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  • APOPTOSIS  (3)
  • 1
    Keywords: brain ; APOPTOSIS ; EXPRESSION ; SURVIVAL ; tumor ; Germany ; DISEASE ; MORTALITY ; PROTEIN ; RESOLUTION ; MICE ; TUMOR-NECROSIS-FACTOR ; NITRIC-OXIDE ; murine ; T-CELLS ; NUMBER ; RATES ; NECROSIS-FACTOR-ALPHA ; IMMUNE-RESPONSE ; CENTRAL-NERVOUS-SYSTEM ; pathology ; TNF-ALPHA ; protein expression ; TNF ; FACTOR-ALPHA ; SYNTHASE ; development ; REACTIVE OXYGEN ; PHASE ; NITRIC-OXIDE-SYNTHASE ; NECROSIS-FACTOR ; TUMOR NECROSIS FACTOR ; nitric oxide synthase ; brain abscess ; INTRACEREBRAL IMMUNE-RESPONSE ; NEUTROPHIL APOPTOSIS ; RECEPTOR-TYPE 1 ; Staphylococcus aureus ; TOXOPLASMA ENCEPHALITIS
    Abstract: Tumor necrosis factor-alpha (TNF-alpha) is a central mediator of the immune response to pathogens, but may also exert neurotoxic effects, thereby contributing to immunopathology. To define the role of TNF during the course of brain abscess, TNF-deficient (TNF0/0) truce were stereotaxically infected with Staphylococcus (S.) aureus-laden agarose beads. In comparison to 100% survival of wild type (WT) mice, TNF0/0 mice displayed high mortality rates (54%) in the initial phase of abscess development as well as significantly increased morbidity in the course of the disease. The worse clinical outcome was due to an increased intracerebral (i.e.) bacterial load in TNF0/0 mice as compared to WT mice. The impaired control of S. aureus was associated with reduced inductible nitric oxide synthase (iNOS) mRNA and protein expression in TNF0/0 mice. Similarly, numbers of inflammatory leukocytes, cytokine expression of IL-6, IL-12p40, IFNgamma, IL-1beta mRNA, and brain edema were significantly increased in TNF0/0 mice as compared to WT animals. In addition, resolution of i.e. infiltrates was delayed in TNF0/0 mice correlating with reduced apoptosis of inflammatory leukocytes and formation of a fibrous abscess capsule. Collectively, these data demonstrate that TNF is of key importance for the control of S. aureus-induced brain abscess and regulates the ensuing host immune response
    Type of Publication: Journal article published
    PubMed ID: 15715082
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  • 2
    Keywords: APOPTOSIS ; EXPRESSION ; SURVIVAL ; CELL ; Germany ; PATHWAY ; SYSTEM ; DISTINCT ; GENE ; GENE-EXPRESSION ; GENES ; NF-KAPPA-B ; ACTIVATION ; FAMILY ; MEMBER ; TARGET ; NERVOUS-SYSTEM ; LYMPHOMA ; gene expression ; FACTOR-KAPPA-B ; RT-PCR ; CENTRAL-NERVOUS-SYSTEM ; NF-kappa B ; TARGETS ; pathology ; fluorescence in situ hybridization ; signaling ; FAMILIES ; CELL LYMPHOMA ; LEVEL ; NUCLEAR ; USA ; B-CELL ; germinal center ; central nervous system ; quantitative ; nuclear factor-kappa B ; primary central nervous system lymphomas (PCNSL)
    Abstract: Recent studies point to a role of nuclear factor (NF)-kappa B signaling in a subset of diffuse large B cell lymphomas. We have analyzed the expression of 21 genes encoding NF-kappa B family members, upstream modulators, and targets in 32 primary central nervous system lymphomas (PCNSLs) by quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), Compared with nonmalignant germinal center centroblasts, expression of BCL10, REL, IAP1, and TRAF1 was significantly lower in PCNSLs, whereas that of BAX, BCLXL, BCL2, MALT1, CARD9, CARD10, CARD11, CARD14, CCND2, cFLIP, RELA, RELB, NFKB1, NFK82, and IRF4 was higher. Hierarchical clustering of gene expression data revealed two distinct subgroups of PCNSLs, which were characterized by significantly different transcriptional levels, predominantly of BCL10, but also of REL and IAPI. Thus, these quantitative RT-PCR data with expression of genes of the NF-kappa B family as well as NF-kappa B-regulated genes together with immunohistochemical detection of nuclear RELA and REL indicate activation of the NF-kappa B pathway in PCNSLs, which may contribute to their high proliferative activity and the low level of apoptosis
    Type of Publication: Journal article published
    PubMed ID: 17356384
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  • 3
    Keywords: APOPTOSIS ; CELLS ; INHIBITOR ; MODEL ; DISEASE ; DAMAGE ; CALCIUM ; MULTIPLE-SCLEROSIS ; inflammation ; SPINAL-CORD ; neurodegeneration ; ENCEPHALOMYELITIS ; DEMYELINATION ; AXONAL-INJURY ; Calpain ; GANGLION-CELL DEATH ; Optic neuritis ; Retinal ganglion cells
    Abstract: Optic neuritis is a common manifestation of multiple sclerosis, an inflammatory demyelinating disease of the CNS. Recently, the neurodegenerative component of multiple sclerosis has come under focus particularly because permanent disability in patients correlates well with neurodegeneration; and observations in both humans and multiple sclerosis animal models highlight neurodegeneration of retinal ganglion cells as an early event. After myelin oligodendrocyte glycoprotein immunization of Brown Norway rats, significant retinal ganglion cell loss precedes the onset of pathologically defined autoimmune optic neuritis. To study the role calcium and calpain activation may play in mediating early degeneration, manganese-enhanced magnetic resonance imaging was used to monitor preclinical calcium elevations in the retina and optic nerve of myelin oligodendrocyte glycoprotein-immunized Brown Norway rats. Calcium elevation correlated with an increase in calpain activation during the induction phase of optic neuritis, as revealed by increased calpain-specific cleavage of spectrin. The relevance of early calpain activation to neurodegeneration during disease induction was addressed by performing treatment studies with the calpain inhibitor calpeptin. Treatment not only reduced calpain activity but also protected retinal ganglion cells from preclinical degeneration. These data indicate that elevation of retinal calcium levels and calpain activation are early events in autoimmune optic neuritis, providing a potential therapeutic target for neuroprotection.
    Type of Publication: Journal article published
    PubMed ID: 23860028
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