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Critical Care

, 20:391

First Online: 07 December 2016DOI: 10.1186-s13054-016-1573-1

Cite this article as: Santos Samary, C., Pelosi, P., Leme Silva, P. et al. Crit Care 2016 20: 391. doi:10.1186-s13054-016-1573-1

Abstract

Brain injuries are often associated with intensive care admissions, and carry high morbidity and mortality rates. Ischemic stroke is one of the most frequent causes of injury to the central nervous system. It is now increasingly clear that human stroke causes multi-organ systemic disease. Brain inflammation may lead to opposing local and systemic effects. Suppression of systemic immunity by the nervous system could protect the brain from additional inflammatory damage; however, it may increase the susceptibility to infection. Pneumonia and urinary tract infection are the most common complications occurring in patients after stroke. The mechanisms involved in lung-brain interactions are still unknown, but some studies have suggested that inhibition of the cholinergic anti-inflammatory pathway and release of glucocorticoids, catecholamines, and damage-associated molecular patterns DAMPs are among the pathophysiological mechanisms involved in communication from the ischemic brain to the lungs after stroke. This review describes the modifications in local and systemic immunity that occur after stroke, outlines mechanisms of stroke-induced immunosuppression and their role in pneumonia, and highlights potential therapeutic targets to reduce post-stroke complications. Despite significant advances towards a better understanding of the pathophysiology of ischemic stroke-induced immunosuppression and stroke-associated pneumonia SAP in recent years, many unanswered questions remain. The true incidence and outcomes of SAP, especially in intensive care unit settings, have yet to be determined, as has the full extent of stroke-induced immunosuppression and its clinical implications.

KeywordsIschemic stroke Immunosuppression Stroke-associated pneumonia Inflammation Damage-associated molecular patterns AbbreviationsAECalveolar epithelial cells

ATPadenosine triphosphate

BBBblood–brain barrier

CBFcerebral blood flow

CNScentral nervous system

CRHcorticotropin-releasing hormone

CTLAcytotoxic T-lymphocyte-associated protein

DAMPsdanger-associated molecular patterns

HMGB1high-mobility group box 1

HPAhypothalamic–pituitary–adrenal

IFN-γinterferon gamma

ILinterleukin

iNKTinvariant natural killer

LPSlipopolysaccharide

MAPmitogen-activated protein

MHCmajor histocompatibility complexes

MIP-2macrophage inflammatory protein-2

nAChRα7nicotinic acetylcholine receptor alpha-7

NF-κBnuclear factor kappa B

NMDARN-methyl-D-aspartate receptor

PNSparasympathetic nervous system

RAGEreceptor for advanced glycation end products

ROSreactive oxygen species

SAPstroke-associated pneumonia

TGFtransforming growth factor

TLRtoll-like receptor

TNFtumor necrosis factor

Tregsregulatory T cells

VNSvagus nerve stimulation

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Autor: Cynthia Santos Samary - Paolo Pelosi - Pedro Leme Silva - Patricia Rieken Macedo Rocco

Fuente: https://link.springer.com/







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