scholarly journals Systemic Inflammation and Clinical Outcomes in COVID-19: a retrospective study

2020 ◽  
Author(s):  
Meijia Wang ◽  
Zhenli Huang ◽  
Kun Tang ◽  
Pengfei Gao ◽  
Yanjiao Lu ◽  
...  
Keyword(s):  
Retrospective Study ◽  
Clinical Outcomes ◽  
Systemic Inflammation ◽  
Trial Registration ◽  
Inflammatory Factors ◽  
Reactive Protein ◽  
Tnf Α ◽  
Registration Number ◽  
Factor Α

Abstract Background：COVID-19 causes epidemics and pandemics worldwide, but the role of pathophysiological parameters particularly systemic inflammation in COVID-19 has not been understood. We aimed to investigate clinical outcomes in view of systemic inflammation in COVID-19.Methods：In this retrospective study, the demographic and clinical data of 225 confirmed COVID-19 cases on admission at Tongji Hospital from January 28 to February 15, 2020, were extracted and analyzed. These patients were categorized by inflammation state on the basis of the expression of inflammatory factors or classified as severe and non-severe according to 2019 American Thoracic Society / Infectious Disease Society of America guidelines.Results: Among 225 patients with confirmed COVID-19, 155 patients (68.9%) categorized into hyperinflammation group and 70 (31.1%) were non- hyperinflammation group. Compared to non-hyperinflammation group, hyperinflammation group more frequently had chest tightness/dyspnea and lymphopenia, aberrant multiple indexes of organ function including the heart, liver, kidney, and coagulation, with higher level of C-reactive protein (hsCRP) as well as interleukin (IL)-6, IL-8, tumour necrosis factor α (TNF-α), etc. Hyperinflammation group were more likely to admit to intensive care unit (ICU) (52.3% vs 5.7%), receive ventilation (84.5% vs 10.0%) and be with higher mortality (44.5% vs 5.7%) than non-hyperinflammation group. The mortality of severe patients with hyperinflammation (60/99, 60.6%) was significantly higher than without hyperinflammation (2/20, 10.0%). Non-severe patients with hyperinflammation even tended to have higher mortality (9/56, 16.1%) than those in severe cases without hyperinflammation (2/20, 10%).Conclusion: Excessive systemic inflammation was correlated highly with poor clinical outcomes in COVID-19, particularly in severe cases. Non-severe patients with hyperinflammation even tended to have higher mortality than those in severe cases without hyperinflammation.Trial registration: This is a retrospective observational study without a trial registration number.

Psoriasis: Tumor Necrosis Factor –α, Interleukin 18, C Reactive Protein Polymorphism , and Osteopontin Role

2018 ◽  
Vol 1 (1) ◽  
pp. 58-62
Author(s):  
Ibrahim Abed
Keyword(s):  
Skin Condition ◽  
Chronic Inflammatory Disease ◽  
Systemic Complications ◽  
Reactive Protein ◽  
Tnf Α ◽  
Inflammatory Processes ◽  
Chronic Skin ◽  
Abnormal Lipid Metabolism ◽  
Factor Α

  Background: Psoriasis is a common chronic skin disorder with prevalence of 2.7% in Iraqi community. Many factors affect the prevalence of psoriasis which include genetic, environmental, infectious, immunological, biochemical, endocrinological and psychological. Psoriasis is a chronic inflammatory disease with unknown exact pathogenesis, which may be started as skin condition that subsequently associated with systemic complications. The recurrent proliferative inflammatory processes in subject with psoriasis may lead to abnormal lipid metabolism and associated with cardiovascular diseases. Gene polymorphisms represent either a protective or risk factors for development of psoriasis and cardiovascular disease. Aim of the Study: The aim of the present study is to provide a picture about the association between psoriasis and atherosclerosis. Objectives: To: 1. Estimate the prevalence of impending atherosclerosis in patients with psoriasis. 2. Identify the pattern of association among inflammatory markers in one hand and lipoproteins as traditional markers in another. 3. Clarify the risk assessment of atherosclerosis in patients with psoriasis using multi- biomarkers score. 4. Appraise the inter – traditional and new markers. 5. Evaluate the role of IL-18, TNF -α, osteopontin in the pathogenesis of psoriasis and atherosclerosis. 6. Illustrate the association between disease susceptibility and different gene polymorphism such as IL-18, TNF-α and CRP.  

scholarly journals The role of HMGB1 in invasive Candida albicans infection

2020 ◽  
Author(s):  
Jiaojiao Wang ◽  
Chuanxin Wu ◽  
Yunying Wang ◽  
Chongxiang Chen ◽  
Jing Cheng ◽  
...  
Keyword(s):  
Ethyl Pyruvate ◽  
Survival Rates ◽  
High Mobility ◽  
Serum Levels ◽  
Bacterial Sepsis ◽  
Reactive Protein ◽  
Tnf Α ◽  
Hmgb1 Expression ◽  
Factor Α

AbstractBackgroundHigh mobility group box 1 (HMGB1) is an important “late” inflammatory mediator in bacterial sepsis. Ethyl pyruvate (EP), an inhibitor of HMGB1, can prevent bacterial sepsis by decreasing HMGB1 levels. However, the role of HMGB1 in fungal sepsis is still unclear. Therefore, we investigated the role of HMGB1 and EP in invasive C. albicans infection.MethodsWe measured serum HMGB1 levels in patients with sepsis with C. albicans infection and without fungal infection, and control subjects. We collected clinical indices to estimate correlations between HMGB1 levels and disease severity. Furthermore, we experimentally stimulated mice with C. albicans and C. albicans + EP. Then, we examined HMGB1 levels from serum and tissue, investigated serum levels of tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), determined pathological changes in tissues, and assessed mortality.ResultsSerum HMGB1 levels in patients with severe sepsis with C. albicans infection were elevated. Increased HMGB1 levels were correlated with procalcitonin (PCT), C-reactive protein (CRP), 1,3-β-D-Glucan (BDG) and C. albicans sepsis severity. HMGB1 levels in serum and tissues were significantly increased within seven days after mice were infected with C. albicans. The administration of EP inhibited HMGB1 levels, decreased tissue damage, increased survival rates and inhibited the release of TNF-α and IL-6.ConclusionsHMGB1 levels were significantly increased in invasive C. albicans infections. EP prevented C. albicans lethality by decreasing HMGB1 expression and release. HMGB1 may provide an effective diagnostic and therapeutic target for invasive C. albicans infections.

scholarly journals Relationship between smoking and indicators of systemic inflammation in patients with coronary heart disease

2017 ◽  
Vol 95 (3) ◽  
pp. 264-271
Author(s):  
E. D. Bazdyrev ◽  
O. M. Polikutina ◽  
N. A. Kalichenko ◽  
Yu. S. Slepynina ◽  
E. G. Uchasova ◽  
...  
Keyword(s):  
Systemic Inflammation ◽  
Inflammatory Markers ◽  
Reactive Protein ◽  
Tnf Α ◽  
History Of ◽  
Artery Disease ◽  
Factor Α ◽  
Metalloproteinase 9 ◽  
Necrosis Factor ◽  
Nonspecific Inflammation

Aim. To estimate the severity of systemic inflammation in subjects with coronary artery disease (CAD) without bronchopulmonary system comorbidity depending on smoking factor. Materials and methods. The subjects were divided into groups depending on smoking factor. We estimated the following laboratory markers of nonspecific inflammation: interleukine (IL)-12, -1β, tumour necrosis factor-α, matrix metalloproteinase-9, C-reactive protein. The examination of lungs respiratory function included spirometry, body plethysmography and assessment of diffusing lung capacity. Results. 29.9% of the subjects with CAD smoked, 40% reported discontinuation of smoking in their histories. Smoking in CAD subjects without the history of bronchopulmonary system comorbidity was associated with a higher level of inflammatory markers (IL-12, IL-1β, TNF-α, ММР-9 and CRP) than in subjects who ceased to smoke and those who have never smoked. No differences in the levels of inflammatory markers were revealed in subjects who had smoked before and never smoked. Conclusion. Smoking is widespread among CAD subjects. It is associated with a higher level of markers of nonspecific inflammation as compared to subjects who have never smoked before or ceased smoking.

scholarly journals The Role of Interleukin-6 (IL-6) in the Systemic Inflammatory Response in Xenograft Recipients and in Pig Kidney Xenograft Failure

2021 ◽  
Vol 12 ◽  
Author(s):  
Guoqiang Zhang ◽  
Hayato Iwase ◽  
Qi Li ◽  
Takayuki Yamamoto ◽  
Abhijit Jagdale ◽  
...  
Keyword(s):  
Serum Creatinine ◽  
Systemic Inflammation ◽  
Graft Function ◽  
Genetically Engineered ◽  
Inflammatory Factors ◽  
Kidney Graft ◽  
Amyloid A ◽  
Pig Kidney ◽  
Tnf Α

BackgroundIn pig-to-baboon transplantation models, there is increasing evidence of systemic inflammation in xenograft recipients (SIXR) associated with pig xenograft failure. We evaluated the relationship between systemic inflammatory factors and pig kidney xenograft failure.MethodsBaboons received kidney transplants from genetically engineered pigs (n=9), and received an anti-CD40mAb-based (n=4) or conventional (n=5) immunosuppressive regimen. The pig kidney grafts were monitored by measurements of serum creatinine, serum amyloid A (SAA), white blood cell (WBC) and platelet counts, plasma fibrinogen, and pro-inflammatory cytokines (baboon and pig IL-6, TNF-α, IL-1β).ResultsSix baboons were euthanized or died from rejection, and 3 were euthanized for infection. Changes in serum creatinine correlated with those of SAA (r=0.56, p<0.01). Serum baboon IL-6 was increased significantly on day 1 after transplantation and at euthanasia (both p<0.05) and correlated with serum creatinine and SAA (r=0.59, p<0.001, r=0.58, p<0.01; respectively). but no difference was observed between rejection and infection. Levels of serum pig IL-6, TNF-α, IL-1β were also significantly increased on day 1 and at euthanasia, and serum pig IL-6 and IL-1β correlated with serum creatinine and SAA. The level of serum baboon IL-6 correlated with the expression of IL-6 and amyloid A in the baboon liver (r=0.93, p<0.01, r=0.79, p<0.05; respectively).ConclusionEarly upregulation of SAA and serum IL-6 may indicate the development of rejection or infection, and are associated with impaired kidney graft function. Detection and prevention of systemic inflammation may be required to prevent pig kidney xenograft failure after xenotransplantation.

Genetic Variation in TNF-α, its Relation with Inflammatory Biomarkers and Susceptibility to Rheumatoid Arthritis

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Khadiga Ahmed Ismail
Keyword(s):  
Rheumatoid Arthritis ◽  
Serum Level ◽  
Functional Disability ◽  
Serum Levels ◽  
Amplification Refractory Mutation System ◽  
Reactive Protein ◽  
Tnf Α ◽  
Mutation System ◽  
Potential Factor ◽  
Factor Α

Background: Tumor necrosis Factor-α (TNF-α) is encoded and controlled by TNF-α gene, which is involved in rheumatoid arthritis (RA) susceptibility. This research aimed to identify genetic variations of TNF-α (G308A) and to establish its association with inflammatory markers in Rheumatoid Arthritis predisposition. Methods: In the present study, fifty RA patients and fifty volunteers were involved and evaluated for the C-reactive protein, rheumatoid factor, and TNF-α were estimated by ELISA, Erythrocyte Sedimentation Rate (ESR) by Wintergreen method and for TNF-α-308 G>A polymorphism by polymerase chain reaction with amplification refractory mutation system (PCR-ARMS). Results: The CRP, RF, ESR and TNF-α were significantly elevated in RA patients relative to controls. The serum level TNF-α was also significantly elevated in female patients and in patients ≥50 years. Analysis of TNF-308 gene polymorphism revealed that GG genotypes were more prevalent in RA patients than in the healthy individuals and that GG genotype may be a potential factor to RA. The G allele was more common in RA than in the control. Elevated TNF-α serum levels were significantly associated the GG genotype and functional disability in RA patients. Conclusion: TNF-α promoter 308polymorphism GG genotype may be considered as a risk factor for RA and the TNF-α serum level was significantly related to the functional disability in the disease.

scholarly journals Manipulation of Quercetin and Melatonin in the Down-Regulation of HIF-1α, HSP-70 and VEGF Pathways in Rat’s Kidneys Induced by Hypoxic Stress

Dose-Response ◽  
2020 ◽  
Vol 18 (3) ◽  
pp. 155932582094979
Author(s):  
Aliah R. Alshanwani ◽  
Sameerah Shaheen ◽  
Laila M. Faddah ◽  
Ahlam M. Alhusaini ◽  
Hanaa M. Ali ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Histopathological Examination ◽  
Hemoglobin Concentration ◽  
Vascular Endothelial ◽  
Hsp 70 ◽  
Reactive Protein ◽  
Defensive Role ◽  
Factor Α ◽  
Endothelial Growth Factor

Hypoxia may lead to inflammatory responses by numerous signaling pathways. This investigation intended to inspect the defensive role of Quercetin (Quer) and/ or Melatonin (Mel) against reno toxicity induced by Sodium nitrite (Sod ntr). Sod ntr injection significantly decreased blood hemoglobin concentration (Hb) with a concurrent increase in serum tumor necrosis factor- α, interleukin-6, C-reactive protein, creatinine, and urea levels. Over protein-expression of vascular endothelial growth factor and heat shock, protein-70 and mRNA of HIF-1α were also observed. Pretreatment of the Sod ntr- injected rats with the aforementioned antioxidants; either alone or together significantly improved such parameters. Histopathological examination reinforced the previous results. It was concluded that the combined administration of Quer and Mel may be useful as a potential therapy against renal injury induced by Sod ntr. HIF-1α and HSP-70 are implicated in the induction of hypoxia and its treatment.

C1QTNF6 participates in the pathogenesis of PCOS by affecting the inflammatory response of granulosa cells

2021 ◽  
Author(s):  
Sisi Yan ◽  
Jinli Ding ◽  
Yi Zhang ◽  
Jiayu Wang ◽  
Sainan Zhang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Mouse Models ◽  
Granulosa Cells ◽  
Polycystic Ovary ◽  
Serum Levels ◽  
Inflammatory Factors ◽  
Low Grade ◽  
Reactive Protein ◽  
Reproductive Endocrine ◽  
Factor Α

Abstract Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disease. It has been reported that chronic low-grade inflammation might participate in its pathogenesis. C1q and TNF related 6 (C1QTNF6) is a newly identified adiponectin paralog associated with inflammation. The aim of the present study was to investigate the role of C1QTNF6 in the development of chronic inflammation in PCOS and the underlying molecular mechanism. After analyzing the expression of C1QTNF6 in the serum and granulosa cells (GCs) of PCOS patients and healthy controls, we verified the roles of C1QTNF6 in inflammation through dehydroepiandrosterone-induced PCOS mouse models and cell models of lipopolysaccharide (LPS)-induced inflammation. The results demonstrated that C1QTNF6 expression in the serum and GCs of patients with PCOS was significantly elevated compared with those of the controls, and similar results were observed in the serum and ovary of PCOS mouse models. In PCOS mice and C1QTNF6-overexpressing PCOS mice, serum levels of pro-inflammatory factors including C-reactive protein (CRP), interleukin 6 (IL6) and tumor necrosis factor-α (TNFα) were increased, while the opposite effects were observed when C1QTNF6 was downregulated in PCOS mice. Furthermore, C1QTNF6 overexpression upregulated the levels of TNFα, IL6, and CRP and activated the AKT/NF-κB pathway in LPS-treated KGN cells, whereas C1QTNF6 knockdown and BAY-117082 (an NF-κB inhibitor) treatment resulted in the opposite effects. Taken together, our results indicate that C1QTNF6 is involved in the pathogenesis of PCOS by affecting the inflammatory response via the AKT/NF-κB signaling pathway.

The Role of Tumor Necrosis Factor-α (TNF-α) Polymorphisms in Gastric Cancer: a Meta-Analysis

2021 ◽  
Author(s):  
Maryam Gholamalizadeh ◽  
Samaneh Mirzaei Dahka ◽  
Hadi Sedigh Ebrahim-Saraie ◽  
Mohammad Esmail Akbari ◽  
Azam Pourtaheri ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Meta Analysis ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals The role of systemic inflammation in heart failure

2021 ◽  
Vol 102 (4) ◽  
pp. 510-517
Author(s):  
E V Khazova ◽  
O V Bulashova
Keyword(s):  
Heart Failure ◽  
Cardiovascular Diseases ◽  
Systemic Inflammation ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
C Reactive Protein ◽  
Ventricular Ejection Fraction ◽  
Reactive Protein ◽  
Highly Sensitive

The discussion continues about the role of systemic inflammation in the pathogenesis of cardiovascular diseases of ischemic etiology. This article reviews the information on the role of C-reactive protein in patients with atherosclerosis and heart failure in risk stratification for adverse cardiovascular events, including assessment of factors affecting the basal level of highly sensitive C-reactive protein. Research data (MRFIT, MONICA) have demonstrated a relationship between an increased level of C-reactive protein and the development of coronary heart disease. An increase in the serum level of highly sensitive C-reactive protein is observed in arterial hypertension, dyslipidemia, type 2 diabetes mellitus and insulin resistance, which indicates the involvement of systemic inflammation in these disorders. Currently, the assessment of highly sensitive C-reactive protein is used to determine the risk of developing myocardial infarction and stroke. It has been proven that heart failure patients have a high level of highly sensitive C-reactive protein compared with patients without heart failure. The level of C-reactive protein is referred to as modifiable risk factors for cardiovascular diseases of ischemic origin, since lifestyle changes or taking drugs such as statins, non-steroidal anti-inflammatory drugs, glucocorticoids, etc. reduce the level of highly sensitive C-reactive protein. In patients with heart failure with different left ventricular ejection fraction values, it was found that the regression of the inflammatory response is accompanied by an improvement in prognosis, which confirms the hypothesis of inflammation as a response to stress, which has negative consequences for the cardiovascular system.

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