Autoimmune Responses to Brain Following Stroke

Becker, Kyra J.

doi:10.1007/s12975-012-0154-0

Cited by 26 publications

(19 citation statements)

References 85 publications

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“…In the absence of systemic inflammation but in the presence of local inflammatory cytokines after brain injury, an anti-inflammatory response may be triggered that is detrimental, because it shuts down defense mechanisms, rendering the body susceptible to infection. Under these conditions, the response could in fact be considered maladaptive or inefficient [4, 20]. …”

Section: The Specific Immune Response To Ischemic Strokementioning

confidence: 99%

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Immunomodulation after ischemic stroke: potential mechanisms and implications for therapy

et al. 2016

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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.

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Section: The Specific Immune Response To Ischemic Strokementioning

confidence: 99%

“…Post-stroke infections result in systemic inflammation, making patients more prone to autoimmunity against brain antigens [20]. However, immune responses against self-antigens may happen as a collateral effect.…”

Section: Systemic Immunosuppressionmentioning

confidence: 99%

Immunomodulation after ischemic stroke: potential mechanisms and implications for therapy

et al. 2016

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“…Injured astrocytes, neurons and oligodendrocytes release brain derived antigens such as glial fibrillary acidic protein, S100, and myelin basic protein (MBP) 107 . DAMPs and brain derived antigens can also pass the ruptured BBB and enter the systemic circulation.…”

Section: Mechanisms Of Brain-heart Interaction After Strokementioning

confidence: 99%

Brain–Heart Interaction

Chen

Venkat

Seyfried

et al. 2017

Circulation Research

420

202

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Neurocardiology is an emerging specialty that addresses the interaction between the brain and the heart, i.e. the effects of cardiac injury on the brain, and the effects of brain injury on the heart. This review article focuses on cardiac dysfunction in the setting of stroke such as ischemic stroke, brain hemorrhage and subarachnoid hemorrhage (SAH). The majority of post stroke deaths are attributed to neurological damage, and cardiovascular complications are the second leading cause of post stroke mortality. Accumulating clinical and experimental evidence suggests a causal relationship between brain damage and heart dysfunction. Thus, it is important to determine whether cardiac dysfunction is triggered by stroke, is an unrelated complication, or is the underlying cause of stroke. Stroke induced cardiac damage may lead to fatality or potentially lifelong cardiac problems (such as heart failure), or to mild and recoverable damage such as neurogenic stress cardiomyopathy (NSC) and Takotsubo cardiomyopathy. The role of location and lateralization of brain lesions after stroke in brain-heart interaction, clinical biomarkers and manifestations of cardiac complications, and underlying mechanisms of brain-heart interaction following stroke, such as: the hypothalamic pituitary adrenal axis (HPA); catecholamine surge; sympathetic and parasympathetic regulation; microvesicles (MV’s); microRNAs; gut microbiome, immunoresponse and systemic inflammation are discussed.

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“…Systemic administration of an IFNγ- neutralizing antibody significantly decreases infarct volume [29] adding further evidence for the negative role of this inflammatory cytokine in stroke. Stroke patients who developed a Th 1 response to brain antigens at 90 days post-stroke were more likely to have a poorer outcome regardless of age or baseline stroke severity [30, 31]. IFNγ is considered a signature cytokine of a Th 1 response, which could implicate IFNγ as being detrimental following stroke in patients when an inflammatory T cell response is generated against brain antigens.…”

mentioning

confidence: 99%

Targeting the Peripheral Inflammatory Response to Stroke: Role of the Spleen

Pennypacker

2014

Transl. Stroke Res.

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Autoimmune Responses to Brain Following Stroke

Cited by 26 publications

References 85 publications

Immunomodulation after ischemic stroke: potential mechanisms and implications for therapy

Immunomodulation after ischemic stroke: potential mechanisms and implications for therapy

Brain–Heart Interaction

Targeting the Peripheral Inflammatory Response to Stroke: Role of the Spleen

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