scholarly journals Role of C-type Lectin Receptor to C.albicans on Promotion of Inflamantory Diseases

DENTA ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 63
Author(s):  
Erna Sulistyani
Keyword(s):  
Immune Cells ◽  
Inflammatory Diseases ◽  
Induce Polarization ◽  
Innate Immune ◽  
Oral Medicine ◽  
Lectin Receptor ◽  
Tnf Α ◽  
Transduction Signal ◽  
Anti Inflammatory Cytokine

<p><em>In early 2010 there was a very rapid progress in the development of immunity to fungi, i.e  the discovery of CLR. CLR is one of the PRR receptors found in immune cells that recognize the cell wall of fungi and then trigger a transduction signal that eventually provoke the production of various proinflamatory include IL1β, IL6, TNF α and induce polarization  Th17.  In the condition of infection the number of innate immune cells increases dramatically, lead to increasing of cytokines produced. Both cytokines and the cells that produce them enter the bloodstream. If there is unbalance level of pro and anti inflammatory cytokine, various inflammatory and/or autoimmune diseases can be occur. Unlike the focal concept infection, where the agent will cause disease if  enters the blood vessels, through this concept a fungal infection at epithelium can lead to inflammatory  diseases in other part of body without having to go through fungus</em></p><p><em> </em></p><p><strong><em>Keywords:</em></strong><em> C. albicans, CLR, Cytokine, Inflamatory Disease</em></p><p><strong><em> </em></strong></p><strong><em>Correspondence:  </em></strong><em>Erna Sulistyani, Department of Oral Medicine, Faculty of Dentistry, Jember Bagian Penyakit Mulut, Fakultas Kedokteran Gigi, Universitas Jember,  Kalimantan 37 Jember, Email: </em><a href="mailto:[email protected]"><em>[email protected]</em></a>

scholarly journals The Role of IL-6, TNF-α, and VDR in Inhibiting the Growth of Salmonella Typhi: in vivo Study

2020 ◽  
Vol 14 (1) ◽  
pp. 65-71
Author(s):  
Ami Febriza ◽  
Rosdiana Natzir ◽  
Mochammad Hatta ◽  
Suryani As'ad ◽  
. Budu ◽  
...  
Keyword(s):  
Immune Cells ◽  
Peritoneal Fluid ◽  
Innate Immune ◽  
Colony Count ◽  
P Value ◽  
Bacterial Colony ◽  
Tnf Α ◽  
Group A ◽  
Group B

Background and aim: The prevalence of typhoid fever is reportedly high, especially in Asia. When a pathogen enters the human body, there are markers in the form of molecules that will be known by the innate immune system. Specific molecular markers of gram negative bacteria, which are Lipopolysaccharides (LPS) and Toll-Like receptors-4 will interact with LPS. The binding between LPS and TLR-4 will give rise to activation signals that will activate innate immune cells. Immune cells will release a number of proinflammatory cytokines, such as TNF-α, IL-1, and IL-6. While Vitamin D Receptors (VDR) are expressed in large amounts in tumor tissue and infected cells. This study aimed to prove the role of IL-6, TNF-α, and VDR in inhibiting bacterial growth in mice that have been induced by S.Typhi. Methods: This research was a real experimental pre-post test design to investigate the level of IL-6, TNF-α and VDR in suppressing the growth of bacteria in the peritoneal fluid of S. Typhi, male, mice BALB/c. Mice were divided into three groups comprised of 10 mice each. All mice in groups A and B were intraperitoneally inoculated with S. Typhi strain Thy1 in study day 0. Group A was treated with antibiotic Levofloxacine, on study day 4th. Another study group, group B, was used as a placebo and received aquades on study day 4th. While group C as a control was not inoculated with S. Typhi. Blood samples from three groups for the calculation of serum Il-6, TNF-α, and VDR were collected. This examination was taken four times; at baseline, 4th day, 10th day, and 30th day. For the calculation of bacterial colony, peritoneal fluid retrieval was collected three times, which is on 4th day, 10th day, and 30th day. Results: A repeated measure ANOVA in group A (antibiotic) and group B (placebo) group showed that mean IL-6, TNF-α, and VDR level differed statistically significant between times (p-value 0.000). There was a strong negative correlation between bacterial colony count and VDR level, which was statistically significant in both groups (group A; r = -0.875, p-value = 0.000 vs group B; r = -0.470, p-value = 0.002). IL-6 and TNF-α didn't give significant statistical correlation with bacterial colony count. Conclusion: VDR, IL-6, and TNF-α play an important role in killing bacteria. From the results of this study, IL-6 level is related to the number of bacterial colonies, the lower the IL-6 level, the less the number of bacterial colonies. Similarly, TNF-α levels have a positive correlation with the number of bacterial colonies. While VDR levels are also related to the number of bacterial colonies, the higher the VDR level, the lower the number of bacterial colonies.

scholarly journals The Role of the Pathogen Dose and PI3Kγ in Immunometabolic Reprogramming of Microglia for Innate Immune Memory

2021 ◽  
Vol 22 (5) ◽  
pp. 2578
Author(s):  
Trim Lajqi ◽  
Christian Marx ◽  
Hannes Hudalla ◽  
Fabienne Haas ◽  
Silke Große ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Immune Tolerance ◽  
Immune Cells ◽  
Low Dose ◽  
Innate Immune ◽  
Immune Memory ◽  
Innate Immune Cells ◽  
Atp Production ◽  
Dose Dependent

Microglia, the innate immune cells of the CNS, exhibit long-term response changes indicative of innate immune memory (IIM). Our previous studies revealed IIM patterns of microglia with opposing immune phenotypes: trained immunity after a low dose and immune tolerance after a high dose challenge with pathogen-associated molecular patterns (PAMP). Compelling evidence shows that innate immune cells adopt features of IIM via immunometabolic control. However, immunometabolic reprogramming involved in the regulation of IIM in microglia has not been fully addressed. Here, we evaluated the impact of dose-dependent microglial priming with ultra-low (ULP, 1 fg/mL) and high (HP, 100 ng/mL) lipopolysaccharide (LPS) doses on immunometabolic rewiring. Furthermore, we addressed the role of PI3Kγ on immunometabolic control using naïve primary microglia derived from newborn wild-type mice, PI3Kγ-deficient mice and mice carrying a targeted mutation causing loss of lipid kinase activity. We found that ULP-induced IIM triggered an enhancement of oxygen consumption and ATP production. In contrast, HP was followed by suppressed oxygen consumption and glycolytic activity indicative of immune tolerance. PI3Kγ inhibited glycolysis due to modulation of cAMP-dependent pathways. However, no impact of specific PI3Kγ signaling on immunometabolic rewiring due to dose-dependent LPS priming was detected. In conclusion, immunometabolic reprogramming of microglia is involved in IIM in a dose-dependent manner via the glycolytic pathway, oxygen consumption and ATP production: ULP (ultra-low-dose priming) increases it, while HP reduces it.

Role of Inflammasome Activation in Systemic Lupus Erythematosus: Are Innate Immune Cells Activated?

2020 ◽  
Author(s):  
Rodolfo Perez-Alamino ◽  
Raquel Cuchacovich ◽  
Luis R. Espinoza ◽  
Constance P. Porretta ◽  
Arnold H. Zea
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Immune Cells ◽  
Lupus Erythematosus ◽  
Innate Immune ◽  
Inflammasome Activation ◽  
Innate Immune Cells ◽  
Systemic Lupus

CD14+CD16+ monocytes in coronary artery disease and their relationship to serum TNF-α levels

2004 ◽  
Vol 92 (08) ◽  
pp. 419-424 ◽  
Author(s):  
Stefan Blankenberg ◽  
Christine Espinola-Klein ◽  
Joern Dopheide ◽  
Christoph Bickel ◽  
Karl Lackner ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Animal Studies ◽  
Inflammatory Diseases ◽  
Serum Concentrations ◽  
Tnf Α ◽  
Hs Crp ◽  
Artery Disease ◽  
Fourth Quartile

SummaryMonocytes play a central role in the inflammatory disease atherosclerosis. CD14+CD16+ monocytes are considered proinflammatory monocytes, as they have an increased capacity to produce proinflammatory cytokines, such as TNF-α, and are elevated in various inflammatory diseases. We hypothesized that patients with coronary artery disease (CAD) have increased levels of CD14+CD16+ monocytes, and that CD14+CD16+ monocytes are associated with inflammation markers. We investigated CD14+CD16+ monocytes in 247 patients with CAD and 61 control subjects using flow cytometry. In addition serum concentrations of TNF-α, IL-6, and Hs-CRP were assessed. Patients with CAD had higher levels of CD14+CD16+ monocytes than controls (13.6% versus 11.4%; p<0.001). Logistic regression analysis including quartiles of CD14+CD16+ monocytes showed that CD14+CD16+ monocytes were associated with prevalence of CAD (OR 4.9, 95% CI 2.5–19.1, for subjects in the fourth quartile in comparison to subjects in the first quartile). The association between CD14+CD16+ monocytes and CAD remained independently significant after adjustment for most potential confounders (OR 5.0, 95% CI 1.2-20.0). Serum concentrations of TNF-α were elevated in subjects within the highest quartiles of CD14+CD16+ monocytes (p=0.018). Our study showed that increased numbers of CD14+CD16+ monocytes are associated with coronary atherosclerosis and TNF-α. In accordance, recent animal studies suggest a possibly important role of these monocytes in the development of atherosclerosis.

scholarly journals Adipocytes, Innate Immunity and Obesity: A Mini-Review

2021 ◽  
Vol 12 ◽  
Author(s):  
Alecia M. Blaszczak ◽  
Anahita Jalilvand ◽  
Willa A. Hsueh
Keyword(s):  
Adipose Tissue ◽  
Immune System ◽  
Immune Cells ◽  
Adaptive Immune System ◽  
Innate Immune ◽  
Lymphoid Cells ◽  
Innate Immune Cells ◽  
Adaptive Immune

The role of adipose tissue (AT) inflammation in obesity and its multiple related-complications is a rapidly expanding area of scientific interest. Within the last 30 years, the role of the adipocyte as an endocrine and immunologic cell has been progressively established. Like the macrophage, the adipocyte is capable of linking the innate and adaptive immune system through the secretion of adipokines and cytokines; exosome release of lipids, hormones, and microRNAs; and contact interaction with other immune cells. Key innate immune cells in AT include adipocytes, macrophages, neutrophils, and innate lymphoid cells type 2 (ILC2s). The role of the innate immune system in promoting adipose tissue inflammation in obesity will be highlighted in this review. T cells and B cells also play important roles in contributing to AT inflammation and are discussed in this series in the chapter on adaptive immunity.

scholarly journals Succinate Is an Inflammation-Induced Immunoregulatory Metabolite in Macrophages

Metabolites ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 372 ◽  
Author(s):  
Karl J. Harber ◽  
Kyra E. de Goede ◽  
Sanne G. S. Verberk ◽  
Elisa Meinster ◽  
Helga E. de Vries ◽  
...  
Keyword(s):  
Immune Responses ◽  
Immune Cells ◽  
Immune Cell ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Cell Phenotype ◽  
Independent Manner ◽  
Inflammatory Macrophages ◽  
Necrosis Factor

Immunometabolism revealed the crucial role of cellular metabolism in controlling immune cell phenotype and functions. Macrophages, key immune cells that support progression of numerous inflammatory diseases, have been well described as undergoing vast metabolic rewiring upon activation. The immunometabolite succinate particularly gained a lot of attention and emerged as a crucial regulator of macrophage responses and inflammation. Succinate was originally described as a metabolite that supports inflammation via distinct routes. Recently, studies have indicated that succinate and its receptor SUCNR1 can suppress immune responses as well. These apparent contradictory effects might be due to specific experimental settings and particularly the use of distinct succinate forms. We therefore compared the phenotypic and functional effects of distinct succinate forms and receptor mouse models that were previously used for studying succinate immunomodulation. Here, we show that succinate can suppress secretion of inflammatory mediators IL-6, tumor necrosis factor (TNF) and nitric oxide (NO), as well as inhibit Il1b mRNA expression of inflammatory macrophages in a SUCNR1-independent manner. We also observed that macrophage SUCNR1 deficiency led to an enhanced inflammatory response without addition of exogenous succinate. While our study does not reveal new mechanistic insights into how succinate elicits different inflammatory responses, it does indicate that the inflammatory effects of succinate and its receptor SUCNR1 in macrophages are clearly context dependent.

scholarly journals Myeloperoxidase Modulates Hydrogen Peroxide Mediated Cellular Damage in Murine Macrophages

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1255
Author(s):  
Chaorui Guo ◽  
Inga Sileikaite ◽  
Michael J. Davies ◽  
Clare L. Hawkins
Keyword(s):  
Hydrogen Peroxide ◽  
Hypochlorous Acid ◽  
Cell Function ◽  
Inflammatory Diseases ◽  
Innate Immune ◽  
Cellular Damage ◽  
Enzymatic System ◽  
Therapeutic Approaches ◽  
Macrophage Cell

Myeloperoxidase (MPO) is involved in the development of many chronic inflammatory diseases, in addition to its key role in innate immune defenses. This is attributed to the excessive production of hypochlorous acid (HOCl) by MPO at inflammatory sites, which causes tissue damage. This has sparked wide interest in the development of therapeutic approaches to prevent HOCl-induced cellular damage including supplementation with thiocyanate (SCN−) as an alternative substrate for MPO. In this study, we used an enzymatic system composed of glucose oxidase (GO), glucose, and MPO in the absence and presence of SCN−, to investigate the effects of generating a continuous flux of oxidants on macrophage cell function. Our studies show the generation of hydrogen peroxide (H2O2) by glucose and GO results in a dose- and time-dependent decrease in metabolic activity and cell viability, and the activation of stress-related signaling pathways. Interestingly, these damaging effects were attenuated by the addition of MPO to form HOCl. Supplementation with SCN−, which favors the formation of hypothiocyanous acid, could reverse this effect. Addition of MPO also resulted in upregulation of the antioxidant gene, NAD(P)H:quinone acceptor oxidoreductase 1. This study provides new insights into the role of MPO in the modulation of macrophage function, which may be relevant to inflammatory pathologies.

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