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Stroke immune modulation

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9 papers 0 to 25 followers Papers on post stroke immune modulation, focussing on immune suppression
Vikramjeet Singh, Stefan Roth, Gemma Llovera, Rebecca Sadler, Debora Garzetti, Bärbel Stecher, Martin Dichgans, Arthur Liesz
UNLABELLED: Acute brain ischemia induces a local neuroinflammatory reaction and alters peripheral immune homeostasis at the same time. Recent evidence has suggested a key role of the gut microbiota in autoimmune diseases by modulating immune homeostasis. Therefore, we investigated the mechanistic link among acute brain ischemia, microbiota alterations, and the immune response after brain injury. Using two distinct models of acute middle cerebral artery occlusion, we show by next-generation sequencing that large stroke lesions cause gut microbiota dysbiosis, which in turn affects stroke outcome via immune-mediated mechanisms...
July 13, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Zhen-Kui Wang, Li Xue, Tao Wang, Xiu-Jie Wang, Zhi-Qiang Su
Invariant natural killer T (iNKT) cells are a unique subset of T cells that have been implicated in inflammation, atopy, autoimmunity, infections, and cancer. Although iNKT cells have been extensively studied over the past decade, its role in the pathogenesis of ischemic brain injury is still largely unknown. In our study, we determined whether iNKT cells infiltration occur in a mouse model of permanent cerebral ischemia. C57BL6/J male mice were treated with either alpha-galactosylceramide (α-GalCer) or vehicle control before undergoing permanent middle cerebral artery occlusion (pMCAO)...
October 28, 2016: Neuroscience Letters
Johanna Ruhnau, Juliane Schulze, Bettina von Sarnowski, Marie Heinrich, Sönke Langner, Christian Pötschke, Anika Wilden, Christof Kessler, Barbara M Bröker, Antje Vogelgesang, Alexander Dressel
BACKGROUND AND PURPOSE: Regulatory T cells (Tregs) have been suggested to modulate stroke-induced immune responses. However, analyses of Tregs in patients and in experimental stroke have yielded contradictory findings. We performed the current study to assess the regulation and function of Tregs in peripheral blood of stroke patients. Age dependent expression of CD39 on Tregs was quantified in mice and men. METHODS: Total FoxP3(+) Tregs and CD39(+)FoxP3(+) Tregs were quantified by flow cytometry in controls and stroke patients on admission and on days 1, 3, 5, and 7 thereafter...
2016: Mediators of Inflammation
Lei Zuo, Luhang Shi, Fuling Yan
BACKGROUND: Sympathetic nervous system(SNS) is involved in the mechanism of immune suppression after stroke. Furthermore, as the pro-inflammatory effect of nuclear factor kappa B(NF-kB) is inhibited after stroke, which is regulated by cyclic adenosine monophosphate(cAMP) and proteinkinase A(PKA). The cAMP-PKA-NF-kB pathway might play an important role in noradrenergic-mediated immune dysfunction. AIM: The purpose of our research is to analyze how SNS interfere with the immune system after acute stroke and the underlying mechanism of cAMP-PKA-NF-kB pathway in regulating the inflammation...
August 3, 2016: Neuroscience Letters
Christine Römer, Odilo Engel, Katarzyna Winek, Sonja Hochmeister, Tian Zhang, Georg Royl, Juliane Klehmet, Ulrich Dirnagl, Christian Meisel, Andreas Meisel
Stroke-induced immunodepression (SIDS) is an essential cause of poststroke infections. Pharmacological inhibition of SIDS appears promising in preventing life-threatening infections in stroke patients. However, SIDS might represent an adaptive mechanism preventing autoreactive immune responses after stroke. To address this, we used myelin oligodendrocyte glycoprotein (MOG) T-cell receptor transgenic (2D2) mice where >80% of peripheral CD4(+) T cells express a functional receptor for MOG. We investigated in a murine model of middle cerebral artery occlusion the effect of blocking SIDS by inhibiting body's main stress axes, the sympathetic nervous system (SNS) with propranolol and the hypothalamic-pituitary-adrenal axis (HPA) with mifepristone...
May 20, 2015: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Trisha R Sippel, Takeru Shimizu, Frank Strnad, Richard J Traystman, Paco S Herson, Allen Waziri
Transient suppression of peripheral immunity is a major source of complication for patients suffering from ischemic stroke. The release of Arginase I (ArgI) from activated neutrophils has recently been associated with T-cell dysfunction in a number of pathologies. However, this pathway has not been previously explored in ischemic stroke. Using the murine model of transient middle cerebral artery occlusion, we explored effects of stroke on peripheral T-cell function and evaluated the role of neutrophils and ArgI...
October 2015: Journal of Cerebral Blood Flow and Metabolism
Arthur Liesz, Stefan Roth, Markus Zorn, Li Sun, Kerstin Hofmann, Roland Veltkamp
BACKGROUND AND PURPOSE: Acute brain injuries induce a systemic immune depression syndrome (SIDS) that predisposes patients to bacterial infections. While cellular compartments of this syndrome have been well characterized, the contribution of humoral immune mechanisms and particularly immunoglobulins to SIDS has not been investigated so far. METHODS: We determined serum immunoglobulin levels and infectious complications at several time points in 159 ischemic and hemorrhagic stroke patients...
September 2015: Experimental Neurology
Cong-Yuan Xia, Shuai Zhang, Yan Gao, Zhen-Zhen Wang, Nai-Hong Chen
Resident microglia are the major immune cells in the brain, acting as the first defense of the central nervous system. Following cerebral ischemia, microglia respond to this injury at first and transform from surveying microglia to active state. The activated microglia play a dual role in the ischemic injury, due to distinct microglia phenotypes, including deleterious M1 and neuroprotective M2. However, microglia show transient M2 phenotype followed by a shift to M1. The high ratio of M1 to M2 is significantly related to ischemic injury...
April 2015: International Immunopharmacology
Arthur Liesz, Alexander Dalpke, Eva Mracsko, Daniel J Antoine, Stefan Roth, Wei Zhou, Huan Yang, Shin-Young Na, Mustafa Akhisaroglu, Thomas Fleming, Tatjana Eigenbrod, Peter P Nawroth, Kevin J Tracey, Roland Veltkamp
Acute brain lesions induce profound alterations of the peripheral immune response comprising the opposing phenomena of early immune activation and subsequent immunosuppression. The mechanisms underlying this brain-immune signaling are largely unknown. We used animal models for experimental brain ischemia as a paradigm of acute brain lesions and additionally investigated a large cohort of stroke patients. We analyzed release of HMGB1 isoforms by mass spectrometry and investigated its inflammatory potency and signaling pathways by immunological in vivo and in vitro techniques...
January 14, 2015: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
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