Cachexia and the acute‐phase protein response in inflammation are regulated by interleukin‐6 Academic Article uri icon

Overview

MeSH Major

  • Acute-Phase Reaction
  • Cachexia
  • Inflammation
  • Interleukin-6

abstract

  • Cachexia and the acute-phase response are common manifestations of inflammation and are presumed to be the product of increased synthesis and release of cytokines, including tumor necrosis factor (TNF), interleukin-1 (IL-1) and interleukin-6 (IL-6). IL-1 receptor blockade has been previously shown to attenuate the weight loss, anorexia and acute-phase protein responses associated with a turpentine abscess. However, IL-1 receptor blockade was also associated with a reduced plasma IL-6 response, suggesting that the benefit achieved by IL-1 receptor blockade may be mediated by reduced systemic IL-6 production. To gain a better understanding of the role of IL-6 in this model of inflammation, C57BL/6 mice were passively immunized with either a monoclonal anti-IL-6 antibody (20F3), an anti-IL-1 type I receptor monoclonal antibody (35F5), a non-immune rat IgG, or a combined therapy of 35F5 and 20F3, before receiving a sterile turpentine abscess. IL-6 or IL-1 receptor blockade equally spared body weight and food intake. Compared to IL-1 receptor blockade, passive immunization against IL-6 further reduced the hepatic acute-phase protein response, as represented by serum amyloid P and complement 3. Combined blockade of IL-6 and IL-1 receptor did not result in a further sparing of body weights or improvement of food intake. These results confirm that IL-1 contributes to host cachexia and the acute-phase response following a turpentine abscess, but also show that these actions are dependent upon an IL-6 response. We conclude that the influence of IL-1 on cachexia and the acute-phase response is mediated, at least in part, through IL-6 and, thus, IL-6 may play a pivotal role in the cachexia and acute-phase response to inflammation.

publication date

  • January 1993

Research

keywords

  • Academic Article

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1002/eji.1830230824

PubMed ID

  • 8344351

Additional Document Info

start page

  • 1889

end page

  • 94

volume

  • 23

number

  • 8