scholarly journals Novel Insights Into the Potential Mechanisms of N6-Methyladenosine RNA Modification on Sepsis-Induced Cardiovascular Dysfunction: An Update Summary on Direct and Indirect Evidences

2021 ◽  
Vol 9 ◽  
Author(s):  
Yang Wang ◽  
Miaomiao Xu ◽  
Peng Yue ◽  
Donghui Zhang ◽  
Jiyu Tong ◽  
...  
Keyword(s):  
Immune Response ◽  
Blood Cells ◽  
Rna Splicing ◽  
Cardiac Development ◽  
Inflammatory Responses ◽  
White Blood Cells ◽  
Inflammatory Factors ◽  
Rna Modification ◽  
Cardiovascular Dysfunction ◽  
Immune System Activation

Sepsis is a life-threatening organ dysfunction caused by a host’s dysfunctional response to infection. As is known to all, septic heart disease occurs because pathogens invading the blood stimulate the activation of endothelial cells, causing a large number of white blood cells to accumulate and trigger an immune response. However, in severe sepsis, the hematopoietic system is inhibited, and there will also be a decline in white blood cells, at which time the autoimmune system will also be suppressed. During the immune response, a large number of inflammatory factors are released into cells to participate in the inflammatory process, which ultimately damages cardiac myocytes and leads to impaired cardiac function. N6-methyladenosine (m6A) is a common RNA modification in mRNA and non-coding RNA that affects RNA splicing, translation, stability, and epigenetic effects of some non-coding RNAs. A large number of emerging evidences demonstrated m6A modification had been involved in multiple biological processes, especially for sepsis and immune disorders. Unfortunately, there are limited results provided to analyze the association between m6A modification and sepsis-induced cardiovascular dysfunction (SICD). In this review, we firstly summarized current evidences on how m6A mediates the pathophysiological process in cardiac development and cardiomyopathy to emphasize the importance of RNA methylation in maintaining heart biogenesis and homeostasis. Then, we clarified the participants of m6A modification in extended inflammatory responses and immune system activation, which are the dominant and initial changes secondary to sepsis attack. After that, we deeply analyzed the top causes of SICD and identified the activation of inflammatory cytokines, endothelial cell dysfunction, and mitochondrial failure. Thus, the highlight of this review is that we systematically collected all the related potential mechanisms between m6A modification and SICD causes. Although there is lack of direct evidences on SICD, indirect evidences had been demonstrated case by case on every particular molecular mechanism and signal transduction, which require further explorations into the potential links among the listed mechanisms. This provides novel insights into the understanding of SICD.

Influence of technological stress on the immunological reactivity of piglets

2020 ◽  
Vol 2 ◽  
pp. 155-161
Author(s):  
O.V. Kryachko ◽  
◽  
A.O. Budnik ◽  
Keyword(s):  
Immune Response ◽  
Blood Cells ◽  
White Blood Cells ◽  
Immunological Reactivity ◽  
Chemical Parameters ◽  
Functional Changes ◽  
Morphological Composition ◽  
The Relationship ◽  
Technological Stress ◽  
Lenin Grad

Hematological leukocyte indexes reflect the relationship between different classes of cells of the leukocyte formula and can provide information about intoxication and the state of the immune response in sick animals. Moreover, calculated leukocyte indexes can become an alternative to complex and expen-sive studies to determine the immunogram, cytokine content, and a number of other bio-chemical parameters. In this paper, we con-sidered the nature of changes in immunologi-cal indicators in piglets under technological stress as a result of weaning and regrouping, and we used calculated leukocyte indexes. To organize the research, we selected clini cally healthy Landrace piglets (n=5) in one of the pig breeding complexes in the Lenin-grad region. The studies were conducted one day before weaning of piglets from sows, age 25 days, and two weeks after weaning at the age of 41 days. Blood was collected us-ing a standard method and examined on a hematological analyzer to determine the morphological composition of white blood cells. The calculation of leukocyte indices was performed using formulas that charac-terize the ratio of the content of various forms of white blood cells, and in some cas-es, the rate of precipitation of red blood cells. The functional changes observed by the piglets 'immune system as a result of regrouping stress confirm the negative im-pact of the technological process on the ani-mals' immunity and provide a prerequisite for studying the ways and mechanisms of increasing their protective forces at this stage of the technological cycle. Analysis of integral leukocyte indexes showed an imbal-ance of specific (adaptive) and non-specific (innate) components of immunity in the dy-namics of changes in immunocompetent blood cells against the background of stress.

scholarly journals The Effect of Low-Dose Atorvastatin on Inflammatory Factors in Patients with Traumatic Brain Injury: A Randomized Clinical Trial

2020 ◽  
Vol 7 (4) ◽  
Author(s):  
Farhad Soltani ◽  
Nozar Nassajian ◽  
Kamalodin Tabatabaee ◽  
Fatemeh Javaherforooshzadeh ◽  
Arash Kiani ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Glasgow Coma Score ◽  
Blood Cells ◽  
Low Dose ◽  
White Blood Cells ◽  
Inflammatory Factors ◽  
Control Group ◽  
Atorvastatin Group

Background: Traumatic brain injury (TBI) is the leading cause of morbidity and mortality. Each year near 1.5 million Americans experience a TBI. Of which about 235,000 are hospitalized. Also, TBI claims 50 000 American lives each year. TBI causes mechanical damage to the blood-brain barrier and white blood cells (WBCs) entry to the brain. Objectives: The current study aimed to evaluate the efficacy of low-dose Atorvastatin on inflammatory factors in patients with traumatic brain injury (TBI). Methods: This double-blind, randomized clinical trial study was conducted in the ICU ward of Golestan Hospital in the city of Ahvaz (Iran) from April 2019-May 2020. Sixty patients with moderate to severe TBI were studied. Patients were randomly assigned into two groups of Atorvastatin and control. The main outcomes included the amount of CRP and ESR as well as white blood cells in the first 14 days of hospitalization. Glasgow Coma Score, the length of ICU stay, and the duration of mechanical ventilation were secondary outcomes. Results: The amount of CRP in the Atorvastatin group on the 14th day of hospitalization was significantly lower than those in the control group (31.99 ± 8.38 vs 59.65 ± 10.43) (P < 0.0001). On the same day, the Atorvastatin group had lower levels of ESR than the control group (14.28 ± 4.18 vs 25.57 ± 5.18) (P < 0.0001). The Atorvastatin group had significantly lower levels of white blood cells than the control group (5247.53 ± 751.93 vs 7143.94 ± 907.64, P < 0.0001). Glasgow Coma Score at the time of discharge from the ICU in the Atorvastatin group was more than control (14.06 ± 1.45 and 11.85 ± 0.75, respectively) (P < 0.05). A significant difference was found concerning the ICU stay between the two groups (P = 0.03). Conclusions: This study demonstrated that Atorvastatin could reduce the rate of inflammatory factors in TBI patients. The inflammatory condition of TBI patients heavily determines their prognosis. Inflammation leads to several reactions as well as interactions between different cells and chemical mediators. The Atorvastatin could reduce the rate of inflammatory factors and improved GCS in TBI patients.

Abstract 2: Loss of Rictor in Macrophages Suppresses Their Viability and Reduces Atherosclerosis in LDLR Null Mice

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Vladimir R Babaev ◽  
Lei Ding ◽  
Youmin Zhang ◽  
James M May ◽  
MacRae F Linton
Keyword(s):  
Gene Expression ◽  
Bone Marrow ◽  
Blood Cells ◽  
Inflammatory Responses ◽  
Bone Marrow Cells ◽  
White Blood Cells ◽  
Mammalian Target Of Rapamycin ◽  
Peritoneal Macrophages ◽  
Blood Monocytes ◽  
Glucose Plasma

The mammalian target of rapamycin (mTOR) is a conserved serine/threonine kinase that plays a central role in the regulation of cell viability, growth and metabolism. mTOR complex 2 (mTORC2) directly activates phosphorylation of Akt at S 473 , promoting pro-survival signaling. Rictor is an essential component of mTORC2, and genetic loss of Rictor inactivates the complex. To examine whether macrophage mTORC2 signaling has an impact on atherosclerosis, we transplanted male Ldlr null mice with bone marrow isolated from male mice with myeloid-specific Rictor deletion ( Rictor -/- , n=9) and control marrow from Rictor flox-flox mice ( Rictor flox/flox ; n=10). Compared to control mice reconstituted with Rictor flox/flox cells, the recipients of Rictor -/- bone marrow cells exhibited dramatic changes in blood cells including lower levels of white blood cells, B-cells, T-cells and monocytes but had similar levels of neutrophils. After 8 weeks of the Western diet, both groups of recipients had similar levels of body weight, blood glucose, plasma total cholesterol and triglycerides. However, Rictor -/- → Ldlr -/- mice developed smaller atherosclerotic lesions in the proximal and distal aorta (46 and 40% reduction, respectively). These lesions contained less macrophage area and more apoptotic macrophages than lesions of control Rictor flox/flox → Ldlr -/- mice. Importantly, blood monocytes and peritoneal macrophages isolated from Rictor -/- → Ldlr -/- mice were more sensitive to apoptotic stimuli compared to control Rictor flox/flox cells. In response to LPS, Rictor -/- macrophages exhibited the M1 phenotype with high levels of pro-inflammatory gene expression. Both Rictor -/- blood monocytes and macrophages had lower levels of Il10 gene expression than Rictor flox/flox cells. Thus, loss of Rictor and, consequently, mTORC2 in monocyte/macrophages significantly compromises their survival, and this markedly diminishes early atherosclerosis in Ldlr -/- mice. Our results indicate that mTORC2 is a key signaling regulator of macrophage survival and inflammatory responses and promote atherosclerosis.

White Blood Cells and the Immune Response

1982 ◽  
pp. 68-89
Author(s):  
N. J. Russell ◽  
G. M. Powell ◽  
J. G. Jones ◽  
P. J. Winterburn ◽  
J. M. Basford
Keyword(s):  
Immune Response ◽  
Blood Cells ◽  
White Blood Cells

scholarly journals Markers of humoral and cell-mediated immune response in primary autoimmune hypophysitis: a pilot study

Endocrine ◽  
2021 ◽  
Author(s):  
Sabrina Chiloiro ◽  
Antonella Giampietro ◽  
Flavia Angelini ◽  
Vincenzo Arena ◽  
Egidio Stigliano ◽  
...  
Keyword(s):  
Immune Response ◽  
Blood Cells ◽  
White Blood Cells ◽  
Cell Mediated Immunity ◽  
Qualitative And Quantitative Analysis ◽  
Qualitative And Quantitative ◽  
Autoimmune Hypophysitis ◽  
Serum Cytokines ◽  
Cell Mediated Immune Response ◽  
Simultaneous Identification

Abstract Introduction Primary autoimmune hypophysitis (PAHs) is a rare inflammatory disease of the pituitary gland. Although largely investigated, the pathogenesis of PAH is not completely clarified. We aimed to investigate the immune response in PAHs. Material and methods Serum anti-pituitary and anti-hypothalamus antibodies (respectively APAs and AHAs) were investigated though an indirect immunofluorescence on monkey hypophysis and hypothalamus slides, serum cytokines though an array membrane and cell-mediated immunity though the white blood cells count. Results Nineteen PAH cases entered the study. APA or AHA were identified in all cases. APA were detected in 13 patients (68.4%) and AHA in 13 patients (68.4%). Ten patients (52.6%) were simultaneously positive for both APA and AHA. The prevalence of APAs and AHAs was higher as compared to those observed in 50 health controls (respectively 14% p < 0.001 and 24% p = 0.004) and in 100 not-secreting pituitary adenoma (NFPAs) (respectively 22% p = 0.002 and 8% p < 0.001). Similarly, the prevalence of simultaneous positivity for APA and AHA (52.9%) was higher as compared to the those detected in patients affected by NFPAs (0%; p < 0.001) and in health controls (16% p = 0.002). No differences were identified between PAHs and controls at qualitative and quantitative analysis of serum cytokines and white blood cells count. Conclusions This study suggest that APA and AHA may be detected in an high percentage of PAH cases and that their simultaneous identification may be useful for the differential diagnosis between PAH and NFPAs, in an appropriate clinical context.

Low Ozone Concentrations Affect the Structural and Functional Features of Jurkat T Cells

Processes ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 1030
Author(s):  
Enrica Cappellozza ◽  
Manuela Costanzo ◽  
Laura Calderan ◽  
Mirco Galiè ◽  
Osvaldo Angelini ◽  
...  
Keyword(s):  
Immune Response ◽  
Blood Cells ◽  
Inflammatory Responses ◽  
Antioxidant Response ◽  
Jurkat Cells ◽  
Therapeutic Effects ◽  
Basic Study ◽  
Human T Lymphocyte ◽  
Functional Features

Autohemotherapy is the most used method to administer O2-O3 systemically. It consists in exposing a limited amount of blood to a gaseous O2-O3 and reinfusing it, thus activating a cascade of biochemical pathways involving plasma and blood cells that gives rise to antioxidant and anti-inflammatory responses. The therapeutic effects strictly depend on the O3 dose; it is therefore necessary to understand the relationship between the O3 concentration and the effects on blood cells involved in antioxidant and immune response. Here we performed a basic study on the effects of the low O3 concentrations used for autohemotherapy on the structural and functional features of the human T-lymphocyte-derived Jurkat cells. Ultrastructural, biomolecular, and bioanalytic techniques were used. Our findings showed that 10, 20, and 30 µg O3 concentrations were able to trigger Nrf2-induced antioxidant response and increase IL-2 secretion. However, viability and proliferation tests as well as ultrastructural observations revealed stress signs after treatment with 20 and 30 µg O3, thus designating 10 µg O3 as the optimal concentration in combining cell safety and efficient antioxidant and immune response in our in vitro system. These data offer novel evidence of the fine regulatory role played by the oxidative stress level in the hormetic response of T lymphocytes to O2-O3 administration.

scholarly journals Keratinocyte Growth Factor-2 Reduces Inflammatory Response to Acute Lung Injury Induced by Oleic Acid in Rats by Regulating Key Proteins of the Wnt/β-Catenin Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Shao Tenghao ◽  
Chen Ning ◽  
Wang Shenghai ◽  
Sun Qinlong ◽  
Wu Jiaqian ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Oleic Acid ◽  
Lung Injury ◽  
Signaling Pathway ◽  
Lung Tissue ◽  
Blood Cells ◽  
Keratinocyte Growth Factor ◽  
White Blood Cells ◽  
Inflammatory Factors ◽  
Control Group

Reducing inflammation can effectively relieve acute lung injury (ALI). Objective. To test whether keratinocyte growth factor-2 (KGF-2) can reduce oleic acid-induced inflammation in ALI of rats and explore its possible mechanism. Methods. 45 Sprague-Dawley rats were randomly divided into control group, ALI group, and ALI + KGF-2 group. The animal model of acute lung injury was established by injecting 0.1 mL/kg oleic acid into the tail vein of rats. Rats in the control group were injected with equal volume of normal saline (NS). Each group needs pretreatment 72 hours before the preparation of the acute lung injury model. The control group and ALI group were instilled with 5 ml/kg NS through the airway, and the same amount of KGF-2 was instilled in the ALI + KGF-2 group. It takes 8 hours to successfully prepare the ALI model. Observe the pathological changes of lung tissue through light microscopy, ultrastructural changes through electron microscopy, and the lung wettability/dry weight (w/d) ratio and lung permeability index (LPI). By detecting changes in inflammatory factors in lung tissue and changes in the number of BALF cells, the changes in inflammation in each group were observed. The expressions of Wnt5a, β-catenin, and APC in lung tissue were detected by immunohistochemistry and Western blot. The changes of key proteins in Wnt/β-catenin signaling pathway in the lung tissue of each group were observed. Result. Compared with the ALI group, after KGF-2 pretreatment, the degree of lung injury was reduced, the expression of inflammatory factors was reduced, and the number of red blood cells and white blood cells in BALF was reduced. It can also be observed that the expression of Wnt5a, β-catenin, and APC, a key protein in the Wnt/β-catenin signaling pathway, is reduced. The analysis showed that the number of inflammatory factors, red blood cells, and white blood cells in BALF was positively correlated with the expression of Wnt5a, β-catenin, and APC. Conclusion. KGF-2 may reduce the inflammatory response in ALI induced by oleic acid by regulating key proteins in the Wnt/β-catenin signaling pathway.

scholarly journals Inflammatory Responses Induced by the Rupture of Intracranial Aneurysms Are Modulated by miRNAs

2019 ◽  
Vol 57 (2) ◽  
pp. 988-996 ◽  
Author(s):  
Michal Korostynski ◽  
Rafal Morga ◽  
Marcin Piechota ◽  
Dzesika Hoinkis ◽  
Slawomir Golda ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Blood Cells ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Immune Cell ◽  
Inflammatory Responses ◽  
Chronic Phase ◽  
Mature Mirnas ◽  
Inflammatory Factors ◽  
Peripheral Blood Cells

Abstract Influence of an intracranial aneurysm (IA) rupture on the expression of miRNAs and the potential significance of the resulting changes remains poorly understood. We aimed to characterize the response to the IA rupture through the analysis of miRNAs in peripheral blood cells. Expression of small RNAs was investigated using deep transcriptome sequencing in patients in the acute phase of an IA rupture (first 72 h), in the chronic phase (3–15 months), and controls. A functional analysis and the potential interactions between miRNAs and target genes were investigated. We also measured the levels of proteins that were influenced by regulated miRNAs. We found that 106 mature miRNAs and 90 miRNA precursors were differentially expressed among the groups. The regulated miRNAs were involved in a variety of pathways, and the top pathway involved cytokine-cytokine receptor interactions. The identified miRNAs targeted the inflammatory factors HMGB1 and FASLG. Changes in their expression were detected at the mRNA and protein levels. IA rupture strongly influences the transcription profiles in peripheral blood cells. The regulated miRNAs were involved in the control of immune cell homeostasis. In summary, these results may aid in the elucidation of the molecular mechanisms that orchestrate the inflammatory response to IA rupture.

Analisa Cross-Infection Virus AI Subtipe H5N1 Berdasarkan Imunoserologi pada Burung Air di Cagar Alam Pulau Dua

2013 ◽  
Vol 2 (2) ◽  
pp. 120
Author(s):  
Dewi Elfidasari ◽  
Riris Lindiawati Puspitasari
Keyword(s):  
Immune Response ◽  
Avian Influenza ◽  
Blood Cells ◽  
Hemagglutination Inhibition ◽  
White Blood Cells ◽  
Cross Infection ◽  
Domestic Poultry ◽  
Infectious Microorganism ◽  
Water Birds ◽  
Antigen Antibody

<p><em>Abstrak</em><em> </em><strong><em>-</em></strong><strong><em> </em></strong><strong>Imunoserologi adalah cara mengidentifikasi terbentuknya antibodi yang diproduksi oleh sel darah putih sebagai respon terhadap masuknya antigen. Salah satu teknik Imunoserologi yang lazim digunakan untuk mendeteksi keberadaan antibodi di dalam darah adalah uji hambatan hemaglutinasi (<em>Hemagglutination-inhibition</em>/HI). Pada uji ini digunakan antigen yang homolog sehingga akan terjadi ikatan antigen-antibodi. Titer antibodi merupakan salah satu indikator dalam menentukan respon imun organisme terhadap suatu infeksi, seperti infeksi Virus <em>Avian Influenza</em> (VAI) subtipe H5N1. Interaksi yang terjadi antara burung air liar dengan unggas domestik dapat menyebabkan <em>cross-infection</em>, baik dari unggas domestik ke burung liar maupun dari burung liar ke unggas domestik. Salah satunya cara yang dapat dilakukan untuk menentukan  pola penularan dan penyebaran VAI subtipe H5N1 pada kawasan CAPD adalah melalui analisa <em>cross-infection</em> berdasarkan imunoserologi dengan melihat titer antibodi yang terbentuk pada unggas (ayam, bebek, mentok) dan burung-burung air liar penetap di kawasan tersebut. Hasil penelitian ini menunjukkan bahwa <em>cross-infection</em> tidak terjadi pada penyebaran virus </strong><strong>V</strong><strong>AI subtipe H5N1 di kawasan CAPD. Penularan terjadi hanya satu arah, dari unggas domestik ke burung-burung air liar penetap di CAPD.</strong></p><p> </p><p><em>Abstract<strong> - Immunoserology is a method to identify the formation of antibodies that produced by white blood cells as a response to agains the antigen. One of Immunoserology assays technique that commonly used to detect the presence of antibodies is hemagglutination test (Hemagglutination-inhibition/HI). In this study we used homologous antigens to observed the antigen-antibody binding. The antibody titer is an indicator to determining the immune response for the infectious microorganism, such as Avian Influenza Virus (AIV) subtype H5N1. Interactions between wild water birds and domestic poultry can lead the cross-infection mechanism. The analysis of cross-infection by imunoserologi is one of the ways to find the patterns of transmission and spread of the AIV subtype H5N1 in CAPD. The results of this study was indicate that cross-infection did not occur in the spread of AIV subtype H5N1 in the CAPD. The mechanism of transmission was occurs by one direction, only from domestic poultry to wild water birds resident in CAPD.</strong></em></p>

scholarly journals Clinical significance of changes in serum inflammatory factors in patients with chronic obstructive pulmonary disease and pulmonary infection

2021 ◽  
Vol 49 (5) ◽  
pp. 030006052110132
Author(s):  
Jun Zhou ◽  
Feng Jin ◽  
Feng Wu
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Pulmonary Infection ◽  
Inflammatory Responses ◽  
White Blood Cells ◽  
Inflammatory Factors ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Tnf Α

Background Chronic obstructive pulmonary disease (COPD) is often accompanied by pulmonary infection, inflammatory responses, decreased immunity, and decreased lung function. The relationships among the pulmonary inflammation index (PII), lung function, and immunity in COPD patients with pulmonary infection remain unclear. Methods This retrospective observational study enrolled 234 participants (patients with COPD and pulmonary infection, patients with COPD without pulmonary infection, and healthy individuals) from January 2017 to December 2019. Results Levels of interleukin (IL)-6 were lower and levels of IL-8 were higher in patients with COPD and pulmonary infection. Levels of white blood cells (WBCs), C-reactive protein (CRP), IL-6, IL-8, tumor necrosis factor (TNF)-α and CD8+ cells were higher, while levels of CD3+ and CD4+ cells, the CD4+/CD8+ ratio, forced expiratory volume in 1 s (FEV1), FEV1 % predicted (FEV1%pred), and FEV1/forced vital capacity (FVC) (FEV1%FVC) were lower in patients with COPD and pulmonary infection. Levels of WBCs, CRP, IL-6, IL-8, and TNF-α were negatively associated with FEV1, FEV1%pred and FEV1%FVC. Conclusions Patients with COPD and pulmonary infection have high PIIs, decreased immunity, and poor lung function. PII is closely related to lung function and may represent a useful biomarker for the assessment of patients with COPD and pulmonary infection.

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