scholarly journals Pro-Inflammatory Cytokines as Potential Early Biomarkers and Therapeutic Targets to Combat Ischemic Stroke

2020 ◽  
Vol 2 (11) ◽  
pp. 5-19
Author(s):  
Megha Agrawal ◽  
Keyword(s):  
Ischemic Stroke ◽  
Inflammatory Cytokines ◽  
Time Window ◽  
Medical Condition ◽  
Brain Area ◽  
Therapeutic Targets ◽  
Ongoing Research ◽  
Stroke Research ◽  
Inflammatory Processes ◽  
Pro Inflammatory Cytokines

Ischemic stroke is a serious medical condition and widely considered one of the most common causes of death and disability in the world today. There have been notable research advances in stroke so far and studies have shown that stroke’s complex pathophysiology process involves the oxidative stress and inflammatory reaction. However, despite the progress in stroke research, currently there are no established biochemical factors available that can be employed in the early diagnostics and intervention in stroke. Mostly, stroke diagnosis is based on neuroimaging, which is not a rapid tool to diagnose stroke. This decreases the survivability rate. Further, conventional therapeutic approaches for ischemic stroke management are based on restoring blood flow to the affected brain area and these therapies are effective only during a limited time window. Hence, this procedure results in benefiting only a very small percentage of patients. In view of these limitations, the ongoing research has focused on seeking alternative treatment methods that can reduce stroke brain damage and improve patients’ outcome. To this end, research goals are targeted towards gaining insights into the inflammatory response triggered by cerebral ischemia that is supposed to play an important role in the progression of stroke, and also the subsequent study of inflammatory molecules in the acute phase of stroke. In this mini-review, we describe the inflammatory processes occurring during ischemic stroke along with the potential for pro-inflammatory cytokines to become stroke biomarkers as well as interesting neuroprotective therapeutic targets that could be blocked or stimulated to modulate inflammation after stroke. Finally, we present a perspective briefly discussing some viewpoints on future studies in the ongoing field of stroke research.

scholarly journals Relationship between the induction of inflammatory processes and infectious diseases in patients with ischemic stroke.

2013 ◽  
Vol 60 (3) ◽  
Author(s):  
Marek Cieślak ◽  
Andrzej Wojtczak ◽  
Michał Cieślak
Keyword(s):  
Ischemic Stroke ◽  
Survival Rate ◽  
Cerebral Ischemia ◽  
Infectious Diseases ◽  
Inflammatory Cytokines ◽  
Brain Ischemia ◽  
Neurological Deficit ◽  
Interleukin 1 ◽  
Inflammatory Processes ◽  
Pro Inflammatory Cytokines

Pro-inflammatory cytokines participate in the induction of ischemic stroke. So far, their participation in the cerebral ischemia was proven for the tumor necrosis factor TNF-α, interleukin-1 (IL-1), and interleukin-6 (IL-6). The release of the pro-inflammatory cytokines into the extracellular space causes the enlargement of the brain damage region, and consequently increases the neurological deficit and negatively affects the survival rate prognoses. That is confirmed by the increased concentration of pro-inflammatory cytokines in blood and the cerebrospinal fluid of patients with brain stroke, as well as by the research on the induced/experimental cerebral ischemia in animals. The pro-inflammatory cytokines participate in the migration of the reactive T lymphocytes to the regions of brain ischemia where they enhance the nerve tissue damage by down-regulation of microcirculation, induce the pro-thrombotic processes and release other neurotoxic cytokines. Also, in the early stage of cerebral ischemia, cytokines activate the axis hypothalamus-pituitary gland-adrenal cortex and increase the cortisol concentration in blood, what results in the decreased resistance to infectious diseases. Administration of the inhibitor of the interleukin-1 receptor (IL-1Ra) inhibits the inflammatory processes in the region of brain ischemia, and subsequently improves the prognosis for the size of the neurological deficit and the survival rate, as well as resistance to infectious diseases.

Acute Ischemic Stroke is Associated with Increased Serum Levels of Pro-inflammatory Cytokines

2020 ◽  
Author(s):  
Bhagirath Ramawat ◽  
Alvee Saluja ◽  
Jayashree Bhatacharjee ◽  
Anshuman Srivastava ◽  
Rajinder K. Dhamija
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Inflammatory Cytokines ◽  
Serum Levels ◽  
Pro Inflammatory Cytokines

Aging and Neuroinflammatory Disorders: New Biomarkers and Therapeutic Targets

2019 ◽  
Vol 25 (39) ◽  
pp. 4168-4174 ◽  
Author(s):  
Caterina M. Gambino ◽  
Bruna Lo Sasso ◽  
Giulia Bivona ◽  
Luisa Agnello ◽  
Marcello Ciaccio
Keyword(s):  
Neurodegenerative Disorder ◽  
Strong Association ◽  
Disease Onset ◽  
Therapeutic Targets ◽  
Low Grade ◽  
Ongoing Research ◽  
Neurodegenerative Process ◽  
Chronic Neuroinflammation ◽  
Inflammatory Processes ◽  
New Biomarkers

: Chronic neuroinflammation is a common feature of the pathogenic mechanisms involved in various neurodegenerative age-associated disorders, such as Alzheimer's disease, multiple sclerosis, Parkinson’s disease, and dementia. : In particular, persistent low-grade inflammation may disrupt the brain endothelial barrier and cause a significant increase of pro-inflammatory cytokines and immune cells into the cerebral tissue that, in turn, leads to microglia dysfunction and loss of neuroprotective properties. : Nowadays, growing evidence highlights a strong association between persistent peripheral inflammation, as well as metabolic alterations, and neurodegenerative disorder susceptibility. The identification of common pathways involved in the development of these diseases, which modulate the signalling and immune response, is an important goal of ongoing research. : The aim of this review is to elucidate which inflammation-related molecules are robustly associated with the risk of neurodegenerative diseases. Of note, peripheral biomarkers may represent direct measures of pathophysiologic processes common of aging and neuroinflammatory processes. In addition, molecular changes associated with the neurodegenerative process might be present many decades before the disease onset. Therefore, the identification of a comprehensive markers panel, closely related to neuroinflammation, could be helpful for the early diagnosis, and the identification of therapeutic targets to counteract the underlying chronic inflammatory processes.

scholarly journals Update in the Early Management and Reperfusion Strategies of Patients with Acute Ischemic Stroke

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Aldo A. Mendez ◽  
Edgar A. Samaniego ◽  
Sunil A. Sheth ◽  
Sudeepta Dandapat ◽  
David M. Hasan ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Mechanical Thrombectomy ◽  
Time Window ◽  
Prehospital Care ◽  
Standard Of Care ◽  
Ongoing Research ◽  
Early Management ◽  
Endovascular Thrombectomy

Acute ischemic stroke (AIS) remains a leading cause of death and long-term disability. The paradigms on prehospital care, reperfusion therapies, and postreperfusion management of patients with AIS continue to evolve. After the publication of pivotal clinical trials, endovascular thrombectomy has become part of the standard of care in selected cases of AIS since 2015. New stroke guidelines have been recently published, and the time window for mechanical thrombectomy has now been extended up to 24 hours. This review aims to provide a focused up-to-date review for the early management of adult patients with AIS and introduce the new upcoming areas of ongoing research.

scholarly journals Testosterone Therapy Could Be a Potential Approach For Treatment of Elderly Male COVID-19 Patients- A Review

2021 ◽  
pp. 181-187
Author(s):  
MR Gofur
Keyword(s):  
Inflammatory Cytokines ◽  
Therapeutic Drug ◽  
Elderly Male ◽  
Testosterone Therapy ◽  
Potential Approach ◽  
Male Predominance ◽  
Inflammatory Processes ◽  
Male Patients ◽  
High Level ◽  
Pro Inflammatory Cytokines

The emerging SARS-CoV-2 (2019-nCoV) is still following the increasing trend of infection worldwide with an elderly male predominance. Studies reported that majority of male patients with COVID-19 suffer from severe testosterone deficiency and are likely to die from the coronavirus mainly due to a less effective immune response and high level of pro-inflammatory cytokines, a condition called cytokine storm. Testosterone (a steroid having protective anti-inflammatory properties) therapy reduces circulating levels of pro-inflammatory cytokines. Testosterone therapy is effective in the management of elderly Alzheimer's disease where pro-inflammatory cytokines are the potent mediators of inflammatory processes, and aged men having HIV infection. As, currently there is no specific therapeutic drug targeting the SARS-CoV-2, and, considering the present pandemic circumstance, and the immunomodulatory and protective findings of testosterone therapy in previous studies, it can be hypothesized that testosterone therapy could be a potential approach for treatment of elderly male COVID-19 patients. J. Bio-Sci. 29(1): 181-187, 2021 (June)

scholarly journals Immunomodulatory sphingosine-1-phosphates as plasma biomarkers of Alzheimer’s disease and vascular cognitive impairment

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Xin Ying Chua ◽  
Yuek Ling Chai ◽  
Wee Siong Chew ◽  
Joyce R. Chong ◽  
Hui Li Ang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Cell Line ◽  
Inflammatory Cytokines ◽  
Vascular Cognitive Impairment ◽  
Cerebrovascular Diseases ◽  
Ongoing Research ◽  
Primary Astrocytes ◽  
Pro Inflammatory Cytokines

Abstract Background There has been ongoing research impetus to uncover novel blood-based diagnostic and prognostic biomarkers for Alzheimer’s disease (AD), vascular dementia (VaD), and related cerebrovascular disease (CEVD)-associated conditions within the spectrum of vascular cognitive impairment (VCI). Sphingosine-1-phosphates (S1Ps) are signaling lipids which act on the S1PR family of cognate G-protein-coupled receptors and have been shown to modulate neuroinflammation, a process known to be involved in both neurodegenerative and cerebrovascular diseases. However, the status of peripheral S1P in AD and VCI is at present unclear. Methods We obtained baseline bloods from individuals recruited into an ongoing longitudinal cohort study who had normal cognition (N = 80); cognitive impairment, no dementia (N = 160); AD (N = 113); or VaD (N = 31), along with neuroimaging assessments of cerebrovascular diseases. Plasma samples were processed for the measurements of major S1P species: d16:1, d17:1, d18:0, and d18:1, along with pro-inflammatory cytokines interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF). Furthermore, in vitro effects of S1Ps on cytokine expression were also studied in an astrocytoma cell line and in rodent primary astrocytes. Results Of the S1Ps species measured, only d16:1 S1P was significantly reduced in the plasma of VaD, but not AD, patients, while the d18:1 to d16:1 ratios were increased in all cognitive subgroups (CIND, AD, and VaD). Furthermore, d18:1 to d16:1 ratios correlated with levels of IL-6, IL-8, and TNF. In both primary astrocytes and an astroglial cell line, treatment with d16:1 or d18:1 S1P resulted in the upregulation of mRNA transcripts of pro-inflammatory cytokines, with d18:1 showing a stronger effect than d16:1. Interestingly, co-treatment assays showed that the addition of d16:1 reduced the extent of d18:1-mediated gene expression, indicating that d16:1 may function to “fine-tune” the pro-inflammatory effects of d18:1. Conclusion Taken together, our data suggest that plasma d16:1 S1P may be useful as a diagnostic marker for VCI, while the d18:1 to d16:1 S1P ratio is an index of dysregulated S1P-mediated immunomodulation leading to chronic inflammation-associated neurodegeneration and cerebrovascular damage.

scholarly journals IL-1β Inhibits TGFβ in the Temporomandibular Joint

2009 ◽  
Vol 88 (6) ◽  
pp. 557-562 ◽  
Author(s):  
W.H. Lim ◽  
J. Toothman ◽  
J.H. Miller ◽  
R.H. Tallents ◽  
S.M. Brouxhon ◽  
...  
Keyword(s):  
Mouse Model ◽  
Temporomandibular Joint ◽  
Inflammatory Cytokines ◽  
Tissue Regeneration ◽  
Inverse Correlation ◽  
Wild Type ◽  
Joint Pathology ◽  
Inflammatory Processes ◽  
Articular Pathology ◽  
Pro Inflammatory Cytokines

Similarly to humans, healthy, wild-type mice develop osteoarthritis, including of the temporomandibular joint (TMJ), as a result of aging. Pro-inflammatory cytokines, such as IL-1β, IL-6, and TNFα, are known to contribute to the development of osteoarthritis, whereas TGFβ has been associated with articular regeneration. We hypothesized that a balance between IL-1β and TGFβ underlies the development of TMJ osteoarthritis, whereby IL-1β signaling down-regulates TGFβ expression as part of disease pathology. Our studies in wild-type mice, as well as the Col1-IL1βXAT mouse model of osteoarthritis, demonstrated an inverse correlation between IL-1β and TGFβ expression in the TMJ. IL-1β etiologically correlated with joint pathology, whereas TGFβ expression associated with IL-1β down-regulation and improvement of articular pathology. Better understanding of the underlying inflammatory processes during disease will potentially enable us to harness inflammation for orofacial tissue regeneration.

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