I.v. immunoglobulin reduces circulating proinflammatory cytokines in Guillain-Barré syndrome.
BACKGROUND
Treatment with human i.v. immunoglobulin (IVIg) modifies the course of Guillain-Barré syndrome (GBS), but its specific mode of action is unknown. Cellular interactions mediated through the release of cytokines play a role in the pathogenesis of GBS and may be regulated by IVIg therapy.


OBJECTIVE
To delineate possible immunoregulatory mechanisms of IVIg in patients with GBS.


METHODS
Circulating levels of the proinflammatory cytokines, tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta, were assayed in 21 patients with GBS before and serially after IVIg therapy. Comparisons were made with serum concentration of the anti-inflammatory cytokines, soluble TNF-alpha receptor and IL-10. Serial measurements were also performed in 12 untreated patients with relatively mild disease and 7 patients treated by plasma exchange.


RESULTS
Circulating levels of TNF-alpha and IL-1beta decreased after treatment with IVIg but remained relatively high in untreated patients and in those treated by plasma exchange. Clinical improvement in patients treated with IVIg was associated with a reduction in unbound TNF-alpha during the acute phase of the illness. Circulating levels of anti-inflammatory cytokines were not affected by IVIg treatment.


CONCLUSIONS
Data presented here suggest a novel mechanism of action of IVIg that involves selective modulation of circulating proinflammatory cytokines.
Sharief
M K
MK
Department of Neurology, United Medical and Dental School, Guy's Hospital, London, England.
Ingram
D A
DA
Swash
M
M
Thompson
E J
EJ
D000328:Adult; D016207:Cytokines / Q000097:blood*; D005500:Follow-Up Studies; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000008:administration & dosage*; D007249:Inflammation / Q000188:drug therapy; D010951:Plasma Exchange; D011129:Polyradiculoneuropathy / Q000188:drug therapy*
D016207:Cytokines; D016756:Immunoglobulins, Intravenous