scholarly journals COVID-19 and Immune Function – “A Significant” Zinc

2020 ◽  
Vol 36 (6) ◽  
pp. 1026-1036
Author(s):  
Mustafa Syed Khalid ◽  
Meshari M.H. Aljohani ◽  
Naser A. Alomrani ◽  
Atif Abdulwahab A. Oyoun ◽  
Othman Alzahrani ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Immune Function ◽  
Transition Element ◽  
Immune Homeostasis ◽  
Human History ◽  
Primary Health ◽  
Vital Cell ◽  
Inflammatory Immune Response ◽  
Two Phases

The pandemic COVID-19 is the most terrible calamity of the present human history also it has led to the worldwide issue of public health as a primary health safety problem. It was assumed that the infection of COVID -19 has two-phases, the immune protective as well as damaging phase. In the immune protective phase, clinicians try to enhance the patient immune response, and in the immune damaging phase, clinicians try to control the inflammatory immune response. Zinc belongs to the d-block or a transition element, it is an indispensable trace metal needed for vital cell activities like growth, as well as cell survival. It has significant contributions to immune homeostasis and functions; zinc inadequacy reduces primary and secondary immune responses equally. Studies have shown people who are deficient in zinc are more susceptible to infection. An inclusive knowledge of the bioavailability of the transition metal Zinc will help to be aware of those that are valuable and protective for the population's health. This work is concentrated on the significance of Zinc for the immune function, the presence of it’s in optimum amounts, and how it is beneficial to health in general and in fighting with COVID 19 in particular until today.

scholarly journals Pattern of inflammatory immune response determines the clinical course and outcome of COVID-19: unbiased clustering analysis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Eunyoung Emily Lee ◽  
Kyoung-Ho Song ◽  
Woochang Hwang ◽  
Sin Young Ham ◽  
Hyeonju Jeong ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Clustering Analysis ◽  
Validation Cohort ◽  
Inflammatory Responses ◽  
Clinical Course ◽  
Severe Disease ◽  
Outcome Data ◽  
Inflammatory Immune Response ◽  
Cluster 2

AbstractThe objective of the study was to identify distinct patterns in inflammatory immune responses of COVID-19 patients and to investigate their association with clinical course and outcome. Data from hospitalized COVID-19 patients were retrieved from electronic medical record. Supervised k-means clustering of serial C-reactive protein levels (CRP), absolute neutrophil counts (ANC), and absolute lymphocyte counts (ALC) was used to assign immune responses to one of three groups. Then, relationships between patterns of inflammatory responses and clinical course and outcome of COVID-19 were assessed in a discovery and validation cohort. Unbiased clustering analysis grouped 105 patients of a discovery cohort into three distinct clusters. Cluster 1 (hyper-inflammatory immune response) was characterized by high CRP levels, high ANC, and low ALC, whereas Cluster 3 (hypo-inflammatory immune response) was associated with low CRP levels and normal ANC and ALC. Cluster 2 showed an intermediate pattern. All patients in Cluster 1 required oxygen support whilst 61% patients in Cluster 2 and no patient in Cluster 3 required supplementary oxygen. Two (13.3%) patients in Cluster 1 died, whereas no patient in Clusters 2 and 3 died. The results were confirmed in an independent validation cohort of 116 patients. We identified three different patterns of inflammatory immune response to COVID-19. Hyper-inflammatory immune responses with elevated CRP, neutrophilia, and lymphopenia are associated with a severe disease and a worse outcome. Therefore, targeting the hyper-inflammatory response might improve the clinical outcome of COVID-19.

scholarly journals A Pro-Inflammatory Gut Microbiome Characterizes SARS-CoV-2 Infected Patients and a Reduction in the Connectivity of an Anti-Inflammatory Bacterial Network Associates With Severe COVID-19

2021 ◽  
Vol 11 ◽  
Author(s):  
Johanna Reinold ◽  
Farnoush Farahpour ◽  
Christian Fehring ◽  
Sebastian Dolff ◽  
Margarethe Konik ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Gut Microbiome ◽  
Tertiary Care Hospital ◽  
Tertiary Care ◽  
Cell Number ◽  
Care Hospital ◽  
Microbiome Composition ◽  
Inflammatory Immune Response ◽  
Anti Inflammatory

The gut microbiota contributes to maintaining human health and regulating immune responses. Severe COVID-19 illness is associated with a dysregulated pro-inflammatory immune response. The effect of SARS-CoV-2 on altering the gut microbiome and the relevance of the gut microbiome on COVID-19 severity needs to be clarified. In this prospective study, we analyzed the gut microbiome of 212 patients of a tertiary care hospital (117 patients infected with SARS-CoV-2 and 95 SARS-CoV-2 negative patients) using 16S rRNA gene sequencing of the V3-V4 region. Inflammatory markers and immune cells were quantified from blood. The gut microbiome in SARS-CoV-2 infected patients was characterized by a lower bacterial richness and distinct differences in the gut microbiome composition, including an enrichment of the phyla Proteobacteria and Bacteroidetes and a decrease of Actinobacteria compared to SARS-CoV-2 negative patients. The relative abundance of several genera including Bifidobacterium, Streptococcus and Collinsella was lower in SARS-CoV-2 positive patients while the abundance of Bacteroides and Enterobacteriaceae was increased. Higher pro-inflammatory blood markers and a lower CD8+ T cell number characterized patients with severe COVID-19 illness. The gut microbiome of patients with severe/critical COVID-19 exhibited a lower abundance of butyrate-producing genera Faecalibacterium and Roseburia and a reduction in the connectivity of a distinct network of anti-inflammatory genera that was observed in patients with mild COVID-19 illness and in SARS-CoV-2 negative patients. Dysbiosis of the gut microbiome associated with a pro-inflammatory signature may contribute to the hyperinflammatory immune response characterizing severe COVID-19 illness.

scholarly journals Leptin’s and antigen-presenting cells’ functions in periodontitis – an overview / Leptin e as funções das células que apresentam antigénios na periodontite - uma visão geral

2021 ◽  
Vol 4 (2) ◽  
pp. 8011-8019
Author(s):  
Giovanna Ganem Favero ◽  
Isabela Lopes Martin ◽  
Fernanda Pereira da Silva Albino ◽  
Carlos Eduardo Fontana ◽  
Sérgio Luiz Pinheiro ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Immune Responses ◽  
Inflammatory Responses ◽  
Antigen Presenting Cells ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Inflammatory Immune Response ◽  
Antigen Presenting ◽  
The Relationship

Leptin is a hormone synthesized predominantly by white adipose tissue. Its production levels are directly proportional to the total mass of this tissue in an individual’s body. Apart from its classic role in the regulation of hunger and satiety, it also plays an important part in scenarios involving innate and adaptive immune responses. It has been discovered that leptin levels are altered in a variety of inflammatory responses, such as periodontitis, a condition which derives from a persistent inflammatory immune response from a host facing bacterial infection. The initial trigger for this reaction is the recognition of the pathogens by antigen presenting cells, such as macrophages and dendritic cells, whose actions can be influenced by leptin. This review aims to present the relationship between leptin, dendritic cells and macrophages in the context of periodontal disease. Thus, we have assembled the most important findings related to leptin’s role in the modulation of the immune response carried out by these cells in periodontitis.

Abstract 286: Immune Dysfunction in a Vasopressin-Induced Mouse Model of Preeclampsia

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Sabrina M Scroggins ◽  
Donna A Santillan ◽  
James Y Min ◽  
Jeremy A Sangren ◽  
Nicole A Pearson ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Statistical Significance ◽  
Immune Dysfunction ◽  
Maternal Plasma ◽  
Specific Model ◽  
Splenic Lymphocytes ◽  
Wild Type ◽  
Immune Alterations ◽  
Inflammatory Immune Response

Preeclampsia is a disease of pregnancy and the postpartum period, affecting 5-7% of all U.S. pregnancies. We recently determined that elevated secretion of arginine vasopressin (AVP) in humans is detected as early as the 6th week of pregnancy in the women that subsequently develop preeclampsia. Further, we have determined that in C57BL/6 mice, chronic AVP infusion serves as a clinically-relevant and pregnancy-specific model of preeclampsia. Although the pathogenesis of preeclampsia is still poorly understood, an inflammatory immune response is clearly involved. AVP secretion is stimulated by proinflammatory cytokines and AVP in turn can act upon receptors present on lymphocytes. We hypothesize that hypersecretion of AVP results in maternal-fetal immune alterations in preeclamptics. Immune responses were evaluated in wild-type C57BL/6 female mice chronically infused with AVP (24 ng/hr or saline s.c.) throughout pregnancy. We observed an increase in the frequency of IL-12 (saline N=7: 1.1±0.2, vs AVP N=9: 2.2±0.4, P<0.05), IL-17 (saline N=7: 1.2±0.17, vs AVP N=9: 2.6±0.4, P<0.05) and TNFa (saline N=8: 0.9±0.1, vs AVP N=9: 1.6±0.1, P<0.005) expressing lymphocytes isolated from AVP mice. Additionally, the frequency of IFNg expressing lymphocytes was increased in AVP mice, approaching statistical significance (saline N=8: 2.2±0.9, vs AVP N=9: 3.0±0.4, P=0.059). The frequency of IL-6, IL-10, and LAP expressing splenic lymphocytes were similar between saline vs. AVP mice. Interestingly, maternal plasma revealed a significant reduction in IL-17 (saline N=4: 1.0e+7±3.8e+6, vs AVP N=5: 3.1e=5±1.3e+5 ng/g, P<0.05) in AVP mice. Neither IL-4 nor IFNg were detectable in maternal plasma of either group. Additionally, IL-17 trended higher in the amnionic fluid and lower in the placenta of AVP mice. IL-4 production trended lower in both the placenta and amnionic fluid of AVP-infused mice, while IFNg was similar between groups. These data support our hypothesis that AVP hypersecretion results in the maternal-fetal immune alterations associated with the development of preeclampsia. Ongoing experiments are aimed at identifying the lymphocytes and cytokines involved as well as local vs. systemic immune dysfunction associated with AVP-induced preeclampsia.

Oral Immune Activation by Disgust and Disease-Related Pictures

2015 ◽  
Vol 29 (3) ◽  
pp. 119-129 ◽  
Author(s):  
Richard J. Stevenson ◽  
Deborah Hodgson ◽  
Megan J. Oaten ◽  
Luba Sominsky ◽  
Mehmet Mahmut ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Innate Immune Response ◽  
Negative Control ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Immune Markers ◽  
Before And After ◽  
Secondary Analyses ◽  
Image Set

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.

The alarmin IL-33 drives a ST2+ Treg-mediated anti-inflammatory immune response during immune-mediated hepatitis

2019 ◽  
Author(s):  
K Neumann ◽  
F Heinrich ◽  
A Ochel ◽  
G Tiegs
Keyword(s):  
Immune Response ◽  
Immune Mediated ◽  
Inflammatory Immune Response ◽  
Anti Inflammatory

scholarly journals Coupled complementation of immune response genes controlling responsiveness to the H-2.2 alloantigen.

1977 ◽  
Vol 146 (2) ◽  
pp. 571-578 ◽  
Author(s):  
M E Dorf ◽  
J H Stimpfling
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Humoral Response ◽  
Mixed Lymphocyte Culture ◽  
Lymphocyte Culture ◽  
F1 Hybrids ◽  
Gene Control ◽  
Low Responder ◽  
Resistant Strains ◽  
High Level

The ability of various B10 congenic resistant strains to respond to the alloantigen H-2.2 was tested. High and low antibody-producing strains were distinguished by their anti-H-2.2 hemagglutinating respones. However, these strains do not differ in their ability to respond to these antigenic differences in the mixed lymphocyte culture. The humoral response to the H-2.2 alloantigen was shown to be controlled by two interacting genes localized within the H-2 complex. Thus, F1 hybrids prepared between parental low responder strains could yield high level immune responses. In addition, strains bearing recombinant H-2 haplotypes were used to map the two distinct genes controlling the immune response. The alleles at each locus were shown to be highly polymorphic as evidenced by the asymmetric complementation patterns observed. The restricted interactions of specific alleles was termed coupled complementation. The significance of the results in the terms of mechanisms of Ir gene control are discussed.

scholarly journals Maintenance of Type 2 Response by CXCR6-Deficient ILC2 in Papain-Induced Lung Inflammation

2019 ◽  
Vol 20 (21) ◽  
pp. 5493 ◽  
Author(s):  
Meunier ◽  
Chea ◽  
Garrido ◽  
Perchet ◽  
Petit ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Nk Cell ◽  
Lymphoid Cells ◽  
Inflammatory Conditions ◽  
Airway Diseases ◽  
Type 2 Cytokines ◽  
Lymphoid Organogenesis ◽  
Deficient Mice

Innate lymphoid cells (ILC) are important players of early immune defenses in situations like lymphoid organogenesis or in case of immune response to inflammation, infection and cancer. Th1 and Th2 antagonism is crucial for the regulation of immune responses, however mechanisms are still unclear for ILC functions. ILC2 and NK cells were reported to be both involved in allergic airway diseases and were shown to be able to interplay in the regulation of the immune response. CXCR6 is a common chemokine receptor expressed by all ILC, and its deficiency affects ILC2 and ILC1/NK cell numbers and functions in lungs in both steady-state and inflammatory conditions. We determined that the absence of a specific ILC2 KLRG1+ST2– subset in CXCR6-deficient mice is probably dependent on CXCR6 for its recruitment to the lung under inflammation. We show that despite their decreased numbers, lung CXCR6-deficient ILC2 are even more activated cells producing large amount of type 2 cytokines that could drive eosinophilia. This is strongly associated to the decrease of the lung Th1 response in CXCR6-deficient mice.

scholarly journals Combining Oncolytic Viruses and Small Molecule Therapeutics: Mutual Benefits

Cancers ◽  
2021 ◽  
Vol 13 (14) ◽  
pp. 3386
Author(s):  
Bart Spiesschaert ◽  
Katharina Angerer ◽  
John Park ◽  
Guido Wollmann
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Tumor Cells ◽  
Small Molecule ◽  
Antiviral Immunity ◽  
Oncolytic Viruses ◽  
Antitumor Immune Response ◽  
Antiviral Responses ◽  
Small Molecule Therapeutics ◽  
Immunosuppressive Factors

The focus of treating cancer with oncolytic viruses (OVs) has increasingly shifted towards achieving efficacy through the induction and augmentation of an antitumor immune response. However, innate antiviral responses can limit the activity of many OVs within the tumor and several immunosuppressive factors can hamper any subsequent antitumor immune responses. In recent decades, numerous small molecule compounds that either inhibit the immunosuppressive features of tumor cells or antagonize antiviral immunity have been developed and tested for. Here we comprehensively review small molecule compounds that can achieve therapeutic synergy with OVs. We also elaborate on the mechanisms by which these treatments elicit anti-tumor effects as monotherapies and how these complement OV treatment.

scholarly journals The immune response of T cells and therapeutic targets related to regulating the levels of T helper cells after ischaemic stroke

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Tian-Yu Lei ◽  
Ying-Ze Ye ◽  
Xi-Qun Zhu ◽  
Daniel Smerin ◽  
Li-Juan Gu ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Immune System ◽  
Immune Responses ◽  
Ischaemic Stroke ◽  
Immune Cells ◽  
Tissue Injury ◽  
Recovery Period ◽  
Vital Functions ◽  
Anti Inflammatory

AbstractThrough considerable effort in research and clinical studies, the immune system has been identified as a participant in the onset and progression of brain injury after ischaemic stroke. Due to the involvement of all types of immune cells, the roles of the immune system in stroke pathology and associated effects are complicated. Past research concentrated on the functions of monocytes and neutrophils in the pathogenesis of ischaemic stroke and tried to demonstrate the mechanisms of tissue injury and protection involving these immune cells. Within the past several years, an increasing number of studies have elucidated the vital functions of T cells in the innate and adaptive immune responses in both the acute and chronic phases of ischaemic stroke. Recently, the phenotypes of T cells with proinflammatory or anti-inflammatory function have been demonstrated in detail. T cells with distinctive phenotypes can also influence cerebral inflammation through various pathways, such as regulating the immune response, interacting with brain-resident immune cells and modulating neurogenesis and angiogenesis during different phases following stroke. In view of the limited treatment options available following stroke other than tissue plasminogen activator therapy, understanding the function of immune responses, especially T cell responses, in the post-stroke recovery period can provide a new therapeutic direction. Here, we discuss the different functions and temporal evolution of T cells with different phenotypes during the acute and chronic phases of ischaemic stroke. We suggest that modulating the balance between the proinflammatory and anti-inflammatory functions of T cells with distinct phenotypes may become a potential therapeutic approach that reduces the mortality and improves the functional outcomes and prognosis of patients suffering from ischaemic stroke.

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