Background: Acute inflammatory demyelinating polyradiculoneuropathy (AIDP) and acute motor axonal neuropathy (AMAN) have been described as two major subtypes of Guillain-Barre syndrome (GBS); however, the possible difference of their immune-inflammatory pathogenesis remains unclear. Methods: In this study, by using FACS and enzyme-linked immunosorbent assays analyses, the role of Th1 cytokines tumour necrosis factor-alpha (TNF-alpha), interleukin-12 (IL-12) and their receptors on peripheral blood mononuclear cells (PBMCs) and in serum concentrations were investigated in AIDP and AMAN. Results: The results showed enhanced IL-12, IL-12R1 in AIDP and TNF-alpha in AMAN during the acute phase, as well as increased TNF-alpha and TNFR1 during the plateau phase of AIDP. Intravenous high dose immunoglobulin decreased IL-12R1 expression on cells in AIDP, but increased TNF-alpha and TNFR2 in AMAN. Conclusions: Our data suggest that IL-12 promotes disease development in AIDP and in contrast to previously inflammatory assumptions, TNF-alpha may play double roles in GBS. The anti-inflammatory role of TNF-alpha realized through TNFR2 in AMAN is possibly a therapeutic mechanism in the IVIg treatment of AMAN.
[1]Jilin Univ, Dept Neurol, Hosp 1, Changchun 130023, Peoples R China.
[2]Karolinska Univ Hosp Huddinge, Karolinska Inst, Dept Neurobiol Care Sci & Soc, SE-14186 Stockholm, Sweden.
[3]Jilin Univ, Dept Pathol, Coll Basic Med, Changchun 130023, Peoples R China.
[4]United Arab Emirates Univ, Fac Med & Hlth Sci, Dept Pharmacol, Abu Dhabi, U Arab Emirates.
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