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Inflammatory Insult (inflammatory + insult)
Selected AbstractsReview: Role of developmental inflammation and blood,brain barrier dysfunction in neurodevelopmental and neurodegenerative diseasesNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 2 2009H. B. Stolp The causes of most neurological disorders are not fully understood. Inflammation and blood,brain barrier dysfunction appear to play major roles in the pathology of these diseases. Inflammatory insults that occur during brain development may have widespread effects later in life for a spectrum of neurological disorders. In this review, a new hypothesis suggesting a mechanistic link between inflammation and blood,brain barrier function (integrity), which is universally important in both neurodevelopmental and neurodegerative diseases, is proposed. The role of inflammation and the blood,brain barrier will be discussed in cerebral palsy, schizophrenia, Parkinson's disease, Alzheimer's disease and multiple sclerosis, conditions where both inflammation and blood,brain barrier dysfunction occur either during initiation and/or progression of the disease. We suggest that breakdown of normal blood,brain barrier function resulting in a short-lasting influx of blood-born molecules, in particular plasma proteins, may cause local damage, such as reduction of brain white matter observed in some newborn babies, but may also be the mechanism behind some neurodegenerative diseases related to underlying brain damage and long-term changes in barrier properties. [source] A link between neutrophils and chronic disease manifestations of Chlamydia muridarum urogenital infection of miceFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 1 2010Hyo Y. Lee Abstract Vigorous acute inflammatory responses accompany Chlamydia muridarum infections in mice and are positively correlated with adverse urogenital and respiratory tract infection outcomes in the mouse model. Thus, we tested the hypothesis that neutrophils induce an acute inflammatory insult that, in the repair phase, leads to the chronic sequelae of hydrosalpinx , a surrogate marker of infertility in the mouse model. To this end, we induced neutropenia in mice using a neutrophil-depleting monoclonal antibody during acute phases of C. muridarum urogenital infection only (days 2,21 postinfection). To prove induced neutropenia, peripheral blood was monitored for neutrophils during the treatment regimen. Neutropenic mice had a similar infection course as control mice, but had significantly reduced levels of certain histopathological parameters, reduced production of matrix metalloproteinase-9 (MMP-9) and reduced rates of hydrosalpinx following resolution of the infection. We conclude that neutrophils are a major source of MMP-9, a previously proved pathological factor in this model. Further, we conclude that acute inflammation in the form of neutrophils and neutrophil activation products are at least partially responsible for inducing the histological changes that ultimately result in fibrosis and infertility in the mouse model of chlamydial upper genital tract disease. [source] Neutrophil mobilization and clearance in the bone marrowIMMUNOLOGY, Issue 3 2008Rebecca C. Furze Summary The bone marrow is the site of neutrophil production, a process that is regulated by the cytokine granulocyte colony-stimulating factor (G-CSF). Mature neutrophils are continually released into the circulation, with an estimated 1011 neutrophils exiting the bone marrow daily under basal conditions. These leucocytes have a short half-life in the blood of ,6·5 hr, and are subsequently destroyed in the spleen, liver and indeed the bone marrow itself. Additionally, mature neutrophils are retained in the bone marrow by the stromal cell-derived factor (SDF-1,)/chemokine (C-X-C motif) receptor 4 (CXCR4) chemokine axis and form the bone marrow reserve. Following infection or inflammatory insult, neutrophil release from the bone marrow reserve is substantially elevated and this process is mediated by the co-ordinated actions of cytokines and chemokines. In this review we discuss the factors and molecular mechanisms regulating the neutrophil mobilization and consider the mechanisms and functional significance of neutrophil clearance via the bone marrow. [source] Neuroprotective effects of Tanshinone IIA on permanent focal cerebral ischemia in mice,PHYTOTHERAPY RESEARCH, Issue 5 2009Kenan Dong Abstract The objective of this study was to evaluate whether Tanshinone IIA (TSA) was neuroprotective in permanent focal cerebral ischemia and to determine the possible mechanisms of its neuroprotection. Mice were subjected to permanent middle cerebral artery occlusion. The neuroprotection of TSA was investigated with respect to neurological deficit scores and infarct volume. Biochemical analyses for malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in serum, and nitric oxide (NO) content and the inducible nitric oxide synthase (iNOS) activity in brain tissue were performed at 24 h after ischemia. Immunohistochemistry was used to measure the expression of iNOS. In vitro, the effects of TSA were tested in the cultured astrocytes exposed to hydrogen dioxide (H2O2). TSA (5, 10 and 20 mg/kg, i.p.) significantly reduced the infarct volume and improve neurological deficit. TSA also significantly increased the activity of SOD after 24 h of ischemia and decreased the MDA level, NO content, and iNOS expression. In vitro, the translocation of NF- ,B was inhibited by TSA and the survival rate of astrocytes was markedly increased and the NO production was decreased. In conclusion, these results illustrated that TSA protected the brain from ischemic injury by suppressing the oxidative stress and the radical-mediated inflammatory insult. Copyright © 2008 John Wiley & Sons, Ltd. [source] Improving the Procedure for Detection of Intrahepatic Transplanted Islets by Magnetic Resonance ImagingAMERICAN JOURNAL OF TRANSPLANTATION, Issue 10 2009M. L. Malosio Islet transplantation is an effective therapy for restoring normoglycemia in type-1 diabetes, but long-term islet graft function is achieved only in a minority of cases. Noninvasive magnetic resonance imaging of pancreatic islets is an attractive option for "real-time" monitoring of graft evolution. So far, previous studies have been performed in the absence of a standardized labeling procedure and, besides a feasibility study in patients, the effectiveness and safety of various labeling approaches were tested only with high field magnets (4.7 T). In this study, we addressed: (a) standardization of a labeling procedure for human islets with clinically-approved contrast agent Endorem®, (b) safety aspects of labeling related to inflammation and (c) quality of imaging both at 7 T and 1.5 T. We have highlighted that the ratio of Endorem®/islet is crucial for reproducible labeling, with a ratio of 2.24 ug/IEQ, allowing successful in vivo imaging both with 1.5 T and 7.0 T magnets up to 143 days after intrahepatic transplant. With this standardized labeling procedure, labeled islets are neither inflamed nor more susceptible to inflammatory insults than unlabeled ones. This report represents an important contribution towards the development of a standardized and safe clinical protocol for the noninvasive imaging of transplanted islets in humans. [source] Airway microvascular extravasation and luminal entry of plasmaCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2003Lennart Greiff Summary Extravasation of plasma from postcapillary venules is a specific in vivo response to inflammatory insults. In the nasal and bronchial airways, extravasated plasma has a widespread distribution in the lamina propria, between the epithelial cells and in the airway lumen. This feature, in combination with the fact that the process involves extravasation of bulk plasma, with all peptides and proteins of plasma, indicates that plasma exudation contributes to the dramatic change of the mucosal milieu that characterizes airway inflammation. Accordingly, this process is of key importance to conditions such as allergic rhinitis and asthma. The means by which extravasated plasma participates in mucosal defence is physiological in the sense that it may operate on the surface of the epithelium without impairing its function as an absorption barrier. The flow of plasma into the airway lumen may thus wash away unwanted material from inter-epithelial cell spaces, exuded binding proteins may bind unwanted solutes non-specifically and extravasated immunoglobulins may neutralize allergens. In addition to the role as defence mechanism, extravasated plasma components may act as important pro-inflammatory factors. Furthermore, experimental data as well as observations in natural disease suggest that luminal levels of plasma proteins can be employed as an accessible index reflecting to what degree the airway mucosa is affected by inflammatory processes. [source] | ||||||||||