Interleukins and Ischemic Stroke

Zhu, Hua; Hu, Siping; Li, Yuntao; Sun, Yao; Xiong, Xiao-Qing; Hu, Xinyao; Chen, Junjing; Sheng, Qing

doi:10.3389/fimmu.2022.828447

Cited by 159 publications

(125 citation statements)

References 176 publications

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“…We found that caspase-1 and IL-10 were elevated in patients with unfavorable outcomes when compared to those with favorable outcomes. IL-10 is secreted by numerous cells of the CNS after injury and has been shown to play a protective role by reducing cytokine activity, proinflammatory activity, and apoptosis [75,76]. Additionally, IL-10 inhibits IL-2 activity, and has been shown in numerous studies to be increased after stroke or TBI [75,76].…”

Section: Discussionmentioning

confidence: 99%

Inflammatory Biomarkers of Traumatic Brain Injury

et al. 2022

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Traumatic brain injury (TBI) has a complex pathology in which the initial injury releases damage associated proteins that exacerbate the neuroinflammatory response during the chronic secondary injury period. One of the major pathological players in the inflammatory response after TBI is the inflammasome. Increased levels of inflammasome proteins during the acute phase after TBI are associated with worse functional outcomes. Previous studies reveal that the level of inflammasome proteins in biological fluids may be used as promising new biomarkers for the determination of TBI functional outcomes. In this study, we provide further evidence that inflammatory cytokines and inflammasome proteins in serum may be used to determine injury severity and predict pathological outcomes. In this study, we analyzed blood serum from TBI patients and respective controls utilizing Simple Plex inflammasome and V-PLEX inflammatory cytokine assays. We performed statistical analyses to determine which proteins were significantly elevated in TBI individuals. The receiver operating characteristics (ROC) were determined to obtain the area under the curve (AUC) to establish the potential fit as a biomarker. Potential biomarkers were then compared to documented patient Glasgow coma scale scores via a correlation matrix and a multivariate linear regression to determine how respective biomarkers are related to the injury severity and pathological outcome. Inflammasome proteins and inflammatory cytokines were elevated after TBI, and the apoptosis-associated speck like protein containing a caspase recruitment domain (ASC), interleukin (IL)-18, tumor necrosis factor (TNF)-α, IL-4 and IL-6 were the most reliable biomarkers. Additionally, levels of these proteins were correlated with known clinical indicators of pathological outcome, such as the Glasgow coma scale (GCS). Our results show that inflammatory cytokines and inflammasome proteins are promising biomarkers for determining pathological outcomes after TBI. Additionally, levels of biomarkers could potentially be utilized to determine a patient’s injury severity and subsequent pathological outcome. These findings show that inflammation-associated proteins in the blood are reliable biomarkers of injury severity that can also be used to assess the functional outcomes of TBI patients.

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Section: Discussionmentioning

confidence: 99%

Inflammatory Biomarkers of Traumatic Brain Injury

et al. 2022

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“…Over-activation of microglial cells releases various pro-inflammatory cytokines that exacerbate cerebral ischemia-reperfusion (I/R) injury [148,149]. There are many different cytokines reported as biomarkers for cerebral ischemia, such as IL-1β, IL-6, IL-8, IL-12, IL-15, IL-16, IL-20, IL-18, IL-23/IL-17, and so on, which play a pro-inflammatory role after ischemic stroke; ILs that have anti-inflammatory effects on ischemic stroke include IL-2, IL-4, IL-10, IL-13, IL-19, IL-33, and so on, as reported recently [150]. In 2019, ischemic stroke affected approximately 77.2 million individuals [151].…”

Section: Role Of Fatty Acids In Microglial Polarization In Cerebral I...mentioning

confidence: 67%

Roles of Fatty Acids in Microglial Polarization: Evidence from In Vitro and In Vivo Studies on Neurodegenerative Diseases

Sanjay

Park

Lee

2022

IJMS

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Microglial polarization to the M1 phenotype (classically activated) or the M2 phenotype (alternatively activated) is critical in determining the fate of immune responses in neurodegenerative diseases (NDs). M1 macrophages contribute to neurotoxicity, neuronal and synaptic damage, and oxidative stress and are the first line of defense, and M2 macrophages elicit an anti-inflammatory response to regulate neuroinflammation, clear cell debris, and promote neuroregeneration. Various studies have focused on the ability of natural compounds to promote microglial polarization from the M1 phenotype to the M2 phenotype in several diseases, including NDs. However, studies on the roles of fatty acids in microglial polarization and their implications in NDs are a rare find. Most of the studies support the role of polyunsaturated fatty acids (PUFAs) in microglial polarization using cell and animal models. Thus, we aimed to collect data and provide a narrative account of microglial types, markers, and studies pertaining to fatty acids, particularly PUFAs, on microglial polarization and their neuroprotective effects. The involvement of only PUFAs in the chosen topic necessitates more in-depth research into the role of unexplored fatty acids in microglial polarization and their mechanistic implications. The review also highlights limitations and future challenges.

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“…[23][24][25] warrants further investigation. Classically, IL-4 and related T h2 -type immune responses were thought to oppose pro-atherogenic T h1 activities, and indeed IL-4 has been demonstrated to aid in tissue recovery/damage resolution following ischemic stroke [26]. Yet, the simplified paradigm of T h2 and IL-4 as purely athero-protective, inflammation-resolving has been challenged by other mechanistic and clinical data implicating these allergic-type responses (e.g.…”

Section: Discussionmentioning

confidence: 99%