IL-10 Prevents Apoptosis of Brain Endothelium during Bacteremia

Londoño, Diana; Carvajal, Jenny; Strle, Klemen; Kim, Kwang S.; Cadavid, Diego

doi:10.4049/jimmunol.1100060

Cited by 32 publications

(24 citation statements)

References 59 publications

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“…IL-10 had a protective effect upon the integrity of the blood–brain barrier [38]. IL-10 has been associated with delirium in non-inflamed, but not in inflamed, critically ill patients [9]; however, we could not find a significant difference in IL-10 levels between delirium and control patients.…”

Section: Discussioncontrasting

confidence: 66%

Inflammation biomarkers and delirium in critically ill patients

et al. 2014

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IntroductionDelirium is a common occurrence in critically ill patients and is associated with an increase in morbidity and mortality. Septic patients with delirium may differ from a general critically ill population. The aim of this investigation was to study the relationship between systemic inflammation and the development of delirium in septic and non-septic critically ill patients.MethodsWe performed a prospective cohort study in a 20-bed mixed intensive care unit (ICU) including 78 (delirium = 31; non-delirium = 47) consecutive patients admitted for more than 24 hours. At enrollment, patients were allocated to septic or non-septic groups according to internationally agreed criteria. Delirium was diagnosed using the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) during the first 72 hours of ICU admission. Blood samples were collected within 12 hours of enrollment for determination of tumor necrosis factor (TNF)-α, soluble TNF Receptor (STNFR)-1 and -2, interleukin (IL)-1β, IL-6, IL-10 and adiponectin.ResultsOut of all analyzed biomarkers, only STNFR1 (P = 0.003), STNFR2 (P = 0.005), adiponectin (P = 0.005) and IL-1β (P < 0.001) levels were higher in delirium patients. Adjusting for sepsis and sedation, these biomarkers were also independently associated with delirium occurrence. However, none of them were significant influenced by sepsis.ConclusionsSTNFR1, STNFR2, adiponectin and IL-1β were associated with delirium. Sepsis did not modify the relationship between the biomarkers and delirium occurrence.

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Section: Discussioncontrasting

confidence: 66%

Inflammation biomarkers and delirium in critically ill patients

et al. 2014

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“…Surprisingly, cerebral bacteremia may result in so much endothelial damage in the absence of IL-10 as to cause ICH and death shortly following peak bacterial loads (37). These findings are associated with increases in the FAS/FAS-ligand apoptotic pathway, which IL-10 reverses (37). However, the effects of IL-10 seem to be specific to the noxious stimuli generating its production.…”

Section: Vascular Endothelium Remodeling and Dysfunctionmentioning

confidence: 99%

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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“…In turn, reduction of BCL10-mediated inflammatory signaling by a novel recombinant protein, CP-CRADD, offers a new strategy to control vascular inflammatory responses not only in non-immune cells (endothelial cells) as demonstrated in this study but also in immune cells. CRADD is also expressed in human brain microvascular endothelial cells (60), suggesting its potential anti-inflammatory function there as well.…”

Section: Discussionmentioning

confidence: 99%

The Adaptor CRADD/RAIDD Controls Activation of Endothelial Cells by Proinflammatory Stimuli

Qiao

Liu

Veach

et al. 2014

Journal of Biological Chemistry

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Background:The role of CRADD in endothelial cells is unknown. Results: CRADD attenuates responses to proinflammatory agonists in endothelial cells and stabilizes their barrier function. Conclusion: CRADD plays a pivotal role in maintaining the integrity of the endothelial barrier. Significance: Understanding the role of CRADD as a physiologic rheostat of perturbed endothelial cells informs development of CRADD-based measures to stabilize endothelial integrity.

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IL-10 Prevents Apoptosis of Brain Endothelium during Bacteremia

Cited by 32 publications

References 59 publications

Inflammation biomarkers and delirium in critically ill patients

Inflammation biomarkers and delirium in critically ill patients

Role of Interleukin-10 in Acute Brain Injuries

The Adaptor CRADD/RAIDD Controls Activation of Endothelial Cells by Proinflammatory Stimuli

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