Cytokine
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Review
Perspectives on anti-IL-1 inhibitors as potential therapeutic interventions for severe COVID-19.
The overproduction of proinflammatory cytokines, resulting in what has been described as a cytokine storm or cytokine release syndrome (CRS), may be the key factor in the pathology of severe coronavirus disease 2019 (COVID-19) and is also a crucial cause of death from COVID-19. With the purpose of finding effective and low-toxicity drugs to mitigate CRS, IL-1 blockade agents, which are one of the safest ways to stop this overwhelming innate immune response, are already available in several preliminary reports or are under observational trials and may offer an important treatment option in hyperinflammatory COVID-19. In this review, we described the key information in both case reports and clinical studies on the potential beneficial features of IL-1 inhibitors in COVID-19 patients.
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Patients with COVID-19 who require ICU admission might have the cytokine storm. It is a state of out-of-control release of a variety of inflammatory cytokines. The molecular mechanism of the cytokine storm has not been explored extensively yet. ⋯ Four molecular axes that may be involved in SARS-CoV-2 driven inflammatory cytokine overproduction are addressed in this work. The virus-mediated down-regulation of ACE2 causes a burst of inflammatory cytokine release through dysregulation of the renin-angiotensin-aldosterone system (ACE/angiotensin II/AT1R axis), attenuation of Mas receptor (ACE2/MasR axis), increased activation of [des-Arg9]-bradykinin (ACE2/bradykinin B1R/DABK axis), and activation of the complement system including C5a and C5b-9 components. The molecular clarification of these axes will elucidate an array of therapeutic strategies to confront the cytokine storm in order to prevent and treat COVID-19 associated acute respiratory distress syndrome.
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β-adrenoceptor antagonist (β-blocker) may have potential in the treatment of septic shock and sepsis. However, the relevant research findings are still controversial. ⋯ β-blocker of esmolol is safe and effective in improving 28-day mortality and controlling ventricular rate in patients with sepsis after fluid resuscitation, and has no significant adverse effect on tissue perfusion.
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Psoriasis and psoriatic arthritis cause significant physical and psychological burdens for afflicted individuals. An accelerated TNF-α/IL-23/IL-17 axis is their major pathomechanism; therefore, anti-TNF-α/IL-23/IL-17 biologics are very effective for the treatment of skin and joint lesions in psoriasis and psoriatic arthritis. Given that the IL-17 signature is more upregulated in the skin than in synovium in psoriatic arthritis, anti-IL-23/IL-17 agents seem to be superior to anti-TNF-α remedies in the treatment of skin lesions. In this review, we focus on the differential efficacy of anti-TNF-α/IL-23/IL-17 biologics in psoriasis and psoriatic arthritis.
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Traumatic Brain Injury (TBI) triggers a cascade of secondary biological and physiological effects that are variable, depending on the severity, location, and complexity of the injury. Improved diagnosis and prognosis of brain injury may be possible by examining changes in protein biomarker concentrations and, determining their role in long-term outcomes may improve treatment. One promising direction for biomarker research surrounds pro- and anti-inflammatory cytokines which may have utility for predicting short and long-term prognosis after TBI, and may also be therapeutic targets in shaping neuronal recovery following a TBI. ⋯ Increased levels of interleukin (IL)-6, IL-1, IL-8, IL-10 and tumor necrosis factor alpha (TNFα) were associated with worse outcomes, with most studies focusing on morbidity and mortality. It is important to identify the biochemical changes that may influence or initiate the presentation of health outcomes after a TBI. Earlier identification of symptoms associated with these biochemical changes can be used to support better treatment planning, targeted interventions and ultimately, improvement in patient outcomes.