Letter by Shenhar-Tsarfaty et al Regarding Article, “Autonomic Shift and Increased Susceptibility to Infections After Acute Intracerebral Hemorrhage”
2011; Lippincott Williams & Wilkins; Volume: 42; Issue: 10 Linguagem: Inglês
10.1161/strokeaha.111.627448
ISSN1524-4628
AutoresShani Shenhar‐Tsarfaty, E Bénassayag, Shlomo Berliner, Natan M. Bornstein, Hermona Soreq,
Tópico(s)Traumatic Brain Injury and Neurovascular Disturbances
ResumoHomeStrokeVol. 42, No. 10Letter by Shenhar-Tsarfaty et al Regarding Article, "Autonomic Shift and Increased Susceptibility to Infections After Acute Intracerebral Hemorrhage" Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBLetter by Shenhar-Tsarfaty et al Regarding Article, "Autonomic Shift and Increased Susceptibility to Infections After Acute Intracerebral Hemorrhage" Shani Shenhar-Tsarfaty, Einor Ben-Assayag, Shlomo Berliner, Natan M. Bornstein and Hermona Soreq Shani Shenhar-TsarfatyShani Shenhar-Tsarfaty , Einor Ben-AssayagEinor Ben-Assayag , Shlomo BerlinerShlomo Berliner , Natan M. BornsteinNatan M. Bornstein and Hermona SoreqHermona Soreq Originally published25 Aug 2011https://doi.org/10.1161/STROKEAHA.111.627448Stroke. 2011;42:e559Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2011: Previous Version 1 To the Editor:In the May issue of Stroke, we read with great interest the recent article by Sykora et al regarding the association of decreased baroreflex sensitivity with infections after intracerebral hemorrhage.1 The authors demonstrated decreased baroreflex sensitivity and an invasive procedure as independent predictors for postintracerebral hemorrhage infection, supporting the concept of autonomic shift toward sympathetic predominance as an independent risk of higher occurrence of infection in intracerebral hemorrhage. Although not discussed by the authors, their findings further confirm a critical role for the cholinergic–anti-inflammatory effect in patients with stroke, as was also shown in several recent studies of other experimental animal and human models.The principal neurotransmitter of the parasympathetic branch of the autonomous nervous system is acetylcholine whose levels are regulated by the closely related enzymes acetyl- and butyrylcholinesterase (AChE, BChE), collectively determining the total cholinesterase activity in the circulation.2 Therefore, the sympathetic/parasympathetic balance could be estimated by measuring these enzyme activities. Thus, recent experimental evidence suggests that the parasympathetic nervous system may be an important contributor to immunodepression. The brain, through vagal secretion of acetylcholine, regulates the innate immune response during infection or injury and suppresses peripheral inflammation by intercepting proinflammatory cytokine production.3We have recently shown that serum AChE activity as well as the cholinergic status, a measurement for the overall capability to hydrolyze acetylcholine in the circulation, predicts the neurological outcome, survival, and inflammatory reactions after acute ischemic stroke in humans.4 Both cholinergic parameters were correlated with multiple inflammatory biomarkers. It is interesting to compare these 2 studies, which use 2 different approaches to estimate the autonomic shift toward sympathetic predominance in 2 types of stroke and to assess the deteriorating effect of this shift on the inflammatory profile and risk of infection. An emerging controller of the cholinergic effect of inflammation is micro-RNA-132,5 whose involvement with poststroke recovery awaits further studies. Taken together, these promising results might open new venues for more rigorous assessment of the poststroke risk of survival and systemic infection and the identification of conceptually novel targets for therapeutic interference.Shani Shenhar-Tsarfaty, PhD The Institute of Life Sciences The Edmond and Lily Safra Center for Brain Sciences The Hebrew University of Jerusalem Jerusalem, IsraelEinor Ben-Assayag, PhDShlomo Berliner, MD, PhDNatan M. Bornstein, MD Departments of Neurology and Internal Medicine-E Tel Aviv Sourasky Medical Center Affiliated with the Sackler Faculty of Medicine Tel Aviv, IsraelHermona Soreq, PhD The Institute of Life Sciences The Edmond and Lily Safra Center for Brain Sciences The Hebrew University of Jerusalem Jerusalem, IsraelDisclosuresNone.FootnotesStroke welcomes Letters to the Editor and will publish them, if suitable, as space permits. Letters must reference a Stroke published-ahead-of-print article or an article printed within the past 3 weeks. The maximum length is 750 words including no more than 5 references and 3 authors. Please submit letters typed double-spaced. Letters may be shortened or edited. Include a completed copyright transfer agreement form (available online at http://stroke.ahajournals.org and http://submit-stroke.ahajournals.org). References 1. Sykora M, Diedler J, Poli S, Rizos T, Turcani P, Veltkamp R, Steiner T. Autonomic shift and increased susceptibility to infections after acute intracerebral hemorrhage. Stroke. 2011; 42:1218–1223.LinkGoogle Scholar2. Soreq H, Seidman S. Acetylcholinesterase—new roles for an old actor. Nat Rev Neurosci. 2001; 2:294–302.CrossrefMedlineGoogle Scholar3. Tracey KJ. Understanding immunity requires more than immunology. Nat Immunol. 2010; 11:561–564.CrossrefMedlineGoogle Scholar4. Ben Assayag E, Shenhar-Tsarfaty S, Ofek K, Soreq L, Bova I, Shopin L, Berg RM, Berliner S, Shapira I, Bornstein NM, Soreq H. Serum cholinesterase activities distinguish between stroke patients and controls and predict 12-month mortality. Mol Med. 2010; 16:278–286.MedlineGoogle Scholar5. Shaked I, Meerson A, Wolf Y, Avni R, Greenberg D, Gilboa-Geffen A, Soreq H. Microrna-132 potentiates cholinergic anti-inflammatory signaling by targeting acetylcholinesterase. Immunity. 2009; 31:965–973.CrossrefMedlineGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetailsCited By Kramer A, Roberts D, Holodinsky J, Todd S, Hill M, Zygun D, Faris P and Wong J (2014) Intraventricular Tissue Plasminogen Activator in Subarachnoid Hemorrhage Patients: A Prospective, Randomized, Placebo-Controlled Pilot Trial, Neurocritical Care, 10.1007/s12028-014-9965-z, 21:2, (275-284), Online publication date: 1-Oct-2014. October 2011Vol 42, Issue 10 Advertisement Article InformationMetrics © 2011 American Heart Association, Inc.https://doi.org/10.1161/STROKEAHA.111.627448PMID: 21868734 Originally publishedAugust 25, 2011 PDF download Advertisement SubjectsIntracranial HemorrhageIschemic Stroke
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