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Inflammatory Cytokine Expression Is Associated with Chikungunya Virus Resolution and Symptom Severity  [PDF]
Alyson A. Kelvin ,David Banner,Giuliano Silvi,Maria Luisa Moro,Nadir Spataro,Paolo Gaibani,Francesca Cavrini,Anna Pierro,Giada Rossini,Mark J. Cameron,Jesus F. Bermejo-Martin,Stéphane G. Paquette,Luoling Xu,Ali Danesh,Amber Farooqui,Ilaria Borghetto,David J. Kelvin,Vittorio Sambri,Salvatore Rubino
PLOS Neglected Tropical Diseases , 2011, DOI: 10.1371/journal.pntd.0001279
Abstract: The Chikungunya virus infection zones have now quickly spread from Africa to parts of Asia, North America and Europe. Originally thought to trigger a disease of only mild symptoms, recently Chikungunya virus caused large-scale fatalities and widespread economic loss that was linked to recent virus genetic mutation and evolution. Due to the paucity of information on Chikungunya immunological progression, we investigated the serum levels of 13 cytokines/chemokines during the acute phase of Chikungunya disease and 6- and 12-month post-infection follow-up from patients of the Italian outbreak. We found that CXCL9/MIG, CCL2/MCP-1, IL-6 and CXCL10/IP-10 were significantly raised in the acute phase compared to follow-up samples. Furthermore, IL-1β, TNF-α, Il-12, IL-10, IFN-γ and IL-5 had low initial acute phase levels that significantly increased at later time points. Analysis of symptom severity showed association with CXCL9/MIG, CXCL10/IP-10 and IgG levels. These data give insight into Chikungunya disease establishment and subsequent convalescence, which is imperative to the treatment and containment of this quickly evolving and frequently re-emerging disease.
Cigarette smoke induces IL-8, but inhibits eotaxin and RANTES release from airway smooth muscle
Ute Oltmanns, Kian F Chung, Matthew Walters, Matthias John, Jane A Mitchell
Respiratory Research , 2005, DOI: 10.1186/1465-9921-6-74
Abstract: HASMC in primary culture were exposed to cigarette smoke extract (CSE) with or without TNFα. Chemokines were measured by enzyme-linked immunosorbent assay (ELISA) and gene expression by real time polymerase chain reaction (PCR). Data were analysed using one-way analysis of variance (ANOVA) followed by Bonferroni's t testCSE (5, 10 and 15%) induced IL-8 release and expression without effect on eotaxin or RANTES release. At 20%, there was less IL-8 release. TNFα enhanced CSE-induced IL-8 release and expression. However, CSE (5–30%) inhibited TNFα-induced eotaxin and RANTES production. The effects of CSE on IL-8 release were inhibited by glutathione (GSH) and associated with the induction of the oxidant sensing protein, heme oxygenase-1.Cigarette smoke may directly cause the release of IL-8 from HASMC, an effect enhanced by TNF-α which is overexpressed in COPD. Inhibition of eotaxin and RANTES by cigarette smoke is consistent with the predominant neutrophilic but not eosinophilic inflammation found in COPD.Chronic obstructive pulmonary disease (COPD) is a major public health problem that is currently ranking as the fourth leading cause of death in the world [1]. It is characterised by progressive and largely irreversible airflow limitation associated with symptoms such as cough, sputum production, and dyspnea. A chronic inflammatory response of the lung to noxious particles, most notably tobacco smoke, but also occupational dusts and air pollution, is currently considered as the underlying pathological mechanism leading to this clinical condition [1]. However, the link between inhalation of harmful substances, such as cigarette smoke, bronchial inflammation and the development of airflow limitation is not completely understood.Currently, cessation of smoking is the only intervention that slows down disease progression in COPD [2]. Although only a minority of smokers develop symptoms of COPD, there is evidence that even in the lungs of asymptomatic smokers the numbers o
银杏内酯b对星形胶质细胞释放no、il-6及趋化因子rantes的影响  [PDF]
药学学报 , 2010,
Abstract: 考察银杏内酯b对星形胶质细胞释放no、il-6及趋化因子rantes的影响,探讨在炎性刺激条件下,银杏内酯b对星形胶质细胞的保护作用机制。采用griess试剂检测培养上清液中no的含量,elisa法测定il-6及rantes的含量,rt-pcr法测定il-6及rantesmrna的表达。结果显示,lps可显著刺激大鼠原代星形胶质细胞释放no,银杏内酯b可显著抑制lps刺激的no释放;il-1β可显著刺激u251星形胶质瘤细胞il-6和rantes的生成,并增加其mrna的表达,银杏内酯b可明显抑制il-1β诱导的il-6和rantes的生成,并可显著抑制il-1β和rantesmrna的表达。因此,银杏内酯b可能是通过减少no的生成,降低星形胶质细胞炎症因子il-6mrna和细胞趋化因子rantesmrna的表达,从而减少il-6及rantes的产生,减轻炎症反应的程度。结果表明,银杏内酯b可能通过降低ad发病和进展过程中的与星形胶质细胞相关的慢性炎症反应,从而缓解ad症状。
Biomarkers for Severity of Spinal Cord Injury in the Cerebrospinal Fluid of Rats  [PDF]
Joanna M. Lubieniecka,Femke Streijger,Jae H. T. Lee,Nikolay Stoynov,Jie Liu,Randy Mottus,Tom Pfeifer,Brian K. Kwon,Jens R. Coorssen,Leonard J. Foster,Thomas A. Grigliatti,Wolfram Tetzlaff
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0019247
Abstract: One of the major challenges in management of spinal cord injury (SCI) is that the assessment of injury severity is often imprecise. Identification of reliable, easily quantifiable biomarkers that delineate the severity of the initial injury and that have prognostic value for the degree of functional recovery would significantly aid the clinician in the choice of potential treatments. To find such biomarkers we performed quantitative liquid chromatography-mass spectrometry (LC-MS/MS) analyses of cerebrospinal fluid (CSF) collected from rats 24 h after either a moderate or severe SCI. We identified a panel of 42 putative biomarkers of SCI, 10 of which represent potential biomarkers of SCI severity. Three of the candidate biomarkers, Ywhaz, Itih4, and Gpx3 were also validated by Western blot in a biological replicate of the injury. The putative biomarkers identified in this study may potentially be a valuable tool in the assessment of the extent of spinal cord damage.
Beyond sepsis pathophysiology with cytokines: what is their value as biomarkers for disease severity?
Bozza, Fernando A;Bozza, Patrícia T;Castro Faria Neto, Hugo C;
Memórias do Instituto Oswaldo Cruz , 2005, DOI: 10.1590/S0074-02762005000900037
Abstract: sepsis is a major challenge in medicine. it is a common and frequently fatal infectious condition. the incidence continues to increase, with unacceptably high mortality rates, despite the use of specific antibiotics, aggressive operative intervention, nutritional support, and anti-inflammatory therapies. typically, septic patients exhibit a high degree of heterogeneity due to variables such as age, weight, gender, the presence of secondary disease, the state of the immune system, and the severity of the infection. we are at urgent need for biomarkers and reliable measurements that can be applied to risk stratification of septic patients and that would easily identify those patients at the highest risk of a poor outcome. such markers would be of fundamental importance to decision making for early intervention therapy or for the design of septic clinical trials. in the present work, we will review current biomarkers for sepsis severity and especially the use of cytokines as biomarkers with important pathophysiological role.
Nuclear NF-κB p65 in Peripheral Blood Mononuclear Cells Correlates with Urinary MCP-1, RANTES and the Severity of Type 2 Diabetic Nephropathy  [PDF]
Bin Yi, Xiaofang Hu, Hao Zhang, Jing Huang, Jishi Liu, Jing Hu, Wei Li, Lihua Huang
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0099633
Abstract: Aims To investigate if nuclear NF-κB p65 expression in ex vivo isolated peripheral blood mononuclear cells correlates with urinary MCP-1 or RANTES and the severity of type 2 diabetic nephropathy. Methods According to their urinary albumin-to-creatinine ratio (uACR), 107 patients with type 2 diabetes (eGFR >60 ml/min) were divided into normal albuminuria group (DN0 group, 38 cases), microalbuminuria group (DN1 group, 38 cases), and macroalbuminuria group (DN2 group, 31 cases), compared with matched healthy normal control group (NC group, 30 cases). Nuclear NF-κB p65 protein expression levels in peripheral blood mononuclear cells were detected by western blotting. Real-time quantitative polymerase chain reaction was used to detect NF-κB p65 mRNA expression and ELISA assay was used to detect the levels of urinary MCP-1 and RANTES. Results Nuclear NF-κB p65 protein and NF-κB p65 mRNA expression levels in peripheral blood mononuclear cells, urinary MCP-1/Cr and RANTES/Cr were all significantly higher in all diabetes groups as compared with NC group. In particular, the increase of nuclear NF-κB p65 protein and NF-κB p65 mRNA expressions, urinary MCP-1/Cr and RANTES/Cr all correlated with the severity of type 2 diabetic nephropathy as indicated by the increase in uACR. Pearson correlation analysis indicated that both urinary MCP-1/Cr and RANTES/Cr were positively correlated with nuclear NF-κB p65 protein or NF-κB p65 mRNA levels. Stepwise multiple regression analysis showed that nuclear NF-κB p65 protein or NF-κB p65 mRNA was an independent variable for urinary MCP-1/Cr, and MCP-1/Cr and RANTES/Cr were two independent variables for uACR. Conclusion Our research demonstrates that nuclear NF-κB p65 protein and mRNA expressions in ex vivo isolated peripheral blood mononuclear cells well correlate with urinary MCP-1/Cr, RANTES/Cr and the severity of type 2 diabetic nephropathy.
Dose-Response Met-RANTES Treatment of Experimental Periodontitis: A Narrow Edge between the Disease Severity Attenuation and Infection Control  [PDF]
Carlos Eduardo Repeke,Samuel Barros Ferreira Jr.,Andreia Espindola Vieira,Elcia Maria Silveira,Mario Julio Avila-Campos,Jo?o Santana da Silva,Carlos Ferreira Santos,Ana Paula Campanelli,Ana Paula Favaro Trombone,Gustavo Pompermaier Garlet
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0022526
Abstract: Chemokines and chemokine receptors have been implicated in the selective migration of leukocyte subsets to periodontal tissues, which consequently influences the disease outcome. Among these chemoattractants, the chemokines CCL3, CCL4 and CCL5 and its receptors, CCR1 and CCR5, have been associated with increased disease severity in mice and humans. Therefore, in this study we investigated the modulation of experimental periodontitis outcome by the treatment with a specific antagonist of CCR1 and 5 receptors, called met-RANTES. C57Bl/6 mice was orally infected with Aggregatibacter actinomycetemcomitans and treated with 0.05, 0.1, 0.5, 1.5 and 5 mg doses of met-RANTES on alternate days, and evaluated by morphometric, cellular, enzymatic and molecular methods. At 0.5 mg up to 5 mg doses, a strong reduction in the alveolar bone loss and inflammatory cell migration were observed. Interestingly, 5 mg dose treatment resulted in the maximum inhibition of inflammatory cell migration, but resulted in a similar inhibition of bone loss when compared with the lower doses, and also resulted in increased bacterial load and CRP response. When 0.5 and 5 mg therapy regimens were compared it was observed that both therapeutic protocols were able to downregulate the levels of pro-inflammatory, Th1-type and osteoclastogenic cytokines, and CD3+ and F4/80+ cells migration to periodontal tissues, but the high dose modulates host response in a more pronounced and unspecific and excessive way, interfering also with the production of antimicrobial mediators such as MPO, iNOS and IgG, and with GR1+ and CD19+ cells migration. Our results demonstrate a thin line between beneficial immunoregulation and impaired host defense during experimental periodontitis, and the determination of the exact equilibrium point is mandatory for the improvement of immune-targeted therapy of periodontitis.
Biomarkers for susceptibility to infection and disease severity in human malaria
Andrade, Bruno Bezerril;Barral-Netto, Manoel;
Memórias do Instituto Oswaldo Cruz , 2011, DOI: 10.1590/S0074-02762011000900009
Abstract: malaria remains a major infectious disease that affects millions of people. once infected with plasmodium parasites, a host can develop a broad range of clinical presentations, which result from complex interactions between factors derived from the host, the parasite and the environment. intense research has focused on the identification of reliable predictors for exposure, susceptibility to infection and the development of severe complications during malaria. although most promising markers are based on the current understanding of malaria immunopathogenesis, some are also focused more broadly on mechanisms of tissue damage and inflammation. taken together, these markers can help optimise therapeutic strategies and reduce disease burden. here, we review the recent advances in the identification of malarial biomarkers, focusing on those related to parasite exposure and disease susceptibility. we also discuss priorities for research in biomarkers for severe malaria.
The diagnostic value of biomarkers of inflammation, angiogenesis and fibrogenesis to assess the severity of urodynamic obstruction in children with congenital megaureter  [PDF]
Morozov D.A.,Krasnova E.I.,Deryugina LA.,Zakharova N.B.
Saratov Journal of Medical Scientific Research , 2012,
Abstract: The aim of the study is to determine the diagnostic value of urine biomarkers of inflammation (interleukin-1p, tumor necrosis factor-a), angiogenesis (vascular endothelial growth factor) and fibrogenesis (monocyte chemoattractant protein-1, matrix metalloproteinase-9) to assess the severity of urodynamic obstruction of the ureter. Materials and Methods — Complex investigation of 47 children with congenital nonrefluxing megaureter at the age from 1 month till 11 years is carried. Results. The correlation between the urine level of IL-1p and main laboratory criteria of inflammation occurred, so IL-1p as an integrative indicator of pyelonephritis activity was appeared. The relation between levels of VEGF and MCP-1 and indicators of renal hemodynamics allowed to consider increased levels of these factors as markers of irreversible nephrosclerosis. The urine level of MMP-9 was strongly correlated with parameters of peristalyic activity of the ureter. The group of children with lower peristalyic activity of the megaureter was significantly different from group with normal ureteral peristalsis by the high urine level of MMP-9. We do not have reliable data about the diagnostic value of determination of the urine level of TNF-a in children with congenital megaureter. Conclusion: The urine level of biological markers investigations are very important for clinical practice for determination of pyelonephritis activity (IL-1p), severity of ischemic deterioration of renal parenchyma (VEGF, MCP-1). Further studies are needed to clarify the pathogenic role of MMP-9 in the regulation of peristalyic activity of the ureter during embryonic and postnatal development in patients with congenital nonrefluxing megaureter.
Genetic polymorphisms of RANTES, IL1-A, MCP-1 and TNF-A genes in patients with prostate cancer
Pablo Sáenz-López, Rafael Carretero, José Cózar, José Romero, Julia Canton, José Vilchez, Miguel Tallada, Federico Garrido, Francisco Ruiz-Cabello
BMC Cancer , 2008, DOI: 10.1186/1471-2407-8-382
Abstract: A case-control study design was used to test the association between prostate cancer risk and the polymorphisms TNF-A-308 A/G (rs 1800629), RANTES-403 G/A (rs 2107538), IL1-A-889 C/T (rs 1800587) and MCP-1 2518 G/A (rs 1024611) in 296 patients diagnosed with prostate cancer and in 311 healthy controls from the same area.Diagnosis of prostate cancer was significantly associated with TNF-A GA + AA genotype (OR, 1.61; 95% CI, 1.09–2.64) and RANTES GA + AA genotype (OR, 1.44; 95% CI, 1.09–2.38). A alleles in TNF-A and RANTES influenced prostate cancer susceptibility and acted independently of each other in these subjects. No epistatic effect was found for the combination of different polymorphisms studied. Finally, no overall association was found between prostate cancer risk and IL1-A or MCP-1 polymorphisms.Our results and previously published findings on genes associated with innate immunity support the hypothesis that polymorphisms in proinflammatory genes may be important in prostate cancer development.Chronic or recurrent inflammation is known to play a causative role in the promotion and progression of many human tumours, including cancers of the liver, oesophagus, stomach, large intestine and urinary bladder [1-3]. Chronic inflammation has also been implicated in the aetiology of prostate cancer [4-7]. Prostate cancer risk has been associated with sexually transmitted infections and prostatitis in some epidemiologic studies [8,9], and its relationship with genetic polymorphisms in inflammatory cytokines has been explored in various case-control studies [10-13]. Chronic inflammation, alongside the intrinsic properties of pre-malignant cells and other determinants, may therefore be one of the driving forces of malignant transformation. Thus, numerous mediators released in dysregulated chronic inflammation have been found to promote cell growth and invasion, induce mutagenesis and increase angiogenicity [1]. By virtue of these properties, inflammatory mediators favo
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