Role of Immune Dysregulation in Increased Mortality Among a Specific Subset of COVID-19 Patients and Immune-Enhancement Strategies for Combatting Through Nutritional Supplements

Rao, K. S.; Vaddi, Suryaprakash; Senthilkumar, Rajappa; Preethy, Senthilkumar; Katoh, Shojiro; Ikewaki, Nobunao; Abraham, S

doi:10.3389/fimmu.2020.01548

Cited by 44 publications

(53 citation statements)

References 69 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Decreased NK cell count may also explain the uncontrolled expansion and activation of other immune effectors [ 20 , 38 ]. Therefore, the dysregulated basal levels and discrepant response of lymphocyte subpopulations in T2D are postulated to have a critical role in the severity and adverse outcome of the disease [ 20 , 39 , 40 ].…”

Section: Discussionmentioning

confidence: 99%

Distinguishable Immunologic Characteristics of COVID-19 Patients with Comorbid Type 2 Diabetes Compared with Nondiabetic Individuals

Zhao

Sun

Zhang

et al. 2020

Mediators of Inflammation

View full text Add to dashboard Cite

Background. COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has threatened every civilian as a global pandemic. The immune system poses the critical interactive chain between the human body and the virus. Here, we make efforts to examine whether comorbidity with type 2 diabetes (T2D) affects the immunological response in COVID-19 patients. Methods. We conducted a retrospective pilot study investigating immunological characteristics of confirmed cases of COVID-19 with or without comorbid T2D. Two subcohorts of sex- and age-matched participants were eligible for data analysis, of which 33 participants were with T2D and the remaining 37 were nondiabetic (NDM). Cellular immunity was assessed by flow cytometric determination of surface markers including CD3, CD4, CD8, CD19, CD16, and CD56 in peripheral blood. Levels of C reactive protein, immunoglobulin (IgG, IgM, IgA, and IgE), and complements (C3, C4) were detected by rate nephelometry immunoassay. And Th1/Th2 cytokines (IL-2, IL-4, IL-6, IL-10, TNF-α, and IFN-γ) were detected by Cytometric Bead Array. Results. Neutrophil counts were found to be significantly higher in the T2D group than in the NDM group and had a significant relevance with clinical severity. Lymphocyte frequencies showed no significant differences in the two groups. However, the proportions and absolute counts of T, Tc, Th, and NK cells decreased in both groups to different degrees. An abnormal increase in neutrophil count and a decrease in lymphocyte subpopulations may represent risk factors of COVID-19 severity. The level of IgG, IgM, IgA, C3, and C4 showed no significant difference between the two groups, while the IgE levels were higher in the T2D group than in the NDM group ( p < 0.05 ). Th1 cytokines including IFN-γ, TNF-α, and IL-6, as well as CRP, appeared significantly higher in the T2D group. Conclusions. The COVID-19 patients comorbid with T2D demonstrated distinguishable immunological parameters, which represented clinical relevancies with the predisposed disease severity in T2D.

show abstract

Section: Discussionmentioning

confidence: 99%

Distinguishable Immunologic Characteristics of COVID-19 Patients with Comorbid Type 2 Diabetes Compared with Nondiabetic Individuals

Zhao

Sun

Zhang

et al. 2020

Mediators of Inflammation

View full text Add to dashboard Cite

show abstract

“…The vulnerability of patients with cardiovascular risk factors such as obesity, hypertension, and diabetes to the disease severity of COVID-19 is well established [7][8][9]44]. Imbalance between coagulation and fibrinolysis with increased levels of clotting factors and relative inhibition of the fibrinolytic system, endothelial dysfunction, and enhanced platelet aggregation and activation, which are complications of diabetes, favour the development of a hypercoagulable pro-thrombotic state, thus explaining the high risk of diabetes patients to COVID-19 in terms of disease severity [44].…”

Section: Coagulopathy and Covid-19incidence And Vulnerable Populationsmentioning

confidence: 99%

“…This BRMG reduces the levels of IL-1β, IL-2, IL-4, IL-6, IL-12, TNF-α, IFN-γ, and sFasL while increasing IL8 and sFAS [34], thereby balancing an effective optimal defence against viral infection without hyperinflammation. Anti-viral defence activities of BRMG occur through increased IL8, which causes activation, migration, and chemotaxis of neutrophils to kill virusinfected cells; increased type-I IFN production, which helps kill virus-infected cells; increased IL-7 production, which leads to development and survival of mature T-cells to maintain homeostasis; activation of B-cells, which results in production of virusspecific antibodies (IgG, IgM and sIgA) for neutralization of virus toxicity; and increased NK cell activity and macrophage activity [7]. Prevention of hyperinflammation occurs by preventing the onset of apoptosis through increased sFAS production, regulation and suppression of CS through activation of Treg cells and decreased IL6, and prevention of chemoattraction of monocytes and macrophages, T cells, NK cells, and dendritic cells through a decrease in CXCL10 and CCL2 (monocyte chemotactic protein 1; MCP-1) [7].…”

Section: Preventive and Therapeutic Aspects Of Coagulopathy In Covid-19mentioning

confidence: 99%

“…However, it should be noted that even in the absence of advanced COVID-19, large artery stroke has been reported [6]. ACE2 receptors are expressed widely within endothelial cells, which could explain their vulnerability to SARS-CoV-2 binding, membrane fusion, and viral entry, thereby leading to infection and direct vascular injury [7] and giving rise to the coagulopathyassociated sequence in COVID-19.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Coagulopathy associated with COVID-19 – Perspectives & Preventive strategies using a biological response modifier Glucan

et al. 2020

Self Cite

View full text Add to dashboard Cite

Direct endothelial injury by viruses and dysregulation of clotting mechanisms due to cytokine storm are the major precipitating factors of mortality in COVID-19; both are attributed to a fundamental dysregulation of the immune system. While immune dysregulation can be attributed to several factors, the risk of associated thrombogenic disruption varies across individuals. This variation depends on several factors, such as comorbidities, including diabetes, hypertension, and cardiovascular diseases. When considering ethnic variations, the vulnerability of Caucasians, African Americans and Hispanics needs to be addressed before arriving at strategies to handle thromboembolic complications, which have been identified in recent reports as the leading causes of mortality in COVID-19. Although evaluation of D-dimer and prothrombin during admission is considered to predict prognosis and mortality, there are no preventive or prophylactic strategies before hospital admission. Herein, we present our perspectives on the effect of regular supplementation with the biological response modifier beta glucan based on its relevance to immune modulation. This effect is of paramount importance in decreasing the development of severe COVID-19 and reducing mortality against the background of coagulopathy, especially in vulnerable populations.

show abstract

“…The infection caused by SARS-CoV-2 produces a hyperinflammation known as cytokine storm that affects antibody production, a very important defense mechanism. COVID-19 severely affects people with comorbidities, such as hypertension, diabetes, and cardiovascular disease (66,67). These comorbidities produce inflammation that exacerbates during SARS-CoV-2 infection, causing an increase in mortality.…”

Section: Sleep and Innate Immunity (Susceptibility To Viral Infections)mentioning

confidence: 99%

A New Hypothesis on Anxiety, Sleep Insufficiency, and Viral Infections; Reciprocal Links to Consider in Today's “World vs. COVID-19” Endeavors

et al. 2020

View full text Add to dashboard Cite

In today's ever-growing concerns about the coronavirus disease (COVID-19) pandemic, many experience sleep insufficiencies, such as difficulty falling or staying asleep, sleep-related behavioral symptoms, and out-of-phase circadian rhythmicity despite the lack of history of earlier such symptoms. Meanwhile, the disruption in sleep bioparameters is experienced more in people with a history of sleep disorders. The behavioral sleep disorders in the current situations are prevalent given the today's amount of anxiety everyone is feeling about COVID-19. On the other hand, evidences indicated that the cross-link between impaired sleep efficiency and disrupted innate immunity makes people susceptible to viral infections. The present brief review highlights the links between psychosocial stress, sleep insufficiency, and susceptibility to viral infections in relevance to COVID-19 situation. The stress management measures, including addressing sleep-related disorders and sleep hygiene, will have a notable impact by harnessing immune response and thus reducing the susceptibility to viral infections.

show abstract

Role of Immune Dysregulation in Increased Mortality Among a Specific Subset of COVID-19 Patients and Immune-Enhancement Strategies for Combatting Through Nutritional Supplements

Cited by 44 publications

References 69 publications

Distinguishable Immunologic Characteristics of COVID-19 Patients with Comorbid Type 2 Diabetes Compared with Nondiabetic Individuals

Distinguishable Immunologic Characteristics of COVID-19 Patients with Comorbid Type 2 Diabetes Compared with Nondiabetic Individuals

Coagulopathy associated with COVID-19 – Perspectives & Preventive strategies using a biological response modifier Glucan

A New Hypothesis on Anxiety, Sleep Insufficiency, and Viral Infections; Reciprocal Links to Consider in Today's “World vs. COVID-19” Endeavors

Contact Info

Product

Resources

About