Association Of Inflammatory Cytokines Research Articles

Association of inflammatory cytokines with lung function, chronic lung diseases, and COVID-19

Association of inflammatory cytokines with lung function, chronic lung diseases, and COVID-19

Association Of IL-6, And IL-10 Gene Snps In Childhood Febrile Seizure

Background: Febrile seizure are typically defined as convulsions=that-occur in children, between/6 months to 5years, who have a fever of more,,than”38 degrees Celsius, that is not associated with an intracranial’ reason such as an infection, ,head .injury, or epilepsy. It is also known as the immature brain's response to fever, which is age-dependent. As a child’s brain develops, there is an increase in neuronal excitability which puts the child at the risk of febrile seizures. Aims: the aim of the present study is to find out the association of Inflammatory cytokines (IL-6, IL-10) SNP with the onset of childhood febrile seizure. Method- Blood samples from patients with childhood febrile seizure will be collected in a sterile condition, and the association of SNP for both IL-6 (-597) G/A, and IL-10 (-819) C/T with disease susceptibility will be studied by using allele specific PCR. Results: The case-control study of 40 patients with Febrile seizure and 40 control without Febrile seizure has revealed that a substantial difference in the frequency distribution of IL-6 genotypes between the patient group and the control group where (p =0.041). Besides, there was no discernible variation in the frequency distribution of IL-10 genotypes and alleles. (p > 0.05); therefore, none of genotypes or alleles can be regarded as risk factor or protective factor. Conclusion: The present study has concluded that IL-6(-597) G/A, (rs:1800797) single nucleotide polymorphism (SNP) was associated with Febrile seizure susceptibility, and GG, genotype considered as, risk factor, while genotype GA act as protective factor. However, it refers that the IL-10-819C/T (rs:1800871), genes may not represent the Febrile-seizure-associated genetic risk factor.

Association of inflammatory cytokines with obesity and pulmonary function testing.

The World Health Organization (WHO) reported that the prevalence of obesity in the Kingdom of Saudi Arabia (KSA) is 33.7% (women 39.5% and men 29.5%), respectively. The effects of obesity on airway inflammation and respiratory mechanics as well as the function of adipose tissue has a key role in the development of various lung diseases. Therefore, this study aimed to compare the level of cytokines between obese (BMI ≥ 30) and non-obese participants and to assess their association with BMI, airways inflammation and pulmonary function. One-hundred and seven non-smoking students (18-25 years of age) were recruited using convenience sampling technique for comparative cross-sectional study. Of them, 80 students were eligible and included in the analysis; 54 were non-obese (BMI<30) and 26 were obese (BMI ≥ 30). All the participants underwent anthropometric measurements, fractional exhaled nitric oxide (FeNO) measurement, spirometry and cytokines measurement (IL-6, IL-1β, GM-CSF, IL-7, IL-8 and IL-10). Measurements were compared between obese and non-obese groups. Then a correlation test was made between pro- and anti-inflammatory cytokines with BMI, pulmonary function test finding and FeNO. The prevalence of obesity was 32.5% in the study population. Levels of pro-inflammatory cytokine IL-6 levels was significantly higher in obese than non-obese participants (p = 0.044). The level of FeNO log was significantly higher in obese participants than non-obese (p = 0.002). The pro-inflammatory cytokine IL-6 showed positive correlation with BMI while GMCSF showed negative correlation with FVC (p<0.05). The levels of pro-inflammatory cytokine IL-6 was found to be significantly higher in obese participants than non-obese participants. Furthermore, it showed positive correlation with BMI whereas pro-inflammatory cytokine GMCSF showed negative correlation with FVC.

Abstract 427: Differential Gene Expression in Survivors versus Non-Survivors of In-Hospital Cardiac Arrest

Background: While association of inflammatory cytokines with outcomes in cardiac arrest have become increasingly studied in both animal and human models, sparse published literature exists regarding gene expression and outcomes in adults with cardiac arrest. Accordingly, the goal of the current investigation was to identify proteins that are associated with survival, gender, and time and in what direction these proteins are associated in patients resuscitated from IHCA. Methods: In this prospective study, we assessed blood samples from adult patients with IHCA who underwent ACLS-guided resuscitation between 2014 and 2019 at an academic tertiary care medical center. Blood obtained at 0, 6, and 24 hours of IHCA) was sent for proteomic analysis. The primary outcome of interest was survival to hospital discharge. Results: Of the 95 patients, 22 (23.2%) survived to hospital discharge while 73 (76.8%) did not. A total of 206 samples were obtained from 95 patients, where each patient was measured at up to 6 time points. Given higher number of samples at 0, 6, and 24 hours following IHCA, modeling data was restricted to these time points. Volcano plot and heat map were generated for significant proteins for the survivor versus non-survivor analysis at each of the listed time points. Gene set enrichment analysis was also utilized to identify the top 10 gene sets associated with survivorship at T0, T6, and T12, and visualized via heatmap and a bar graph. Conclusions: In this contemporary proteomic study of 95 adults with IHCA receiving ACLS-guided resuscitative and post-resuscitative care, gene sets associated with survival exist and significant proteins associated with survivorship can be identified. To our knowledge, this is one of the first studies to assess differential gene expression in men and women with IHCA with respect to survival.

Association of Inflammatory Cytokines with Clonal Hematopoiesis and Progression to Acute Myeloid Leukemia

Association of Inflammatory Cytokines with Clonal Hematopoiesis and Progression to Acute Myeloid Leukemia

Changes in extracellular cytokines in predicting disease severity and final clinical outcome of patients with blunt chest trauma

BackgroundChest trauma causes substantial morbidity and mortality and its severity is assessed using clinical diagnosis or scoring systems like Injury severity score (ISS) and thoracic trauma severity score (TTSS). Association of inflammatory cytokines with severity of disease and final clinical outcome is not clearly defined in patients with chest trauma. In this study, we thought to evaluate the inflammatory response in serum and bronchoalveolar lavage fluid (BALF) in chest trauma patients and correlate the level of extracellular cytokines with diseases severity and final outcome. MethodsA total of 65 patients with blunt chest trauma and 30 healthy controls were enrolled in this prospective observational study. Assessment of inflammatory cytokines such as Interleukin (s) - IL-5, IL-13, IL-2, IL-6, IL-9, IL-1β, IFN-γ, TNF-α, IL-17A, IL-17F,IL-4, IL-21 and IL-22 was performed in both serum and bronchoalveolar lavage fluid using 13-plex multiplex kit using fluorescence–encoded bead based immunoassays. ResultsA significantly higher level of IL-13, IL-2, IL-6, IL-9, IL-1β, IFN-γ, TNF-α, IL-17A, IL-17F, IL-21 and IL-22 cytokines were observed in patients with blunt chest trauma compared to healthy controls. Level of IL-2, IL-6, IL-1β and IL-17A was significantly raised in the patients with blunt chest trauma who had a fatal outcome during the hospital stay. An elevated cytokine response of IL-13, IL-4, and IL-21 was noted in the group of patients with high (>5) thoracic trauma severity score. ConclusionRoutine monitoring of the inflammatory cytokine level in patients with chest trauma may be used routinely. Longer prospective studies should be encouraged to determine the role of cytokines in patients with chest trauma in predicting the patient final clinical outcome.

Association of ACEI/ARB, inflammatory cytokines, and antiviral drugs with liver dysfunction in patients with hypertension and COVID-19

ABSTRACT Background: Currently, SARS-CoV-2 liver invasion, inflammatory cytokines, and antiviral drugs are widely thought to be associated with liver dysfunction in COVID-19 patients. Besides, previous studies indicated that ACEI/ARB drugs can increase the expression of hepatic ACE2, a cell entry receptor for SARS-CoV-2. This study aims to investigate whether ACEI/ARB aggravates liver injury and the association of inflammatory cytokines and antiviral drugs with liver dysfunction in patients with hypertension and COVID-19.Method: This retrospective study included 127 hypertensive patients with long-term use or nonuse of ACEI/ARBs hospitalized for COVID-19 from January 30 to April 7, 2020, in Tongji hospital of Wuhan, China. Demographic, clinical, laboratory, treatment, and outcome data were collected.Results: Of the 127 patients with COVID-19 and hypertension, 43 taking long-term of ACEI/ARBs and 84 without using ACEI/ARBs. Abnormal liver function was observed in part of ACEI/ARB and non-ACEI/ARB users but without significant differences between these two groups. Serum inflammatory cytokines, IL-6, IL-8, and TNFα, as well as inflammation-related markers, ferritin, procalcitonin, and C-reactive protein, were significantly elevated in patients with liver dysfunction. IL-6 level was positively correlated with liver function tests on admission and highly consistent with the changes of abnormal ALT, AST, and GGT during hospitalization, but the correlations of other inflammatory cytokines were low. There was no significant association between the use of antiviral drugs and liver dysfunction in these patients.Conclusion: The elevation of inflammatory cytokine, IL-6, but not ACEI/ARB and antiviral drugs, is closely associated with liver dysfunction in patients with hypertension and COVID-19.

The Association of Inflammatory Cytokines in the Pulmonary Pathophysiology of Respiratory Failure in Critically Ill Patients With Coronavirus Disease 2019.

The majority of coronavirus disease 2019 mortality and morbidity is attributable to respiratory failure from severe acute respiratory syndrome coronavirus 2 infection. The pathogenesis underpinning coronavirus disease 2019-induced respiratory failure may be attributable to a dysregulated host immune response. Our objective was to investigate the pathophysiological relationship between proinflammatory cytokines and respiratory failure in severe coronavirus disease 2019. Multicenter prospective observational study. ICU. Critically ill patients with coronavirus disease 2019 and noncoronavirus disease 2019 critically ill patients with respiratory failure (ICU control group). Daily measurement of serum inflammatory cytokines. Demographics, comorbidities, clinical, physiologic, and laboratory data were collected daily. Daily serum samples were drawn for measurements of interleukin-1β, interleukin-6, interleukin-10, and tumor necrosis factor-α. Pulmonary outcomes were the ratio of Pao2/Fio2 and static lung compliance. Twenty-six patients with coronavirus disease 2019 and 22 ICU controls were enrolled. Of the patients with coronavirus disease 2019, 58% developed acute respiratory distress syndrome, 62% required mechanical ventilation, 12% underwent extracorporeal membrane oxygenation, and 23% died. A negative correlation between interleukin-6 and Pao2/Fio2 (rho, -0.531; p = 0.0052) and static lung compliance (rho, -0.579; p = 0.033) was found selectively in the coronavirus disease 2019 group. Diagnosis of acute respiratory distress syndrome was associated with significantly elevated serum interleukin-6 and interleukin-1β on the day of diagnosis. The inverse relationship between serum interleukin-6 and Pao2/Fio2 and static lung compliance is specific to severe acute respiratory syndrome coronavirus 2 infection in critically ill patients with respiratory failure. Similar observations were not found with interleukin-β or tumor necrosis factor-α.

Betalain exerts a protective effect against glaucoma is majorly through the association of inflammatory cytokines

The present research aimed at evaluating the protective role of betalain on the in vitro glaucoma model using PC12 neuronal cells. The cultured neuronal cells in a customized pressurized chamber were analyzed for the onset of glutathione, myeloperoxidase (MPO), cathepsin, expression of inflammatory enzymes such as cyclooxygenase (COX-1), lipoxygenase (5- LOX), sPLA2 caveolin-1, glaucoma markers and other inflammatory cytokines in the presence and absence of betalain. The results have shown that a significant increase in the expression of oxidative stress with increased activity of cathepsin B and D. On the other hand, the activity of inflammatory enzymes such as COX-1, 5- LOX, sPLA2 were significantly increased in pressure exposed cells. In addition, glaucoma simulated cells demonstrated a significant increase in the VEGF, TGF-β, BDGF, and neuroserpin compared to control. Moreover, cells predisposed to hydrostatic pressure demonstrated an increase in (p < 0.01) inflammatory cytokines such as IL-6, CXCR4, IL-17, IL-1β, and TNF-α levels. However, cells pre-treated with betalain improved the glutathione levels with attenuated MPO activity. Simultaneously, the levels of inflammatory cytokines and other glaucoma marker genes found restored in drug pre-treated cells. Thus, the results of the present study demonstrate that the use of betalain on ocular cells can prevent the progression of the disease that can be a suggestive therapeutic for controlling glaucoma like conditions.

Advances in the pathogenesis representing definite outcomes in chronic urticaria.

We reviewed in this article, the recent advances in CSU physiopathology and potential clinical and laboratory biomarkers in CSU. In addition to the central role of mast cells in urticaria physiopathology, increased interest in basophils has arisen. Recent data corroborate the autoimmunity pathway as one of the main pathways in mast cell activation. The association of inflammatory cytokines, heat shock proteins and staphylococcal infection with CSU are also reviewed. C-reactive protein, D-dimers, autologous serum skin test, IgE levels and FcεRI expression in basophils have shown their potential as biomarkers for disease duration, activity, severity and/or response to treatment. A comprehensive understanding of chronic spontaneous urticaria mechanisms is essential to find novel biomarkers and treatments. The use of these biomarkers in clinical practice will guide us in choosing the best treatment option for our patients.

Association of Inflammatory Cytokines With the Symptom Cluster of Pain, Fatigue, Depression, and Sleep Disturbance in Chinese Patients With Cancer

ContextPain, fatigue, depression, and sleep disturbance are common in patients with cancer and usually co-occur as a symptom cluster. However, the mechanism underlying this symptom cluster is unclear. ObjectivesThis study aimed to identify subgroups of cluster symptoms, compare demographic and clinical characteristics between subgroups, and examine the associations between inflammatory cytokines and cluster symptoms. MethodsParticipants were 170 Chinese inpatients with cancer from two tertiary hospitals. Inflammatory markers including interleukin-6 (IL-6), interleukin-1 receptor antagonist, and tumor necrosis factor alpha were measured. Intergroup differences and associations of inflammatory cytokines with the cluster symptoms were examined with one-way analyses of variance and logistic regression. ResultsBased on cluster analysis, participants were categorized into Subgroup 1 (all low symptoms), Subgroup 2 (low pain and moderate fatigue), or Subgroup 3 (moderate-to-high on all symptoms). The three subgroups differed significantly in Eastern Cooperative Oncology Group (ECOG) performance status, sex, residence, current treatment, education, economic status, and inflammatory cytokines levels (all P < 0.05). Compared with Subgroup 1, Subgroup 3 had a significantly poorer ECOG physical performance status and higher IL-6 levels, were more often treated with combined chemoradiotherapy, and were more likely to be rural residents. IL-6 and ECOG physical performance status were significantly associated with 1.246-fold (95% CI 1.114–1.396) and 31.831-fold (95% CI 6.017–168.385) increased risk of Subgroup 3. ConclusionOur findings suggest that IL-6 levels are associated with cluster symptoms in cancer patients. Clinicians should identify patients at risk for more severe symptoms and formulate novel target interventions to improve symptom management.

Association of inflammatory cytokines with obesity and prevention with ASA or DHA/EPA supplementation.

e14619 Background: Obesity is associated with poor breast cancer outcomes. Our prior data suggested a positive feedback loop whereby circulating factors associated with obesity induce the COX-2 enzyme, resulting in increased pro-inflammatory cytokine prostaglandin E2 (PGE2), which can then increase aromatase levels. In order to establish a better understanding of baseline PGE2 levels, as well as select the proper COX2 inhibitor for prospective study, we performed a randomized study of aspirin (ASA), fish oil (DHA/EPA), and the combination in postmenopausal women of varying body habitus and assessed changes in cytokines. Methods: Women were recruited and randomly assigned into 3 interventions: ASA 81mg, docosahexaenoic acid (DHA, 1500mg) with eicosapentaenoic acid (EPA, 2500mg), or combination ASA and DHA/EPA (DUAL). Blood was collected before and after 28 days of supplementation, and 27 cytokines were assessed by Luminex array (Millipore); PGE2 was measured by ELISA. Investigators were blinded until analysis was complete. Statistical analyses were performed in R. Results: 110 patients were included: 90% participants white; of which 50% Hispanic; average BMI 31.5±0.67; and age: 60.1±0.58. Cytokines were not correlated with demographic variables. At baseline inflammatory cytokines IL-6 and Eotaxin were correlated with BMI ((p &gt; 0.029 and p &gt; 0.017, respectively). After 28 days of DHA/EPA BMI was correlated with Eotaxin, Il-2, IL-7 and GM-CSF (p &lt; 0.05), in ASA group correlation was significant only with IL-2 (cor.coef= 0.58). Two sample t-test showed significant difference between DUAL and ASA or DHA/EPA for IL-6 (p = 0.008 and p = 0.034, respectively), and for IL-2 only between DUAL and ASA (p = 0.039). Furthermore, impact on PGE2 was observed with ASA with 81% obtaining a decrease from baseline (median change -28%); by comparison 55.1% (-1%) and 65.6% (-22%) of subjects showed decrease in the DUAL and DHA/EPA groups respectively. Level of macrophage inflammatory proteins (MIP-1b) were lower in the DUAL group compare to ASA (p &lt; 0.014). Conclusions: Chronic inflammatory cytokines are correlated with obesity, and may be modified by use of ASA and DHE/EPA. This strategy may be useful in the secondary prevention setting. Clinical trial information: NCT02062255.

Association of inflammatory cytokines with mortality in peritoneal dialysis patients.

Aims: Previous study on association between pro-inflammatory cytokines and mortality in PD population is limited. We aimed to investigate here.Methods: Total 50 patients who underwent incident PD were enrolled in this study. We measured the titers of pro-inflammatory cytokines Interleukin-18(IL-18), Interleukin-6 (IL-6), and Interleukin-1ß (IL-1ß). Study outcomes were all-cause mortality, cardiovascular-related mortality, and infection-caused mortality. Cox-regression model was used.Results: In this 7 year prospective study, IL-18 ≥ 804.3pg/ml, IL-6 ≥ 3.92 pg/ml, IL-1ß ≥ 0.86pg/ml, age ≥ 50 years-old, and existence of diabetes could be used as individual significant predictors for mortality in PD patients. Higher titers of IL-6 were associated with lower averaging albumin levels within 1st year of PD. Increasing numbers of these risk markers of mortality was associated with decreasing survival advantages (P = 0.001).Conclusion: Age ≥ 50 years-old, diabetes, and inflammatory cytokines profiles at the start of PD therapy could predict for 7-year mortality in PD population.

Global Cytokine Profiles and Association With Clinical Characteristics in Patients With Irritable Bowel Syndrome.

Evidence suggests that patients with irritable bowel syndrome (IBS) have an altered cytokine profile, although it is unclear whether cytokines are linked with symptom severity. We aimed to determine whether global serum and mucosal cytokine profiles differ between IBS patients and healthy subjects and whether cytokines are associated with IBS symptoms. Serum from 144 IBS patients and 42 healthy subjects was analyzed for cytokine levels of interleukin (IL)-5, IL-6, IL-8, IL-10, IL-12p70, IL-13, IL-17A, interferon (IFN)-γ, and tumor necrosis factor (TNF) by MSD MULTI-ARRAY. In total, 109 IBS and 36 healthy sigmoid colon biopsies were analyzed for mRNA expression of IL-8, IL-10, TNF, and FOXP3 by quantitative reverse transcription PCR. Multivariate discrimination analysis evaluated global cytokine profiles. Rectal sensitivity, oroanal transit time, and psychological and gastrointestinal symptom severity were also assessed. Global cytokine profiles of IBS patients and healthy subjects overlapped, but cytokine levels varied more in IBS patients. Serum levels of IL-6 and IL-8 tended to be increased and levels of IFN-γ tended to be decreased in IBS patients. Mucosal mRNA expression of IL-10 and FOXP3 tended to be decreased in IBS patients. Within both the full study cohort and IBS patients alone, serum level of TNF was associated with looser stool pattern, while subjects with more widespread somatic symptoms had increased serum levels of IL-6. Although neither IBS bowel habit subgroups nor patients with possible post-infectious IBS were associated with distinct cytokine profiles, a small cluster of IBS patients with comparatively elevated immune markers was identified. Global cytokine profiles did not discriminate IBS patients from healthy subjects, but cytokine profiles were more varied among IBS patients than among healthy subjects, and a small subgroup of patients with enhanced immune activity was identified. Also, association of inflammatory cytokines with some clinical symptoms suggests that immune activation may be of importance in a subset of IBS patients.

Association of Inflammatory Cytokines with Traditional and Nontraditional Cardiovascular Risk Factors in Indians with known Coronary Artery Disease.

Background:Inflammatory processes are implicated in the etiology of cardiovascular disease (CVD). Data on the association of inflammatory markers with cardiovascular risk factors in Indian patients with CVD are limited.Aim:This study was conducted with the aim to evaluate the association of inflammatory markers with traditional and nontraditional cardiovascular risk factors in angiographically proven coronary artery disease (CAD) patients.Subjects and Methods:We studied the association of serum highly sensitive C-reactive protein (hsCRP) (0.1-37.9 mg/l), interleukin-6 (IL-6) (2-253.2 pg/ml) and tumor necrosis factor-alpha (TNF-α) (8-525.8 pg/ml) with cardiovascular risk factors in 300 (M: 216, F: 84; mean age: 60.9 (12.4) years) CAD patients. All patients were evaluated for anthropometry and cardiovascular risk factors, and blood samples were collected for biochemical and inflammatory markers. Statistical analysis was carried out using SPSS Version 20.Results:Mean hsCRP, IL-6 and TNF-α in study population were 11.7 (9.7) mg/l, 64.5 (75.2) pg/ml, and 25.3 (40.9) pg/ml respectively. A total of 73.6% (221/300) patients had hsCRP levels >3.0 mg/l. All inflammatory markers were significantly higher and showed a positive correlation with dyslipidemia, diabetes mellitus, and/or hypertension (HTN). TNF-α had a negative correlation with age and positive correlation with smoking. Only IL-6 and hsCRP had a positive correlation with insulin resistance and negative correlation with insulin secretion. Among lipid parameters, triglyceride had a positive correlation, and high density lipoprotein had a negative correlation with all inflammatory markers. There was a progressive increase in the percentage of subjects with diabetes, HTN, and dyslipidemia with increasing levels of inflammatory markers.Conclusions:Indian patients with CAD had significantly high levels of inflammatory markers, which were related to cardiovascular risk factors.

Association of inflammatory cytokines, lipid peroxidation end products and nitric oxide with the clinical severity and fetal outcome in preeclampsia in Indian women.

Preeclampsia is a multisystem disorder associated with maternal hypertension, placental abnormalities and adverse fetal outcomes. The various pathways involved in its etiology include endothelial dysfunction, inflammatory milieu, lipid peroxidation and immunological imbalance. The present study was conducted to evaluate the causative and predictive role of nitric oxide, lipid peroxidation end products (MDA) and inflammatory cytokines (IL-6, TNF-α) in clinical presentation, severity and fetal outcome in preeclampsia. The study population was divided into 3 groups- Non- pregnant females comprising the control population; G1 and G2 groups included normal pregnant and pregnant females with preeclampsia with 50 patients in each group. Nitric Oxide and MDA levels were found to be highest in the preeclamptic patients as compared to other two groups. ROC curve analysis shows the superiority of the inflammatory markers as determinants of severity of preeclampsia which suggests the emerging role of pro inflammatory markers in the various pathological changes in preeclampsia. TNF-α emerged as the best marker in multivariate analysis and thus, has the potential for being used as a marker for PIH. Our study illustrates the multifactorial etiology of preeclampsia involving oxidative stress, proinflammatory milieu and endothelial dysfunction.

Expression of Selected Inflammatory Cytokine Genes in Bladder Biopsies

Besides the deregulation of oncogene and tumour suppressor gene, bladder carcinoma can also be caused byinflammation. To date, the association of inflammatory cytokines with carcinoma of the bladder (especially thetransitional cell carcinomas) is not fully understood. In this study, we report an attempt to examine expressionpatterns of pro- and anti- inflammatory cytokine genes from normal and tumour tissue biopsies of the humanbladder. Our molecular assays involved the use of the GeneXP™ Human Cyto-3 kit and the ReverseTranscription – Polymerase Chain Reaction test. Due to limitation in our experimental process, mainly attributedby inconsistencies in the results obtained between the two assay systems, we cannot reach a conclusionregarding the association of the six selected inflammatory cytokine genes (IL-8, IL-12A, IL-18, TGF-β1, TGF-β2, and TGF-β3) with bladder carcinoma. However, our data provided early novel evidence of expression offour inflammatory cytokine genes, namely IL-12A, TGF-β1, TGF-β2, and TGF-β3 in tissues derived from thehuman bladder.