Immune depression in musculoskeletal trauma

Inflamm Res. 2010 Jun;59(6):409-14. doi: 10.1007/s00011-010-0167-7. Epub 2010 Feb 11.


The immune responses after musculoskeletal trauma are physiological reactions of the organism to restore homeostasis. An imbalance between the early systemic inflammatory response syndrome and the later compensatory anti-inflammatory response syndrome may be responsible for organ dysfunction and increased susceptibility to infections. Cytokines are known to be integral components of the immune response, and the balance or imbalance of the different cytokines partly controls the clinical course in the patients. The major pro-inflammatory cytokines include tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), IL-6, and IL-8. These cytokines are predominantly produced by monocytes and macrophages, they mediate overlapping effects, and their actions can be additive. TNF-alpha and IL-1beta are early regulators of the immune response, and both induce the release of secondary pro-inflammatory cytokines. IL-10 is an anti-inflammatory cytokine which reduces the synthesis of pro-inflammatory mediators. The extent of traumatic damage correlates with the immunological changes and determines a graded depression of leucocytes to express cytokines on edotoxin exposure. Correspondingly, it has become clinically evident that in unstable traumatised patients, the recommendation today is damage control orthopaedics, i.e. initial stabilisation of long bone fractures by external fixation followed by definitive stabilisation at about 1 week.

Publication types

  • Review

MeSH terms

  • Animals
  • Endotoxins / toxicity
  • Humans
  • Immune System / physiology
  • Inflammation / immunology
  • Inflammation / pathology
  • Musculoskeletal System / immunology*
  • Musculoskeletal System / injuries*
  • Wounds and Injuries / immunology*


  • Endotoxins