دورية أكاديمية
أعرض في EDS

Protein expression profiling of inflammatory mediators in human temporal lobe epilepsy reveals co-activation of multiple chemokines and cytokines.

التفاصيل البيبلوغرافية
العنوان: Protein expression profiling of inflammatory mediators in human temporal lobe epilepsy reveals co-activation of multiple chemokines and cytokines.
المؤلفون: Kan AA; Department of Neuroscience and Pharmacology, Rudolf Magnus Institute of Neuroscience, Universiteitsweg 100, 3584 CG, Utrecht, The Netherlands., de Jager W, de Wit M, Heijnen C, van Zuiden M, Ferrier C, van Rijen P, Gosselaar P, Hessel E, van Nieuwenhuizen O, de Graan PN
المصدر: Journal of neuroinflammation [J Neuroinflammation] 2012 Aug 30; Vol. 9, pp. 207. Date of Electronic Publication: 2012 Aug 30.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: BioMed Central Country of Publication: England NLM ID: 101222974 Publication Model: Electronic Cited Medium: Internet ISSN: 1742-2094 (Electronic) Linking ISSN: 17422094 NLM ISO Abbreviation: J Neuroinflammation Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : BioMed Central, c2004-
مواضيع طبية MeSH: Cytokines/*metabolism , Epilepsy, Temporal Lobe/*pathology , Hippocampus/*metabolism , Immune System/*metabolism , Neocortex/*metabolism , Up-Regulation/*physiology, Adult ; Aged ; Aged, 80 and over ; Analysis of Variance ; Cytokines/genetics ; Epilepsy, Temporal Lobe/immunology ; Female ; Hippocampus/pathology ; Humans ; Male ; Middle Aged ; Neocortex/pathology ; Neuroglia/metabolism ; Neurons/metabolism ; Principal Component Analysis
مستخلص: Mesial temporal lobe epilepsy (mTLE) is a chronic and often treatment-refractory brain disorder characterized by recurrent seizures originating from the hippocampus. The pathogenic mechanisms underlying mTLE remain largely unknown. Recent clinical and experimental evidence supports a role of various inflammatory mediators in mTLE. Here, we performed protein expression profiling of 40 inflammatory mediators in surgical resection material from mTLE patients with and without hippocampal sclerosis, and autopsy controls using a multiplex bead-based immunoassay. In mTLE patients we identified 21 upregulated inflammatory mediators, including 10 cytokines and 7 chemokines. Many of these upregulated mediators have not previously been implicated in mTLE (for example, CCL22, IL-7 and IL-25). Comparing the three patient groups, two main hippocampal expression patterns could be distinguished, pattern I (for example, IL-10 and IL-25) showing increased expression in mTLE + HS patients compared to mTLE-HS and controls, and pattern II (for example, CCL4 and IL-7) showing increased expression in both mTLE groups compared to controls. Upregulation of a subset of inflammatory mediators (for example, IL-25 and IL-7) could not only be detected in the hippocampus of mTLE patients, but also in the neocortex. Principle component analysis was used to cluster the inflammatory mediators into several components. Follow-up analyses of the identified components revealed that the three patient groups could be discriminated based on their unique expression profiles. Immunocytochemistry showed that IL-25 IR (pattern I) and CCL4 IR (pattern II) were localized in astrocytes and microglia, whereas IL-25 IR was also detected in neurons. Our data shows co-activation of multiple inflammatory mediators in hippocampus and neocortex of mTLE patients, indicating activation of multiple pro- and anti-epileptogenic immune pathways in this disease.
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المشرفين على المادة: 0 (Cytokines)
تواريخ الأحداث: Date Created: 20120901 Date Completed: 20130419 Latest Revision: 20240318
رمز التحديث: 20240318
مُعرف محوري في PubMed: PMC3489559
DOI: 10.1186/1742-2094-9-207
PMID: 22935090
قاعدة البيانات: MEDLINE
الوصف
تدمد:1742-2094
DOI:10.1186/1742-2094-9-207