Interleukin-18 is induced in acute inflammatory demyelinating polyneuropathy. Export

@article{citeulike:5711512, abstract = {T lymphocytes of the Th1 subset producing the proinflammatory cytokine interferon-gamma (IFN-gamma) have been implicated in the pathogenesis of immune-mediated diseases of the peripheral nervous system (PNS) such as the acute Guillain-Barr\'{e} syndrome (GBS) and its animal model experimental autoimmune neuritis (EAN). Interleukin-18 (IL-18) is a potent IFN-gamma-inducing cytokine that is synthesized as an inactive precursor molecule and cleaved by caspase-1 into its mature active form. In our present study we analyzed the expression of IL-18 and caspase-1 in the nerve roots of EAN rats using reverse transcriptase-polymerase chain reaction and immunocytochemistry. Using an enzyme-linked immunosorbent assay, we furthermore determined IL-18 protein levels in paired serum and cerebrospinal fluid (CSF) samples from patients with GBS as well as from noninflammatory neurologic disease (NIND) controls. In EAN, IL-18 and caspase-1 mRNA levels in the nerve roots increased during the stage of active disease progression. Immunocytochemically, both perivascular and parenchymal IL-18 protein expression was increased in the roots of EAN rats and mainly associated with ED1+ macrophages stained on serial sections. IL-18 serum levels were significantly higher in GBS patients than in NIND controls (238+/-71 vs. 42+/-7 pg/ml, P<0.001). Our data implicate the Th1-inducing cytokine IL-18 in the pathogenesis of acute immune-mediated PNS demyelination.}, author = {Jander, S. and Stoll, G.}, citeulike-article-id = {5711512}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/11240039}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=11240039}, day = {1}, issn = {0165-5728}, journal = {Journal of neuroimmunology}, keywords = {diabetic-complications, il-18}, month = {March}, number = {1-2}, pages = {253--258}, posted-at = {2009-09-03 05:17:04}, priority = {2}, title = {Interleukin-18 is induced in acute inflammatory demyelinating polyneuropathy.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/11240039}, volume = {114}, year = {2001} }

TY - JOUR ID - citeulike:5711512 L3 - citeulike-article-id:5711512 N2 - T lymphocytes of the Th1 subset producing the proinflammatory cytokine interferon-gamma (IFN-gamma) have been implicated in the pathogenesis of immune-mediated diseases of the peripheral nervous system (PNS) such as the acute Guillain-Barré syndrome (GBS) and its animal model experimental autoimmune neuritis (EAN). Interleukin-18 (IL-18) is a potent IFN-gamma-inducing cytokine that is synthesized as an inactive precursor molecule and cleaved by caspase-1 into its mature active form. In our present study we analyzed the expression of IL-18 and caspase-1 in the nerve roots of EAN rats using reverse transcriptase-polymerase chain reaction and immunocytochemistry. Using an enzyme-linked immunosorbent assay, we furthermore determined IL-18 protein levels in paired serum and cerebrospinal fluid (CSF) samples from patients with GBS as well as from noninflammatory neurologic disease (NIND) controls. In EAN, IL-18 and caspase-1 mRNA levels in the nerve roots increased during the stage of active disease progression. Immunocytochemically, both perivascular and parenchymal IL-18 protein expression was increased in the roots of EAN rats and mainly associated with ED1+ macrophages stained on serial sections. IL-18 serum levels were significantly higher in GBS patients than in NIND controls (238+/-71 vs. 42+/-7 pg/ml, P<0.001). Our data implicate the Th1-inducing cytokine IL-18 in the pathogenesis of acute immune-mediated PNS demyelination. IS - 1-2 JF - Journal of neuroimmunology SN - 0165-5728 EP - 258 TI - Interleukin-18 is induced in acute inflammatory demyelinating polyneuropathy. VL - 114 SP - 253 KW - diabetic-complications KW - il-18 AU - Jander, S AU - Stoll, G PY - 2001/03/01/ UR - http://view.ncbi.nlm.nih.gov/pubmed/11240039 ER -