» Articles » PMID: 2738153

Anti-peripheral Nerve Myelin Antibodies in Guillain-Barre Syndrome Bind a Neutral Glycolipid of Peripheral Myelin and Cross-react with Forssman Antigen

Overview
Journal J Clin Invest
Specialty General Medicine
Date 1989 Jul 1
PMID 2738153
Citations 18
Authors
Affiliations
Soon will be listed here.
Abstract

During acute-phase illness, serum of patients with Guillain-Barre syndrome (GBS) contain complement-fixing antibodies (Ab) to peripheral nerve myelin (PNM). We investigated PNM lipids as putative antigens for these Ab since GBS serum retained significant reactivity to PNM treated with protease. Ab binding to specific lipids was studied with a C1 fixation and transfer (C1FT) assay using fractions of PNM lipid reincorporated into liposomes as antigen targets or to lipids on HPTLC plates with peroxidase-labeled goat Ab to human IgM. Reactivity was detected to a neutral glycolipid (NGL) of human PNM with a similar number of carbohydrates residues to that of Forssman hapten (Forss). Anti-NGL Ab titers in GBS patients (50-220 U/ml) were significantly elevated over disease and normal controls (0-5 and 0-6 U/ml). We studied possible antigenic cross-reactivity of these Ab with Forss by first quantitating Ab activity with C1FT assay and liposomes containing Forss. All 12 GBS sera tested showed titers (54-272 U/ml) significantly elevated over 11 disease controls (0-22 U/ml) and 25 normal controls (0-11 U/ml). GBS serum Ab reacted with Forss isolated from dog nerve or sheep erythrocytes on HPTLC plates. Further, absorption of 80-100% of anti-NGL Ab activity and 17-97% of anti-PNM Ab activity from eight GBS patient serums was accomplished with liposomes containing Forss but not with control liposomes. In seven GBS patients anti-NGL Ab activity represented only a portion of anti-PNM Ab activity. These results suggest that a glycolipid with antigenic cross-reactivity to Forssman hapten may be responsible for some of the anti-PNM Ab activity in GBS.

Citing Articles

Forssman and the staphylococcal hemolysins.

Ingmer H, Leisner J, Fulaz S APMIS. 2024; 133(1):e13459.

PMID: 39188243 PMC: 11669744. DOI: 10.1111/apm.13459.


Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention.

Ubogu E Acta Neuropathol. 2015; 130(4):445-68.

PMID: 26264608 PMC: 4575885. DOI: 10.1007/s00401-015-1466-4.


Immunopathology and Th1/Th2 immune response of Campylobacter jejuni-induced paralysis resembling Guillain-Barré syndrome in chicken.

Nyati K, Prasad K, Kharwar N, Soni P, Husain N, Agrawal V Med Microbiol Immunol. 2011; 201(2):177-87.

PMID: 22102098 DOI: 10.1007/s00430-011-0220-3.


Acute paretic syndrome in juvenile White Leghorn chickens resembles late stages of acute inflammatory demyelinating polyneuropathies in humans.

Bader S, Kothlow S, Trapp S, Schwarz S, Philipp H, Weigend S J Neuroinflammation. 2010; 7:7.

PMID: 20109187 PMC: 2825213. DOI: 10.1186/1742-2094-7-7.


Can antiglycolipid antibodies present in HIV-infected individuals induce immune demyelination?.

Petratos S, Gonzales M Neuropathology. 2001; 20(4):257-72.

PMID: 11211050 PMC: 7167963. DOI: 10.1046/j.1440-1789.2000.00356.x.


References
1.
Norton W . Isolation of myelin from nerve tissue. Methods Enzymol. 1974; 31:435-44. DOI: 10.1016/0076-6879(74)31049-x. View

2.
Melnick S . Thirty-eight cases of the Guillain-Barre syndrome: an immunological study. Br Med J. 1963; 1(5327):368-73. PMC: 2123832. DOI: 10.1136/bmj.1.5327.368. View

3.
Propp R, Means E, DEIBEL R, Sherer G, Barron K . Waldenström's macroglobulinemia and neuropathy. Deposition of M-component on myelin sheaths. Neurology. 1975; 25(10):980-8. DOI: 10.1212/wnl.25.10.980. View

4.
Shin M, Paznekas W, Abramovitz A, Mayer M . On the mechanism of membrane damage by C: exposure of hydrophobic sites on activated C proteins. J Immunol. 1977; 119(4):1358-64. View

5.
Brostoff S, Levit S, Powers J . Induction of experimental allergic neuritis with a peptide from myelin P2 basic protein. Nature. 1977; 268(5622):752-3. DOI: 10.1038/268752a0. View