross-sectional surface area, increased PMN infiltration into the liver, increased liver necrosis, increased signal transducer and activator of transcription 3 activation, and increased nuclear factor-κB activity. These findings indicate that IL-6 is an essential component of the postresuscitation inflammatory cascade in HS and that the local proinflammatory effects of IL-6 on PMN infiltration and organ damage in HS dominate over the anti-inflammatory effects of systemic IL-6.

Original languageEnglish
Pages (from-to)C343-C351
JournalAmerican Journal of Physiology - Cell Physiology
Issue number2 49-2
StatePublished - 2001
Externally publishedYes


  • Alveolar wall cross-sectional surface area
  • Focal liver necrosis
  • Interleukin-6
  • Myeloperoxidase
  • Neutrophils
  • Nuclear factor-κB
  • Signal transducers and activators of transcription proteins


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