Interleukin-10 may protect against progressing injury during the acute phase of ischemic stroke

Protti, G; Gagliardi, Rubens José; Forte, Wilma Carvalho Neves; Sprovieri, Sandra Regina Schwarzwälder

doi:10.1590/0004-282x20130168

Cited by 38 publications

(31 citation statements)

References 15 publications

(10 reference statements)

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“…As compared to those who die, IS patients who improve have been shown to have lower IL-10 at 24 h, but increased levels at 72 h and 144 h (79). In other studies, low IL-10 levels are associated with acute neurologic decline post-stroke (76, 77). Yet another small study found no correlation with IL-10 and other cytokines and IS patient prognosis (86).…”

Section: Ischemic Strokementioning

confidence: 68%

Role of Interleukin-10 in Acute Brain Injuries

et al. 2017

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Interleukin-10 (IL-10) is an important anti-inflammatory cytokine expressed in response to brain injury, where it facilitates the resolution of inflammatory cascades, which if prolonged causes secondary brain damage. Here, we comprehensively review the current knowledge regarding the role of IL-10 in modulating outcomes following acute brain injury, including traumatic brain injury (TBI) and the various stroke subtypes. The vascular endothelium is closely tied to the pathophysiology of these neurological disorders and research has demonstrated clear vascular endothelial protective properties for IL-10. In vitro and in vivo models of ischemic stroke have convincingly directly and indirectly shown IL-10-mediated neuroprotection; although clinically, the role of IL-10 in predicting risk and outcomes is less clear. Comparatively, conclusive studies investigating the contribution of IL-10 in subarachnoid hemorrhage are lacking. Weak indirect evidence supporting the protective role of IL-10 in preclinical models of intracerebral hemorrhage exists; however, in the limited number of clinical studies, higher IL-10 levels seen post-ictus have been associated with worse outcomes. Similarly, preclinical TBI models have suggested a neuroprotective role for IL-10; although, controversy exists among the several clinical studies. In summary, while IL-10 is consistently elevated following acute brain injury, the effect of IL-10 appears to be pathology dependent, and preclinical and clinical studies often paradoxically yield opposite results. The pronounced and potent effects of IL-10 in the resolution of inflammation and inconsistency in the literature regarding the contribution of IL-10 in the setting of acute brain injury warrant further rigorously controlled and targeted investigation.

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Section: Ischemic Strokementioning

confidence: 68%

Role of Interleukin-10 in Acute Brain Injuries

et al. 2017

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“…In this study, patients with lower IL-10 levels deteriorated neurologically within the irst 72 h. Thus, IL-10 may be involved in protective mechanisms during the acute phase of AIS [181]. However, IL-10's role in AIS and post-stroke recovery may be inluenced by additional patient characteristics, such as sex.…”

Section: Anti-inlammatory Il-10 In Aismentioning

confidence: 59%

Roles of Pro- and Anti-inflammatory Cytokines in Traumatic Brain Injury and Acute Ischemic Stroke

Dugue¹,

Nath²,

Dugue³

et al. 2017

Mechanisms of Neuroinflammation

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This chapter will introduce the reader to the pathophysiology of two devastating neurologic events, traumatic brain injury (TBI) and acute ischemic stroke (AIS). Here we focus on the role of key pro-inlammatory and anti-inlammatory cytokines. Several experimental interventions have been found to modulate cytokine production and brain injury after AIS or TBI. Here minocycline, biological response modiiers, hormonal therapies, omega-3 faty acids, N-acetylcysteine, and cannabinoids will be discussed. In addition, the role of cytokine-induced inlammasomes in both TBI and AIS will be addressed and followed by discussion of pro-inlammatory cytokines (e.g., TNF-α, IL-1β, IL-18, and IFN-γ). Finally, the main anti-inlammatory cytokines, IL-33, IL-10, IL-6, and IL-4, will be discussed in the context of both TBI and AIS. It should be noted that the role of these cytokines is diverse and the dichotomization of classically pro-versus anti-inlammatory cytokines is being re-examined, as many of these cytokines have been found to play dual roles in TBI and AIS brain injury.Keywords: traumatic brain injury, ischemic stroke, cytokines, interleukins, inlammasome Pathophysiology of traumatic brain injuryTraumatic brain injury (TBI) is a major cause of death and disability worldwide [1,2]. It is one of the most commonly diagnosed neurological disorders in the United States, impacting people of a variety of ages and segments of society [3]. In Europe, the economic cost of © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.TBI is over 33 billion euros per year [4]. Continued surveillance and research is being done to reduce primary and secondary TBI [as well as acute ischemic stroke(AIS)]-induced brain injury [1].The pathophysiology of TBI begins with the initial brain trauma (i.e., the primary injury). This primary injury results from mechanical damage that disrupts the blood-brain barrier (BBB), alters the vasculature and damages brain tissue. The resulting injured glia and neurons release their intracellular contents (i.e., damage-associated molecular paterns; (DAMPs)) into the extracellular space and activate neighboring glia and neurons. Activated glia and neurons then produce molecular signals that can both exacerbate and mend the acute injury and contribute to long-term recovery [5][6][7][8][9]. These downstream molecular and cellular processes (i.e., the secondary injury in TBI) are the focus of many pre-clinical and clinical therapeutic studies. Secondary injury in TBI involves a host of molecular and cellular responses to the The pathophysiology of AIS and TBI share common mechanisms. The initial insult in AIS, an occlusion of blood low resulting in a core infarct zone surrounded by a poorly perfused penumbra, versus the initial primary physical impact in TBI both result in pe...

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“…Previous clinical studies have established a positive association between higher IL-10 levels during the acute phase and good outcome in IS [25,[31][32][33][34][35]. Nevertheless, no studies had previously investigated the role of IL-10 as a possible action mechanism of Treg-cells in acute phase of IS in humans.…”

Section: Discussionmentioning

confidence: 99%

Role of regulatory T-cells on ischemic stroke outcome: new clinical evidences

Santamaría-Cadavid

Rodríguez‐Castro

Rodríguez‐Yáñez

et al. 2019

Preprint

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Background: Recent preclinical studies have shown that regulatory T (Treg) cells play a key role in the immune response after ischemic stroke (IS). However, the role of Treg-cells in human acute IS has been poorly investigated. Our aim was to study the relationship between circulating Treg-cells and outcome in human IS patients.Methods Methods: A total of 204 IS patients and 22 control subjects were recruited. The main study variable was good functional outcome at 3 months (modified Rankin scale ≤2) considering infarct volume, Early Neurological Deterioration (END) and risk of infections as secondary variables. The percentage of circulating Treg-cells was measured at admission, 48, 72h and at day 7 after stroke onset.Results Results: Circulating Treg-cell levels were higher in IS patients compared to control subjects. Treg-cells at 48h were independently associated with good functional outcome (OR, 3.5; CI: 1.9-7.8) after adjusting by confounding factors. Patients with lower Treg-cells at 48h showed higher frequency of END and risk of infections. In addition, a negative correlation was found between circulating Treg-cells at 48h (r=-0.414) and 72h (r=-0.418) and infarct volume. Conclusions: These findings suggest that Treg-cells may participate in the recovery of IS patients. Therefore, Treg-cells may be considered a potential therapeutic target in acute ischemic stroke.

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Interleukin-10 may protect against progressing injury during the acute phase of ischemic stroke

Cited by 38 publications

References 15 publications

Role of Interleukin-10 in Acute Brain Injuries

Role of Interleukin-10 in Acute Brain Injuries

Roles of Pro- and Anti-inflammatory Cytokines in Traumatic Brain Injury and Acute Ischemic Stroke

Role of regulatory T-cells on ischemic stroke outcome: new clinical evidences

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