Background Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a neuroinflammatory disorder with a predilection for females. Males present differently, with seizures rather than the better-recognized constellation of psychiatric and behavioral symptoms dominating the initial stages of the disease, providing a potential substrate for delayed recognition and treatment. Case Presentation An 18-year-old man presented with fever and “seizures. When examined, he was febrile but alert and coherent. His neurologic, respiratory, cardiovascular, and abdominal examinations were unremarkable. Diagnosed with infective meningoencephalitis, he was started on intravenous ceftriaxone and acyclovir concurrently with anti-epileptic medications. However, he deteriorated into refractory status epilepticus. Electroencephalograms showed left temporo-parietal seizures. Cerebrospinal fluid analysis revealed inflammatory features, but the virologic assays and bacterial cultures returned negative. Magnetic resonance imaging scans performed in the first and second week from symptom-onset demonstrated the interval development of widespread sulcal T2 hyperintensity, with florid and diffuse leptomeningeal enhancement. Anti-NMDAR antibodies were subsequently detected in his cerebrospinal fluid by indirect immunofluorescence. Diagnosed with anti-NMDAR encephalitis, he received plasmapheresis, methylprednisolone and immunoglobulin infusions. Conclusion Anti-NMDAR encephalitis should be considered in patients, especially males, who are treated for suspected infectious meningoencephalitis, but continue to deteriorate, even in the absence of prominent psychiatric or behavioral symptoms, considering how the initial symptoms differ between the genders. The interval development of diffuse and florid leptomeningeal enhancement on sequential magnetic resonance imaging scans of our patient has not been described in prior reports, and may be reflective of the underlying inflammatory processes.
Objective To explore the prevention of IL-18 or anti-IL-18-mAb to the immune liver fibrosis model induced by repeated injection of concanavalin A in BALB/c mice and its mechanism. Methods Total of 120 BALB/c mice were divided into four groups, control group mice (Ga) were injected weekly with normal saline, concanavalin A group was divided into Gb, Gc, Gd. All mice were injected with concanavalin A (15 mg/kg) once a week. Moreover, Gc, Gd mice were injected weekly with IL-18 (7.5 mg/kg) and anti-IL-18-mAb (10 mg/kg) 2 hours before treatment with concanavalin A, respectively. Twenty-four hours after concanavalin A challenge at 1, 5, 12 and 20 weeks, 3 mice were killed by vena orbitalis, repectively. The sera were storaged at 4℃ for detecting of up TNF-α and IFN-γ by ELISA. The liver of mice in different groups were excised and fixed in 10% formalin for HE staining and Masson staining or frozen in liquid nitrogen for immunohistochemical staining for α-SMA. After extracting of total RNA from liver tissue, MMP-2 and TIMP-1 A messenger RNA were amplified by reverse transcription polymerase chain reaction (PCR). Products were electrophoresed on agrose gel containing ethidium bromide and visualized under ultraviolet light. Densitometric RT-PCR data were standardized with β-actin signals.Results After experiment, the number of dead mice of Ga, Gb, Gc and Gd were 0, 6, 15 and 3, respectively. There were significant difference on each group (P < 0.05). At the fifth week of experiment, hepatocellular necrosis in IL-18 administered group mice had become widespread throughout the lobule. Evidence of liver fibrosis was observed during this period. However, at the twelfth week of experimemt, bridging fibrosis and large fibrosis strip in the parenchyma with hepatocellular necrosis was detectable in Gb, but at twentieth week, only the small fibrosis strip had been found in anti-IL-18-mAb administered group mice by HE staining and Masson staining. The serum levels of TNF-α and IFN-γ in IL-18 administered group were higher than that in concanavalin A group and anti-IL-18 administered groups (P < 0.05). Moreover, immunohistochemical staining for α-SMA indicated that the semi-quantu scores in IL-18 administered group were more than concanavalin A group and anti-IL-18-mAb administered groups (P < 0.05). MMP-2-mRNA, TIMP-1-mRNA expression levels increased signifigantly compared with concanavalin A group and anti-IL-18-mAb administered group (P < 0.05). Conclusions The immune liver fibrosis model induced by repeated injection of concanavalin A in BALB/c mice could be worsened by IL-18 administration and block by anti-IL-18 mAb administraion.
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