Signaling the brain in systemic inflammation: the role of complement

10.2741/1297 ◽  
2004 ◽  
Vol 9 (1-3) ◽  
pp. 915 ◽  
Author(s):  
Clark, M. Blatteis
Keyword(s):  
Systemic Inflammation ◽  
The Brain

Signaling the brain in systemic inflammation: role of sensory circumventricular organs

10.2741/1241 ◽  
2004 ◽  
Vol 9 (1-3) ◽  
pp. 290 ◽  
Author(s):  
Joachim Roth
Keyword(s):  
Systemic Inflammation ◽  
Circumventricular Organs ◽  
The Brain

Signaling the brain in systemic inflammation the role of perivascular cells

10.2741/1211 ◽  
2003 ◽  
Vol 8 (6) ◽  
pp. s1321-1329 ◽  
Author(s):  
Paul E Sawchenko
Keyword(s):  
Systemic Inflammation ◽  
Perivascular Cells ◽  
The Brain

scholarly journals Elucidating the role of leptin in systemic inflammation: a study targeting physiological leptin levels in rats and their macrophages

2017 ◽  
Vol 313 (5) ◽  
pp. R572-R582 ◽  
Author(s):  
Elizabeth A. Flatow ◽  
Evilin N. Komegae ◽  
Monique T. Fonseca ◽  
Camila F. Brito ◽  
Florin M. Musteata ◽  
...  
Keyword(s):  
Food Deprivation ◽  
Systemic Inflammation ◽  
Peritoneal Macrophages ◽  
Tnf Α ◽  
Macrophage Subpopulations ◽  
Limited Food ◽  
The Brain

To elucidate the role of leptin in acute systemic inflammation, we investigated how its infusion at low, physiologically relevant doses affects the responses to bacterial lipopolysaccharide (LPS) in rats subjected to 24 h of food deprivation. Leptin was infused subcutaneously (0–20 μg·kg−1·h−1) or intracerebroventricularly (0–1 μg·kg−1·h−1). Using hypothermia and hypotension as biomarkers of systemic inflammation, we identified the phase extending from 90 to 240 min post-LPS as the most susceptible to modulation by leptin. In this phase, leptin suppressed the rise in plasma TNF-α and accelerated the recoveries from hypothermia and hypotension. Suppression of TNF-α was not accompanied by changes in other cytokines or prostaglandins. Leptin suppressed TNF-α when infused peripherally but not when infused into the brain. Importantly, the leptin dose that suppressed TNF-α corresponded to the lowest dose that limited food consumption; this dose elevated plasma leptin within the physiological range (to 5.9 ng/ml). We then conducted in vitro experiments to investigate whether an action of leptin on macrophages could parallel our in vivo observations. The results revealed that, when sensitized by food deprivation, LPS-stimulated peritoneal macrophages can be inhibited by leptin at concentrations that are lower than those reported to promote cytokine release. It is concluded that physiological levels of leptin do not exert a proinflammatory effect but rather an anti-inflammatory effect involving selective suppression of TNF-α via an action outside the brain. The mechanism of this effect might involve a previously unrecognized, suppressive action of leptin on macrophage subpopulations sensitized by food deprivation, but future studies are warranted.

scholarly journals Metabolomic and lipidomic changes triggered by lipopolysaccharide-induced systemic inflammation in transgenic APdE9 mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Elena Puris ◽  
Štěpán Kouřil ◽  
Lukáš Najdekr ◽  
Sanna Loppi ◽  
Paula Korhonen ◽  
...  
Keyword(s):  
Disease Progression ◽  
Brain Tissue ◽  
Systemic Inflammation ◽  
Metabolic Pathways ◽  
Wild Type ◽  
The Impact ◽  
The Brain ◽  
Lps Treatment

AbstractPeripheral infections followed by systemic inflammation may contribute to the onset of Alzheimer`s disease (AD) and accelerate the disease progression later in life. Yet, the impact of systemic inflammation on the plasma and brain tissue metabolome and lipidome in AD has not been investigated. In this study, targeted metabolomic and untargeted lipidomic profiling experiments were performed on the plasma, cortices, and hippocampi of wild-type (WT) mice and transgenic APdE9 mice after chronic lipopolysaccharide (LPS) treatment, as well as saline-treated APdE9 mice. The lipidome and the metabolome of these mice were compared to saline-treated WT animals. In the brain tissue of all three models, the lipidome was more influenced than the metabolome. The LPS-treated APdE9 mice had the highest number of changes in brain metabolic pathways with significant alterations in levels of lysine, myo-inositol, spermine, phosphocreatine, acylcarnitines and diacylglycerols, which were not observed in the saline-treated APdE9 mice. In the WT mice, the effect of the LPS administration on metabolome and lipidome was negligible. The study provided exciting information about the biochemical perturbations due to LPS-induced inflammation in the transgenic AD model, which can significantly enhance our understanding of the role of systemic inflammation in AD pathogenesis.

Role of nitric oxide in the brain during lipopolysaccharide-evoked systemic inflammation

2007 ◽  
Vol 85 (8) ◽  
pp. 1694-1703 ◽  
Author(s):  
Grzegorz A. Czapski ◽  
Magdalena Cakala ◽  
Malgorzata Chalimoniuk ◽  
Barbara Gajkowska ◽  
Joanna B. Strosznajder
Keyword(s):  
Nitric Oxide ◽  
Systemic Inflammation ◽  
The Brain

The Role of Mitochondria in the Genesis of Neuroaxonal Dystrophy in the Brains of Aging Mice

1975 ◽  
Vol 33 ◽  
pp. 372-373
Author(s):  
J.E. Johnson
Keyword(s):  
Electron Microscopy ◽  
Present Report ◽  
Light And Electron Microscopy ◽  
Dorsal Column ◽  
Neuroaxonal Dystrophy ◽  
Nucleus Gracilis ◽  
Dystrophic Axons ◽  
The Brain ◽  
Nucleus Cuneatus

Although neuroaxonal dystrophy (NAD) has been examined by light and electron microscopy for years, the nature of the components in the dystrophic axons is not well understood. The present report examines nucleus gracilis and cuneatus (the dorsal column nuclei) in the brain stem of aging mice.Mice (C57BL/6J) were sacrificed by aldehyde perfusion at ages ranging from 3 months to 23 months. Several brain areas and parts of other organs were processed for electron microscopy.At 3 months of age, very little evidence of NAD can be discerned by light microscopy. At the EM level, a few axons are found to contain dystrophic material. By 23 months of age, the entire nucleus gracilis is filled with dystrophic axons. Much less NAD is seen in nucleus cuneatus by comparison. The most recurrent pattern of NAD is an enlarged profile, in the center of which is a mass of reticulated material (reticulated portion; or RP).

Restraint stress exacerbates carbon tetrachloride-induced liver injury in rats: A role of endogenous corticotropin-releasing factor (CRF) in the brain

2001 ◽  
Vol 120 (5) ◽  
pp. A715-A715
Author(s):  
Y NAKADE ◽  
M YONEDA ◽  
S TAKAMOTO ◽  
T ITO ◽  
S OKAMOTO ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Restraint Stress ◽  
Corticotropin Releasing Factor ◽  
The Brain

Fibrinolytic Activity of Cerebro-Spinal Fluid and the Development of Artificial Cerebral Haematomas in Dogs

1969 ◽  
Vol 21 (02) ◽  
pp. 294-303 ◽  
Author(s):  
H Mihara ◽  
T Fujii ◽  
S Okamoto
Keyword(s):  
Cerebrospinal Fluid ◽  
Carboxylic Acid ◽  
Fibrinolytic Activity ◽  
Clinical Implications ◽  
Trans Form ◽  
Plate Method ◽  
Blood Samples ◽  
Fibrin Plate ◽  
The Brain

SummaryBlood was injected into the brains of dogs to produce artificial haematomas, and paraffin injected to produce intracerebral paraffin masses. Cerebrospinal fluid (CSF) and peripheral blood samples were withdrawn at regular intervals and their fibrinolytic activities estimated by the fibrin plate method. Trans-form aminomethylcyclohexane-carboxylic acid (t-AMCHA) was administered to some individuals. Genera] relationships were found between changes in CSF fibrinolytic activity, area of tissue damage and survival time. t-AMCHA was clearly beneficial to those animals given a programme of administration. Tissue activator was extracted from the brain tissue after death or sacrifice for haematoma examination. The possible role of tissue activator in relation to haematoma development, and clinical implications of the results, are discussed.

Neuromyelitis optica spectrum: novel concept of pathogenesis, diagnosis and treatment of Devic’s disease

2009 ◽  
Vol 150 (46) ◽  
pp. 2101-2109 ◽  
Author(s):  
Péter Csécsei ◽  
Anita Trauninger ◽  
Sámuel Komoly ◽  
Zsolt Illés
Keyword(s):  
Neuromyelitis Optica ◽  
Water Channel ◽  
Diagnostic Procedures ◽  
Diagnosis And Treatment ◽  
Clinical Settings ◽  
Permanent Disability ◽  
Therapeutic Decisions ◽  
Novel Concept ◽  
The Brain

The identification of autoantibodies generated against the brain isoform water channel aquaporin4 in the sera of patients, changed the current diagnostic guidelines and concept of neuromyelitis optica (NMO). In a number of cases, clinical manifestation is spatially limited to myelitis or relapsing optic neuritis creating a diverse. NMO spectrum. Since prevention of relapses provides the only possibility to reduce permanent disability, early diagnosis and treatment is mandatory. In the present study, we discuss the potential role of neuroimaging and laboratory tests in differentiating the NMO spectrum from other diseases, as well as the diagnostic procedures and therapeutic options. We also present clinical cases, to provide examples of different clinical settings, diagnostic procedures and therapeutic decisions.

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