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Post-stroke infections associated with spleen volume reduction: A pilot study.

PLoS One

July 2020

Department of Neurology, Universitair Ziekenhuis Brussel, Center for Neurosciences, Vrije Universiteit Brussel, Brussels, Belgium.

Background: Spleen volume reduction followed by re-expansion has been described in acute ischemic stroke in both animal and human studies. Splenic contraction might be partially due to sympathetic hyperactivity and might be accompanied by release of splenocytes in the peripheral circulation, leading to immunodepression.

Aims: To investigate whether spleen volume changes in the first week after stroke are associated with post-stroke infections, changes in lymphocytes count and autonomic dysfunction.

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β-arrestin2 functions as a key regulator in the sympathetic-triggered immunodepression after stroke.

J Neuroinflammation

April 2018

Department of Neurology, Affiliated ZhongDa Hospital, School of Medicine, Southeast University, Dingjiaqiao 87, Nanjing, 210009, People's Republic of China.

Background: Stroke-induced immunodeficiency syndrome (SIDS) is regarded as a protective mechanism for secondary inflammatory injury as well as a contributor to infection complications. Although stroke-induced hyperactivation of the sympathetic system is proved to facilitate SIDS, the involved endogenous factors and pathways are largely elusive. In this study, we aim to investigate the function of beta-arrestin-2 (ARRB2) in the sympathetic-mediated SIDS.

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Background: Suitable biomarkers that have prognostic values are one of the key points of interest in ischaemic stroke. Increased sympathetic nervous system activity in ischaemic stroke causes multiple local and systemic effects that can be detrimental to the outcome. The mechanism of action is increased secretion and activity of catecholamines, whose end metabolic products are vanillylmandelic acid and homovanilic acid.

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Background: Evidence has led to the consideration of immunodepression after stroke as an important contributor to stroke associated infection (SAI). However, so far no specific immunological indicator has been identified for SAI, and the underlying mechanism remains poorly understood.

Results: SAI patients had significantly higher IL-6 and IL-10 levels and lower HLA-DR levels than no-infection patients within 48h after stroke onset.

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Cholinergic Pathway Suppresses Pulmonary Innate Immunity Facilitating Pneumonia After Stroke.

Stroke

November 2015

From the Department of Experimental Neurology (O.E., K.W., M.T., U.D., A.M.), Department of Neurology (U.D., A.M.), NeuroCure Clinical Research (U.D., A.M.), Institute for Medical Immunology (L.A., C.D., H.D.V., C.M.), BCRT Berlin Brandenburg Centre for Regenerative Medicine (L.A., H.D.V.), Department of Neuropsychiatry and Laboratory of Molecular Psychiatry (C.B., J.P.), and Center for Stroke Research Berlin (O.E., K.W., M.T., U.D., A.M.), Charité University Medicine Berlin, Berlin, Germany; German Center for Neurodegeneration Research (DZNE), partner site Berlin, Germany (J.P., U.D.); Department of Internal Medicine II, Justus-Liebig-University, Universities Giessen and Marburg Lung Center, Member of the German Center for Lung Research (DZL) (S.H.); and Max Delbrück Center for Molecular Medicine, Berlin, Germany (A.C.d.C.G.).

Article Synopsis
  • Temporary immunosuppression post-central nervous system injury, particularly after stroke, increases the risk of pneumonia, while the parasympathetic nervous system’s role in immune response post-stroke is not well understood.
  • Using a mouse model of stroke, researchers found that parasympathetic activity significantly increased following a stroke and that inhibiting this signaling led to improved immune responses in the lungs, preventing pneumonia.
  • The findings highlight the importance of cholinergic pathways in lung immunity after neurological injuries, indicating that targeting these pathways could be vital in managing infection risks post-stroke.
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