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How Inflammatory Disease Causes Fatigue

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  • scarletpaolicchi
    http://www.sciencedaily.com/ releases/ 2009/02/09021717 3034.htm How Inflammatory Disease Causes Fatigue ScienceDaily (Feb. 28, 2009) - New animal research in
    Message 1 of 1 , Mar 6, 2009
      http://www.sciencedaily.com/ releases/ 2009/02/09021717 3034.htm

      How Inflammatory Disease Causes Fatigue

      ScienceDaily (Feb. 28, 2009) - New animal research in the February 18 issue of
      The Journal of Neuroscience may indicate how certain diseases make people feel
      so tired and listless. Although the brain is usually isolated from the immune
      system, the study suggests that certain behavioral changes suffered by those
      with chronic inflammatory diseases are caused by the infiltration of immune
      cells into the brain. The findings suggest possible new treatment avenues to
      improve patients' quality of life.

      Chronic inflammatory diseases like rheumatoid arthritis, inflammatory bowel
      disease, psoriasis, and liver disease cause "sickness behaviors," including
      fatigue, malaise, and loss of social interest. However, it has been unclear how
      inflammation in other organs in the body can impact the brain and behavior.
      The researchers found that in mice with inflamed livers, white blood cells
      called monocytes infiltrated the brain. These findings support previous research
      demonstrating the presence of immune cells in the brain following organ
      inflammation, challenging the long-held belief that the blood-brain barrier
      prevents immune cells from accessing the brain.
      "Using an experimental model of liver inflammation, our group has demonstrated
      for the first time the existence of a novel communication pathway between the
      inflamed liver and the brain," said the study's senior author Mark Swain, MD,
      Professor of Medicine at the University of Calgary.
      Swain and his colleagues found that liver inflammation triggered brain cells
      called microglia to produce CCL2, a chemical that attracts monocytes. When the
      researchers blocked CCL2 signaling, monocytes did not enter the brain despite
      ongoing inflammation in the liver.
      Liver inflammation also stimulated cells in the blood to make an immune chemical
      (TNFá). When the researchers blocked the signaling of this immune chemical,
      microglia produced less CCL2, and monocytes stayed out of the brain.
      In the mice with inflamed livers, preventing the entry of monocytes into the
      brain reduced sickness behaviors; mice showed more mobility and social
      interaction. These findings suggest that people with chronic inflammatory
      diseases may benefit from treatments that limit monocyte access to the brain.
      "Sickness behavior significantly impacts quality of life. Our findings further
      our understanding and may generate potential new avenues for treatment of these
      often crippling symptoms," said Swain.
      "The brain is the master coordinator of many of our bodies' defense responses,
      so it must be able to sense injury and inflammation in distant body organs. This
      study starts to explain the peripheral communication signals that activate the
      brain," said Nancy Rothwell, PhD, DSc, at the University of Manchester, an
      expert on brain inflammation who is unaffiliated with the study.
      The research was supported by the Canadian Institutes of Health Research, the
      Canadian Liver Foundation, and the Alberta Heritage Foundation for Medical

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      Adapted from materials provided by Society for Neuroscience, via EurekAlert!, a
      service of AAAS.

      Best Wishes,
      Alternative Treatments for Hepatitis C
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