HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Baron, P. Articles by Scarlato, G. Search for Related Content PubMed PubMed Citation Articles by Baron, P. Articles by Scarlato, G. Related Collections All Immunology Muscle disease

Production of IL-6 by human myoblasts stimulated with Aß

Relevance in the pathogenesis of IBM

From the Department of Neurological Sciences, Centro Dino Ferrari, University of Milan School of Medicine, IRCCS Ospedale Maggiore, Milan, Italy.

Address correspondence and reprint requests to Dr. Pierluigi Baron, Department of Neurological Sciences, IRCCS Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122 Milan, Italy; e-mail: neuromil{at}mailserver.unimi.it

Objective:— To determine whether amyloid-ß protein (Aß) can induce the production of proinflammatory cytokines by cultured normal muscle cells.

Background:— Sporadic inclusion body myositis (IBM) is characterized by the presence of rimmed vacuoles and fibrillary inclusions of Aß in muscle fibers, and often inflammatory cells. Endomysial expression of proinflammatory molecules has suggested an ongoing immune process, but the site of sensitization and the mechanisms that trigger an inflammatory reaction is unknown.

Method:— The authors used Northern blot analysis and specific immunoassays to study the expression and secretion in cell-free supernatants of tumor necrosis factor- (TNF), interleukin-1ß (IL-1ß), and interleukin-6 (IL-6) by purified human myoblasts and C2C12 mouse skeletal muscle cells incubated with Aß[1-42] or Aß[25-35] peptides.

Results:— Nonstimulated muscle cells produced detectable IL-6, whereas secretion of IL-1ß and TNF was absent. Incubation with Aß peptides increased IL-6 production, whereas TNF and IL-1ß levels remained undetectable. Northern blot analysis of Aß-stimulated human myoblasts revealed an increase in IL-6 mRNA expression.

Conclusions:— Cultured muscle cells increase the constitutive production of IL-6 in response to local deposition of Aß in sporadic IBM. IL-6 could be a CD8⁺ proliferation and differentiation agent, an autocrine proteolysis-inducing factor of damaged myotubes, and a proliferation-stimulating agent for satellite cells to replace the destroyed myofibers in IBM.

This article has been cited by other articles:

				S. A Greenberg How citation distortions create unfounded authority: analysis of a citation network BMJ, July 23, 2009; 339(jul20_3): b2680 - b2680. [Abstract] [Full Text] [PDF]

				P. Arner Novel Target Genes for Catecholamines in Skeletal Muscle J. Clin. Endocrinol. Metab., May 1, 2004; 89(5): 1998 - 1999. [Full Text] [PDF]

				G. Luo, D. D. Hershko, B. W. Robb, C. J. Wray, and P.-O. Hasselgren IL-1beta stimulates IL-6 production in cultured skeletal muscle cells through activation of MAP kinase signaling pathway and NF-kappa B Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2003; 284(5): R1249 - R1254. [Abstract] [Full Text] [PDF]