Ethanol prevents development of destructive arthritis

Research output: Contribution to journalArticle


Environmental factors are thought to play a major role in the development of rheumatoid arthritis. Because the use of ethanol is widespread, we assessed the role of ethanol intake on the propensity to develop chronic arthritis. Collagen type II-immunized mice were given water or water containing 10% (vol/vol) ethanol or its metabolite acetaldehyde. Their development of arthritis was assessed, as well as the impact of ethanol on leukocyte migration and activation of intracellular transcription factors. Mice exposed daily to this dose of ethanol did not display any liver toxicity, and the development of erosive arthritis was almost totally abrogated. In contrast, the anti body-mediated effector phase of collagen-induced arthritis was not influenced by ethanol exposure. Also, the major ethanol metabolite, acetaldehyde, prevented the development of arthritis. This antiinflammatory and antidestructive property of ethanol was mediated by (i) down-regulation of leukocyte migration and (ii) up-regulation of testosterone secretion, with the latter leading to decreased NF-kappa B activation. We conclude that low but persistent ethanol consumption delays the onset and halts the progression of collagen-induced arthritis by interaction with innate immune responsiveness.


  • Ing-Marie Jonsson
  • Margareta Verdrengh
  • Mikael Brisslert
  • Sofia Lindblad
  • Maria Bokarewa
  • Ulrika Islander
  • Hans Carlsten
  • Claes Ohlsson
  • Kutty Selva Nandakumar
  • Rikard Holmdahl
  • Andrej Tarkowski
Research areas and keywords

Subject classification (UKÄ) – MANDATORY

  • Immunology in the medical area


  • antibodies, sex hormones, inflammation, cytokines, immunity
Original languageEnglish
Pages (from-to)258-263
JournalProceedings of the National Academy of Sciences
Issue number1
Publication statusPublished - 2007
Publication categoryResearch

Bibliographic note

The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Medical Inflammation Research (013212019)