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NEUROLOGY 1998;51:1661-1665
© 1998 American Academy of Neurology

Inflammatory cytokines inhibit upregulation of glycolipid expression by Schwann cells in vitro

Robert P. Lisak, MD, Beverly Bealmear, BS, Joyce Benjamins, PhD and Anne Skoff, PhD

From the Division of Neuroimmunology, Department of Neurology (Drs. Lisak, Benjamins, and Skoff, and B. Bealmear), Department of Immunology and Microbiology (Drs. Lisak and Benjamins), and Department of Biochemistry (Dr. Benjamins), Wayne State University School of Medicine, Detroit Medical Center, MI.

Address correspondence and reprint requests to Dr. Robert P. Lisak, Department of Neurology, Wayne State University School of Medicine, 6E-University Health Center, 4201 St. Antoine, Detroit, MI 48201.

Objective: To determine whether products of inflammatory cells can inhibit differentiation and synthesis of myelin glycolipids by Schwann cells.

Background: Infiltration of the peripheral nervous system by inflammatory cells is a feature of acquired demyelinating neuropathies. It is not clear what role these cells have in causing demyelination or inhibiting myelin synthesis.

Methods: Nonmyelinating rat Schwann cells were incubated with 1) different concentrations of activated supernatants (AS) from mitogen-activated inflammatory cells; 2) 8-bromo cyclic adenosine monophosphate (8Br cAMP), known to induce Schwann cell differentiation and synthesis of glycolipids; 3) 8Br cAMP and varying concentrations of AS; 4) 8Br cAMP and cytosine arabinoside (Ara C), which inhibits Schwann cell proliferation; 5) 8Br cAMP, AS, and Ara C; or 6) additional medium.

Results: AS inhibits the capacity of cAMP to induce Schwann cell expression of myelin-associated glycolipids. Inhibition of glycolipid expression was independent of the capacity of these AS to induce Schwann cell proliferation.

Conclusions: These data suggest that inflammatory mediators are capable of inhibition of Schwann cell differentiation and synthesis of myelin.


Supported by grant NS 31287, National Institute for Neurological Disorders and Stroke.

Received April 16, 1998. Accepted in final form August 14, 1998.