Quoted message said:Subject: New Pain Therapy
From: [email hidden] (doe)
Date: 12/24/2003 1:27 PM Mountain Standard Time
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New Pain Therapy Reverses Glial Activation
By medinews.com staff writers Posted on 17 December 2003
Researchers believe that delivering the gene for interleukin-10 (IL-10) to the affected region may
reverse glial activation and relieve chronic pain. Their findings from a number of studies showing
proof of principle were presented at the annual meeting of the Society of Neuroscience in New
Orleans (LA, USA).
Glial cells have an important role in pain. When they are activated in response to nerve damage,
tumors, or viruses, they produce increased levels of substances that enhance the neuron’s
response to pain signals. These substances then activate other glia. When a critical level is
reached, it produces a self-perpetuating feedback loop that can continue even after the original
cause of pain has been resolved. The researchers have focused on the effectiveness of the
powerful, naturally occurring anti-inflammatory protein IL-10 to block or reverse glial
activation. Studies in rats have demonstrated that it can prevent or reverse every enhanced pain
state examined to date.
“A new model for the etiology of chronic pain is quickly emerging as researchers around the world
are developing a better understanding of the underlying causes of chronic pain,†said Linda
Watkins, Ph.D., professor in the department of psychology and the Center for Neuroscience at the
University of Colorado at Boulder (USA; www.colorado.edu) and co-author of a paper published in the
December 1, 2003, issue of Nature Reviews Drug Discovery.
Dr.Watkins and colleagues are working with Avigen, Inc. (San Francisco, CA, USA) on the development
of a new pain treatment.
Seems like it works DUE TO sequestering of .. iron.
J Immunol. 2002 Aug 15;169(4):2204-9. Related Articles, Links
Role of IL-10 for induction of anemia during inflammation.
Tilg H, Ulmer H, Kaser A, Weiss G.
Division of Gastroenterology and Hepatology, Department of Medicine, University Hospital Innsbruck,
Innsbruck, Austria.
Anemia is frequently observed in patients suffering from chronic inflammatory disorders. Recent in
vitro data suggest that Th2 cytokines, such as IL-10, could be involved in its pathogenesis. We
analyzed 1) changes in hemoglobin values in 329 patients with chronic active Crohn's disease
receiving the anti-inflammatory cytokine IL-10 as part of a randomized, double-blind, placebo-
controlled study, 2) serum iron parameters in a subgroup of these patients (n = 54), and 3) the in
vitro effects of IL-10 on ferritin transcription and translation in human monocytic cells (THP-1) by
means of Northern blot and immunoprecipitation after metabolic labeling. Patients receiving higher
doses of IL-10 developed anemia and presented with a dose-dependent increase of ferritin and soluble
transferrin receptor levels, an indicator of iron restriction to erythroid progenitor cells.
According to our in vitro data, hyperferritinemia may result from direct stimulation of ferritin
translation by IL-10 in activated monocytic cells, most likely by cytokine-mediated reduction of the
binding affinity of translational repressors, iron-regulatory proteins, to the 5'-untranslated
region of ferritin mRNA. In patients, all observed changes were most pronounced at the end of
therapy (day +29), and thereafter hemoglobin levels and serum iron parameters returned to baseline
levels within 4 wk of follow-up. Our data demonstrate that IL-10 causes anemia in patients with
inflammatory bowel disease which may be referred to the induction of imbalances in iron homeostasis
by the cytokine, leading to hyperferritinemia and limited iron availability to erythroid progenitor
cells, a condition typically seen in the anemia of chronic inflammation.
Publication Types: Clinical Trial Multicenter Study Randomized Controlled Trial
PMID: 12165551 [PubMed - indexed for MEDLINE]
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