scholarly journals Cytokine antibody array-based analysis of IL-37 treatment effects in asthma

Aging ◽  
2021 ◽  
Author(s):  
Shengnan Gao ◽  
Jingru Wang ◽  
Qing Zhang ◽  
Jun Shu ◽  
Chunxiao Li ◽  
...  
2019 ◽  
Author(s):  
Ruyi Zhai ◽  
Huan Xu ◽  
Xinghuai Sun ◽  
Xiangmei Kong

Abstract Purpose: This study was aimed to analyze the profile of vascular and inflammatory cytokines in aqueous humor of primary open angle glaucoma (POAG) patients. Methods: Aqueous humor samples were acquired from 6 POAG patients and 7 age-related cataract patients that constituted the control group. A human cytokine antibody array was used to detect 37 proteins related to inflammation and vascular regulation. Characteristics including age, gender, and intraocular pressure (IOP) of POAG and age-related cataract patients were compared. Correlation analyses between aqueous humor cytokines and characteristics were performed. Results: The cytokine antibody array results showed that the signal intensities of soluble vascular endothelial growth factor receptor 1 (sVEGFR-1), von Willebrand factor (vWF), tumor necrosis factor (TNF)-α, and angiopoietin-2 in POAG patients were significantly higher in aqueous samples compared to controls (p < 0.05, Student’s test or Mann-Whitney U-test). Among cytokines of all aqueous samples, preoperative IOP was positively associated with expression quantity of sVEGFR-1 (r = 0.647, p = 0.02) and VEGF-A (r = 0.602, p = 0.04) and negatively associated with plasminogen activator inhibitor 1 expression (r = -0.593, p = 0.04). Values for sVEGFR-1 were positively correlated with vWF (r = 0.646, p = 0.02) and TNF-α (r = 0.824, p < 0.001) with statistical significance. Conclusion: Pathogenesis of primary open angle glaucoma may be associated with both vascular dysfunction and inflammatory responses. The vascular factors may include endothelial dysfunction and damaged vascular permeability as indicated by abnormal expression of vWF, sVEGFR-1 and angiopoietin-2. Keywords: POAG, aqueous humor, cytokines, sVEGFR-1, vWF, angiopoietin-2


2021 ◽  
Vol 12 ◽  
Author(s):  
Shan-Shan Guo ◽  
Yu-Jing Liang ◽  
Li-Ting Liu ◽  
Qiu-Yan Chen ◽  
Yue-Feng Wen ◽  
...  

Background: Despite the development of such multiple therapeutic approaches, approximately 20% patients experience recurrence. Identification of molecular markers for stratifying the different risks of tumour recurrence and progression is considered imperative.Methods: We used a RayBio Human Cytokine Antibody Array that simultaneously detected the levels of 297 proteins and profiled the conditioned medium of HONE1 cells and the radioresistant NPC cells HONE1-IR. We found Angiogenin(ANG) expression to be significantly increased in HONE1-IR and HONE1-IR cells exposed to 4-Gy X-ray radiation.Results: We investigated the expression of ANG in NPC tissues and explored its prognostic significance in patients with NPC. We found that ANG expression was increased in recurrent NPC tissues. Elevated expression of ANG induced radio-resistance in NPC cells, in addition to being significantly associated with shorter PFS, OS, and LRFS in patients with NPC. Multivariate analysis results revealed that ANG was an independent prognostic factor that predicted PFS, OS, and LRFS. Furthermore, a nomogram model was generated to predict OS in terms of ANG expression.Conclusion: Our results found the radioresistant function of ANG and proved the clinical prognostic significance of ANG, and the results could help predict radio-sensitivity and stratify high-risk patients or tumour recurrence.


2016 ◽  
Vol 106 (3) ◽  
pp. e187
Author(s):  
M. Pavone ◽  
J.M. Kelsh ◽  
S. Malpani ◽  
R. Confino ◽  
S. Jasti ◽  
...  

2011 ◽  
Vol 34 (5) ◽  
pp. 387-397 ◽  
Author(s):  
Denise M. Newsom ◽  
H. Denny Liggitt ◽  
Katherine O’Rourke ◽  
Dongyue Zhuang ◽  
David A. Schneider ◽  
...  

Cell Stress ◽  
2021 ◽  
Vol 6 (1) ◽  
pp. 6-16
Author(s):  
Yushan Zhang ◽  
Chao Xu ◽  
Nelson I. Agudelo Higuita ◽  
Resham Bhattacharya ◽  
Jennifer Holter Chakrabarty ◽  
...  

The COVID-19 pandemic has led to significant global health and economic consequences. There is an unmet need to define a molecular fingerprint of severity of the disease that may guide an early, rational and directed intervention preventing severe illness. We collected plasma from patients with moderate (nine cases), severe (22 cases) and critical (five cases) COVID-19 within three days of hospitalization (approximately one week after symptom onset) and used a cytokine antibody array to screen the 105 cytokines included in the array. We found that I-TAC, IP-10, ST2 and IL-1ra were significantly upregulated in patients with critical disease as compared to the non-critical (moderate and severe combined). ELISA further quantified I-TAC levels as 590.24±410.89, 645.35±517.59 and 1613.53±1010.59 pg/ml in moderate, severe and critical groups, respectively. Statistical analysis showed that I-TAC levels were significantly higher in patients with critical disease when compared with moderate (p = 0.04), severe (p = 0.03) or the combined non-critical (p = 0.02) group. Although limited by the low sample numbers, this study may suggest a role of I-TAC as a potential early marker to discriminate between critical and non-critical COVID-19 cases. Such knowledge is urgently needed for appropriate allocation of resources and to serve as a platform for future research towards early interventions that could mitigate disease severity and save lives.


2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Xue Mei Fan ◽  
Chun Lian Huang ◽  
Yi Ming Wang ◽  
Ning Li ◽  
Qiong Lin Liang ◽  
...  

Objective. Cytokines are essential promoters in the pathogenesis of diabetic nephropathy (DN) in type 2 diabetes. The following study investigates the adjustment mechanism of Tangshen formula (TSF) on cytokine expressions in db/db mice (DN animal model). Materials and Methods. Db/db mice were randomly divided into three groups. The treated groups were orally administered with TSF and losartan for 12 weeks. Biochemical and histological examinations were determined at 8 and 12 weeks posttreatment, while the cytokine antibody array analysis was applied to analyze the expression of 144 cytokines in kidney tissues at the end of the 12th week posttreatment. Results. TSF significantly reduced urinary albumin excretion and the levels of blood glucose, cholesterol, triglyceride, creatinine, and urea nitrogen. Furthermore, a significant decrease in glomerulus and mesangial area, as well as the downregulation of 24 cytokines and upregulated expressions of 5 cytokines, was found in the TSF-treated mice. Conclusions. The present study reveals that TSF could ameliorate the metabolic anomalies and renal injury in db/db mice. One of the important mechanisms for treatment of DN using the treatment of TSF is the control of the JAK/STAT signaling pathway via regulation of IL-2, IL-6, IL-13, Il-15, and IFN-γ expression.


2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 5113-5113
Author(s):  
J. Perez-Gracia ◽  
C. Prior ◽  
F. Guillen-Grima ◽  
A. Gonzalez ◽  
A. Panizo ◽  
...  

5113 Background: Several drugs are available for treatment of MRCC and predictive markers to select the most appropriate therapy for each patient are needed to improve efficacy and to avoid unnecessary toxicities and costs. Methods: Serum samples were collected prospectively in 31 patients treated with sunitinib at baseline and at the time of response evaluation by RECIST criteria. Serums of 6 patients with extreme phenotypes of marked responses (3) or clear progressions (3) were analyzed with a Human Cytokine Antibody Array (Series 2000, RayBiotech, Norcross, GA. USA) which evaluates 174 cytokines related to angiogenesis and tumor proliferation pathways and has been validated in clinical studies. Cytokine intensity levels were compared between both groups at baseline and after response evaluation and fold-change differences were calculated. Following array data normalization, the most relevant cytokines based on statistical significance and on biological plausibility, were assessed with ELISA in the whole group of patients and the results were correlated with clinical benefit (response or disease stabilization) or progression. Results: 27 of the 174 cytokines varied significantly between patients presenting response or progression. Six of them (TNF-α, MMP-9, ICAM-1, BDNF, SDF-1α and VEGF) were assessed with ELISA in 22 evaluable patients. TNF-α and MMP-9 baseline levels were significantly increased in non-responders and they were significantly associated with progression-free and overall survival respectively. The area under the ROC curves of TNF-α and MMP-9 as predictive factors of sunitinib clinical benefit were respectively 0.8287 and 0.7685, indicating good accuracy. Conclusions: Baseline serum levels of TNF-α and MMP-9 warrant further study as predictive markers of sunitinib activity in patients with MRCC. Selection of patients with extreme phenotypes seems a valid method to identify potential predictive factors of response. [Table: see text] [Table: see text]


2006 ◽  
Vol 2006 ◽  
pp. 1-8 ◽  
Author(s):  
Ulla Jalonen ◽  
Riina Nieminen ◽  
Katriina Vuolteenaho ◽  
Hannu Kankaanranta ◽  
Eeva Moilanen

In inflammation, the post-transcriptional regulation of transiently expressed genes provides a potential therapeutic target. Tristetraprolin (TTP) is of the factors regulating decay of cytokine mRNAs. The aim of the present study was to identify cytokines whose expression is regulated by TTP. We established a TTP knock-down cell line by expressing shRNA against TTP (shTTP cell line). A cytokine antibody array was used to measure cytokine production in macrophages exposed to lipopolysaccharide (LPS). Cytokines IL-6, IL-12, TNF-α, and MIP-2 (a homologue to human IL-8) were expressed at higher levels whereas MIP-3αwas produced at lower levels in LPS-treated shTTP cells than in control cells suggesting that the expression of these cytokines is regulated by TTP. The present data provide IL-12, MIP-2, and MIP-3αas novel inflammatory cytokine targets for TTP-mediated mRNA decay and stress the role of TTP in the regulation of the inflammatory process.


2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Chen Yan ◽  
Le Yu ◽  
Xiu-Ling Zhang ◽  
Jing-Jing Shang ◽  
Jie Ren ◽  
...  

Background. Systemic lupus erythematosus (SLE) is a chronic, systemic autoimmune disease that commonly causes kidney damage. Therefore, we measured plasma levels of cytokines that may be related to renal dysfunction in SLE patients. Methods. To explore the differences between SLE patients with renal dysfunction and healthy volunteers, the levels of cytokines in plasma were screened using a human cytokine antibody array. Then, we chose fourteen of the elevated cytokines for verification with an expanded sample size by a human magnetic Luminex assay. Plasma samples were isolated from SLE patients (n=72) and healthy volunteers (n=8). Results. Cytokine antibody array data showed elevated plasma cytokines in SLE patients with renal dysfunction compared with healthy volunteers. By using the human magnetic Luminex assay, we found that plasma levels of CHI3L1, GDF-15, IGFBP-2, MIF, ST2, TFF3, and uPAR were significantly higher in SLE patients than in healthy volunteers. Plasma levels of CXCL4 were significantly lower in the active group than in the inactive group, and plasma levels of CHI3L1, IGFBP-2, MIF, and MPO were significantly higher in the active group than in the inactive group. We also analyzed the correlation between plasma cytokine levels and the SLEDAI-2K, and our results showed that the plasma levels of the fourteen selected cytokines were weakly correlated or not correlated with the SLEDAI-2K. We further analyzed the correlation between cytokines and renal dysfunction. Plasma levels of GDF-15 and TFF3 were highly positively correlated with serum creatinine levels and 24-hour urine protein levels. Conclusion. Our data suggest that plasma levels of GDF-15 and TFF3 are potential renal dysfunction markers in SLE patients, but plasma levels of these cytokines are not correlated with the SLEDAI-2K. Further study is warranted to determine how these cytokines regulate inflammatory responses and renal dysfunction in SLE.


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