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Search Results: 1 - 10 of 220755 matches for " Cornelia C Bergmann "
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Intrathecal Humoral Immunity to Encephalitic RNA Viruses
Timothy W. Phares,Stephen A. Stohlman,Cornelia C. Bergmann
Viruses , 2013, DOI: 10.3390/v5020732
Abstract: The nervous system is the target for acute encephalitic viral infections, as well as a reservoir for persisting viruses. Intrathecal antibody (Ab) synthesis is well documented in humans afflicted by infections associated with neurological complications, as well as the demyelinating disease, multiple sclerosis. This review focuses on the origin, recruitment, maintenance, and biological relevance of Ab-secreting cells (ASC) found in the central nervous system (CNS) following experimental neurotropic RNA virus infections. We will summarize evidence for a highly dynamic, evolving humoral response characterized by temporal alterations in B cell subsets, proliferation, and differentiation. Overall local Ab plays a beneficial role via complement-independent control of virus replication, although cross or self-reactive Ab to CNS antigens may contribute to immune-mediated pathogenesis during some infections. Importantly, protective Ab exert anti-viral activity not only by direct neutralization, but also by binding to cell surface-expressed viral glycoproteins. Ab engagement of viral glycoproteins blocks budding and mediates intracellular signaling leading to restored homeostatic and innate functions. The sustained Ab production by local ASC, as well as chemokines and cytokines associated with ASC recruitment and retention, are highlighted as critical components of immune control.
Enhanced CD8 T-cell anti-viral function and clinical disease in B7-H1-deficient mice requires CD4 T cells during encephalomyelitis
Phares Timothy W,Stohlman Stephen A,Hinton David R,Bergmann Cornelia C
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-269
Abstract: Background Anti-viral CD8 T-cell activity is enhanced and prolonged by CD4 T-cell-mediated help, but negatively regulated by inhibitory B7-H1 interactions. During viral encephalomyelitis, the absence of CD4 T cells decreases CD8 T cell activity and impedes viral control in the central nervous system (CNS). By contrast, the absence of B7-H1 enhances CD8 T-cell function and accelerates viral control, but increases morbidity. However, the relative contribution of CD4 T cells to CD8 function in the CNS, in the absence of B7-H1, remains unclear. Methods Wild-type (WT) and B7-H1 / mice were infected with a gliatropic coronavirus and CD4 T cells depleted to specifically block T helper function in the CNS. Flow cytometry and gene expression analysis of purified T-cell populations from lymph nodes and the CNS was used to directly monitor ex vivo T-cell effector function. The biological affects of altered T-cell responses were evaluated by analysis of viral control and spinal-cord pathology. Results Increased anti-viral activity by CD8 T cells in the CNS of B7-H1 / mice was lost upon depletion of CD4 T cells; however, despite concomitant loss of viral control, the clinical disease was less severe. CD4 depletion in B7-H1 / mice also decreased inducible nitric oxide synthase expression by microglia and macrophages, consistent with decreased microglia/macrophage activation and reduced interferon (IFN)-γ. Enhanced production of IFN-γ, interleukin (IL)-10 and IL-21 mRNA was seen in CD4 T cells from infected B7-H1 / compared with WT mice, suggesting that over-activated CD4 T cells primarily contribute to the increased pathology. Conclusions The local requirement of CD4 T-cell help for CD8 T-cell function is not overcome if B7-H1 inhibitory signals are lost. Moreover, the increased effector activity by CD8 T cells in the CNS of B7-H1 / mice is attributable not only to the absence of B7-H1 upregulation on major histocompatibility complex class I-presenting resident target cells, but also to enhanced local CD4 T-cell function. B7-H1-mediated restraint of CD4 T-cell activity is thus crucial to dampen both CD8 T-cell function and microglia/macrophage activation, thereby providing protection from T-cell-mediated bystander damage.
IFN-γ protects from lethal IL-17 mediated viral encephalomyelitis independent of neutrophils
Carine Savarin, Stephen A Stohlman, David R Hinton, Richard M Ransohoff, Daniel J Cua, Cornelia C Bergmann
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-104
Abstract: Encephalitis induced by a gliatropic murine coronavirus was used as a model to assess the direct contributions of neutrophils, IFN-γ and IL-17 to virus-induced mortality. CNS inflammatory conditions were selectively manipulated by adoptive transfer of virus-primed wild-type (WT) or IFN-γ deficient (GKO) memory CD4+ T cells into infected SCID mice, coupled with antibody-mediated neutrophil depletion and cytokine blockade.Transfer of GKO memory CD4+ T cells into infected SCID mice induced rapid mortality compared to recipients of WT memory CD4+ T cells, despite similar virus control and demyelination. In contrast to recipients of WT CD4+ T cells, extensive neutrophil infiltration and IL-17 expression within the CNS in recipients of GKO CD4+ T cells provided a model to directly assess their contribution(s) to disease. Recipients of WT CD4+ T cells depleted of IFN-γ did not express IL-17 and were spared from mortality despite abundant CNS neutrophil infiltration, indicating that mortality was not mediated by excessive CNS neutrophil accumulation. By contrast, IL-17 depletion rescued recipients of GKO CD4+ T cells from rapid mortality without diminishing neutrophils or reducing GM-CSF, associated with pathogenic Th17 cells in CNS autoimmune models. Furthermore, co-transfer of WT and GKO CD4+ T cells prolonged survival in an IFN-γ dependent manner, although IL-17 transcription was not reduced.These data demonstrate that IL-17 mediates detrimental clinical consequences in an IFN-γ-deprived environment, independent of extensive neutrophil accumulation or GM-CSF upregulation. The results also suggest that IFN-γ overrides the detrimental IL-17 effector responses via a mechanism downstream of transcriptional regulation.
Interferon-Induced Ifit2/ISG54 Protects Mice from Lethal VSV Neuropathogenesis
Volker Fensterl,Jaime L. Wetzel,Srividya Ramachandran,Tomoaki Ogino,Stephen A. Stohlman,Cornelia C. Bergmann,Michael S. Diamond,Herbert W. Virgin,Ganes C. Sen
PLOS Pathogens , 2012, DOI: 10.1371/journal.ppat.1002712
Abstract: Interferon protects mice from vesicular stomatitis virus (VSV) infection and pathogenesis; however, it is not known which of the numerous interferon-stimulated genes (ISG) mediate the antiviral effect. A prominent family of ISGs is the interferon-induced with tetratricopeptide repeats (Ifit) genes comprising three members in mice, Ifit1/ISG56, Ifit2/ISG54 and Ifit3/ISG49. Intranasal infection with a low dose of VSV is not lethal to wild-type mice and all three Ifit genes are induced in the central nervous system of the infected mice. We tested their potential contributions to the observed protection of wild-type mice from VSV pathogenesis, by taking advantage of the newly generated knockout mice lacking either Ifit2 or Ifit1. We observed that in Ifit2 knockout (Ifit2?/?) mice, intranasal VSV infection was uniformly lethal and death was preceded by neurological signs, such as ataxia and hind limb paralysis. In contrast, wild-type and Ifit1?/? mice were highly protected and survived without developing such disease. However, when VSV was injected intracranially, virus replication and survival were not significantly different between wild-type and Ifit2?/? mice. When administered intranasally, VSV entered the central nervous system through the olfactory bulbs, where it replicated equivalently in wild-type and Ifit2?/? mice and induced interferon-β. However, as the infection spread to other regions of the brain, VSV titers rose several hundred folds higher in Ifit2?/? mice as compared to wild-type mice. This was not caused by a broadened cell tropism in the brains of Ifit2?/? mice, where VSV still replicated selectively in neurons. Surprisingly, this advantage for VSV replication in the brains of Ifit2?/? mice was not observed in other organs, such as lung and liver. Pathogenesis by another neurotropic RNA virus, encephalomyocarditis virus, was not enhanced in the brains of Ifit2?/? mice. Our study provides a clear demonstration of tissue-, virus- and ISG-specific antiviral action of interferon.
RNase L Mediated Protection from Virus Induced Demyelination
Derek D. C. Ireland,Stephen A. Stohlman,David R. Hinton,Parul Kapil,Robert H. Silverman,Roscoe A. Atkinson,Cornelia C. Bergmann
PLOS Pathogens , 2009, DOI: 10.1371/journal.ppat.1000602
Abstract: IFN-α/β plays a critical role in limiting viral spread, restricting viral tropism and protecting mice from neurotropic coronavirus infection. However, the IFN-α/β dependent mechanisms underlying innate anti-viral functions within the CNS are poorly understood. The role of RNase L in viral encephalomyelitis was explored based on its functions in inhibiting translation, inducing apoptosis, and propagating the IFN-α/β pathway through RNA degradation intermediates. Infection of RNase L deficient (RL?/?) mice with a sub-lethal, demyelinating mouse hepatitis virus variant revealed that the majority of mice succumbed to infection by day 12 p.i. However, RNase L deficiency did not affect overall control of infectious virus, or diminish IFN-α/β expression in the CNS. Furthermore, increased morbidity and mortality could not be attributed to altered proinflammatory signals or composition of cells infiltrating the CNS. The unique phenotype of infected RL?/? mice was rather manifested in earlier onset and increased severity of demyelination and axonal damage in brain stem and spinal cord without evidence for enhanced neuronal infection. Increased tissue damage coincided with sustained brain stem infection, foci of microglia infection in grey matter, and increased apoptotic cells. These data demonstrate a novel protective role for RNase L in viral induced CNS encephalomyelitis, which is not reflected in overall viral control or propagation of IFN-α/β mediated signals. Protective function is rather associated with cell type specific and regional restriction of viral replication in grey matter and ameliorated neurodegeneration and demyelination.
IFN-γ Signaling to Astrocytes Protects from Autoimmune Mediated Neurological Disability
Claudia Hindinger, Cornelia C. Bergmann, David R. Hinton, Timothy W. Phares, Gabriel I. Parra, Shabbir Hussain, Carine Savarin, Roscoe D. Atkinson, Stephen A. Stohlman
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0042088
Abstract: Demyelination and axonal degeneration are determinants of progressive neurological disability in patients with multiple sclerosis (MS). Cells resident within the central nervous system (CNS) are active participants in development, progression and subsequent control of autoimmune disease; however, their individual contributions are not well understood. Astrocytes, the most abundant CNS cell type, are highly sensitive to environmental cues and are implicated in both detrimental and protective outcomes during autoimmune demyelination. Experimental autoimmune encephalomyelitis (EAE) was induced in transgenic mice expressing signaling defective dominant-negative interferon gamma (IFN-γ) receptors on astrocytes to determine the influence of inflammation on astrocyte activity. Inhibition of IFN-γ signaling to astrocytes did not influence disease incidence, onset, initial progression of symptoms, blood brain barrier (BBB) integrity or the composition of the acute CNS inflammatory response. Nevertheless, increased demyelination at peak acute disease in the absence of IFN-γ signaling to astrocytes correlated with sustained clinical symptoms. Following peak disease, diminished clinical remission, increased mortality and sustained astrocyte activation within the gray matter demonstrate a critical role of IFN-γ signaling to astrocytes in neuroprotection. Diminished disease remission was associated with escalating demyelination, axonal degeneration and sustained inflammation. The CNS infiltrating leukocyte composition was not altered; however, decreased IL-10 and IL-27 correlated with sustained disease. These data indicate that astrocytes play a critical role in limiting CNS autoimmune disease dependent upon a neuroprotective signaling pathway mediated by engagement of IFN-γ receptors.
Forma??o da eflorescência em ceramica vermelha: fatores de influência no transporte dos íons SO4(2-) e Ca2+
Ferreira, C. C.;Bergmann, C. P.;
Ceramica , 2011, DOI: 10.1590/S0366-69132011000300016
Abstract: the displacement of so42- and ca2+ ions in a red-clay ceramic, simulating the process of efflorescence, was studied. ceramic bodies were molded (70 × 27 × 9 mm3) by vacuum extrusion formulated with different contents of caso4.2h2o (0%, 2%, 4%, 8%, and 16% in weight) and fired at different temperatures (800, 850, 900, and 950 °c) for 12 h. ceramic bodies were characterized in terms of water absorption, apparent porosity and pore size distribution. efflorescence was evaluated according to the norms of astmc67/2003. the solubilization of so42- and ca2+ ions was tested after 1 h with the ceramic bodies immersed in hot water as well as after 7, 14 and 28 consecutive days with the ceramic bodies immersed in cold water. electrical conductivity tests were also carried out in the solubilized material from ceramic bodies 1 h and 7 days after the beginning of the assay, where the potential of these ions in the formation of efflorescence as a function of temperature was evaluated. in the quantification of efflorescence, a new image analysis methodology was developed. the results allowed establishing a relationship between the efflorescence of the investigated ions, physical properties (water absorption and apparent porosity), pore size distribution, solubilization and electrical conductivity.
Mechanisms of stomatal development: an evolutionary view
Anne Vatén, Dominique C Bergmann
EvoDevo , 2012, DOI: 10.1186/2041-9139-3-11
Abstract: Plants conquered land more than 400 million years ago. In the fossil record, the appearance of these pioneer species is contemporaneous with the appearance of structures on their surfaces called stomata. Each stoma (plural, stomata) consists of paired epidermal guard cells, a pore between them and an airspace in the photosynthetic mesophyll tissue subtending it. The function of stomata is to regulate gas exchange between the plant and its surroundings. On short timescales (minutes to hours), the opening and closing of the stomatal pore by turgor-driven changes in guard cell shape is a key regulatory step in maintaining water and carbon dioxide balance. Work from many laboratories has defined the intracellular signal transduction cascades that mediate changes in pore size in response to hormone and environmental signals [1].The current view is that stomata arose only once during evolution [2]. In early land plants, stomatal density was low [3]. During intervening millennia, the stomatal density (SD, number of stomata/unit leaf area) increased, probably in response to reduced aerial CO2 concentration [4]. The stomatal complex has been fine-tuned by several innovations including recruitment of neighboring subsidiary cells to facilitate stomatal opening/closing, relocation of stomatal complexes under protective epidermal cells and incorporation of multiple asymmetric cell divisions in precursors to create a variety of stomatal distributions. Despite the variation, the basic core structure has remained unchanged: two guard cells flank the stomal pore. In nearly all species, two stomata are separated at least by one non-stomatal cell, an arrangement thought to be essential for efficient opening and closing. Stomata are located on aerial organs including leaves, stems, flowers, fruits and seeds and they develop gradually during organ growth such that young organs have fewer total stomata than mature organs, though SD often decreases as the neighboring epidermal cells expan
Aspectos teóricos e práticos sobre a resistência mecanica de porcelanas
Bragan?a, S. R.;Bergmann, C. P.;
Ceramica , 2004, DOI: 10.1590/S0366-69132004000200012
Abstract: the properties of traditional porcelain, including its mechanical strength, are a consequence of the ceramic processing that formed the piece, and then, raw materials and their characteristics, forming process, firing atmosphere, time and temperature. these parameters determine the complexities of microstructure and phase development, which are difficult to be controlled and makes almost impossible to predict porcelain final properties. since the last century, many theories have been developed to explain the strength of porcelain, and some have recently been revised and improved due to the development of new analytical techniques. this work shows an overview on the literature, which comprises new discussions and theories about porcelain strength, including authors′ own investigations.
Influência da adi??o de alumina na microestrutura da espuma vítrea
Pokorny, A.;Vicenzi, J.;Bergmann, C. P.;
Ceramica , 2008, DOI: 10.1590/S0366-69132008000100014
Abstract: in this work, the influence of the alumina addition on the properties of foam glass was studied. alumina was introduced to the mixture in order to increase the refractoriness of the final product. ceramic bodies were composed by ground soda-lime glass from transparent glass bottles, dolomitic lime and alumina. the ceramic bodies were formulated with 3 and 5 wt.% of dolomite lime, both without alumina and with 4 wt.% of this material, uniaxially pressed, and fired in the temperature range from 600 oc to 1000 oc at a heating rate of 150 k/h. the technological characterization of the ceramic bodies involved the determination of the volume expansion. the microstructure was investigated by optical microscopy and scanning electron microscopy. the experimental results show that the addition of alumina influenced the volume expansion of the ceramic bodies, decreasing the foaming.
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