Recruitment of Eosinophils in Vivo Enhances CCL11/Eotaxin
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CXCL4/Platelet Factor 4 Is an Agonist of CCR1 and Drives Human Monocyte Migration
This is a repository copy of CXCL4/Platelet Factor 4 is an agonist of CCR1 and drives human monocyte migration. White Rose Research Online URL for this paper: https://eprints.whiterose.ac.uk/132464/ Version: Published Version Article: Fox, James Martin orcid.org/0000-0002-2473-7029, Kausar, Fahima, Day, Amy et al. (7 more authors) (2018) CXCL4/Platelet Factor 4 is an agonist of CCR1 and drives human monocyte migration. Scientific Reports. 9466. ISSN 2045-2322 Reuse This article is distributed under the terms of the Creative Commons Attribution (CC BY) licence. This licence allows you to distribute, remix, tweak, and build upon the work, even commercially, as long as you credit the authors for the original work. More information and the full terms of the licence here: https://creativecommons.org/licenses/ Takedown If you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing [email protected] including the URL of the record and the reason for the withdrawal request. [email protected] https://eprints.whiterose.ac.uk/ www.nature.com/scientificreports OPEN CXCL4/Platelet Factor 4 is an agonist of CCR1 and drives human monocyte migration Received: 10 March 2016 James M. Fox 1,3, Fahima Kausar1, Amy Day1, Michael Osborne1, Khansa Hussain1, Accepted: 5 June 2018 Anja Mueller1,4, Jessica Lin1, Tomoko Tsuchiya 2, Shiro Kanegasaki2 & James E. Pease1 Published: xx xx xxxx Activated platelets release micromolar concentrations of the chemokine CXCL4/Platelet Factor-4. Deposition of CXCL4 onto the vascular endothelium is involved in atherosclerosis, facilitating monocyte arrest and recruitment by an as yet, unidentified receptor. -
Systemic Immune Activity Predicts Overall Survival in Treatment-Naïve Patients with Metastatic Pancreatic Cancer Matthew R
Published OnlineFirst December 30, 2015; DOI: 10.1158/1078-0432.CCR-15-1732 Biology of Human Tumors Clinical Cancer Research Systemic Immune Activity Predicts Overall Survival in Treatment-Naïve Patients with Metastatic Pancreatic Cancer Matthew R. Farren1, Thomas A. Mace1, Susan Geyer2, Sameh Mikhail1, Christina Wu1, Kristen Ciombor1, Sanaa Tahiri1, Daniel Ahn1, Anne M. Noonan1, Miguel Villalona-Calero1, Tanios Bekaii-Saab1, and Gregory B. Lesinski1 Abstract Purpose: Pancreatic ductal adenocarcinoma (PDAC) is an respectively), whereas higher levels of the monocyte chemoat- aggressive cancer with a 5-year survival rate <7% and is ultimately tractant MCP-1 were associated with significantly longer OS refractory to most treatments. To date, an assessment of immu- (P ¼ 0.045; HR ¼ 0.69). Patients with a greater proportion þ nologic factors relevant to disease has not been comprehensively of antigen-experienced T cells (CD45RO )hadlongerOS(CD4 performed for treatment-na€ve patients. We hypothesized that P ¼ 0.032; CD8 P ¼ 0.036; HR ¼ 0.36 and 0.61, respectively). systemic immunologic biomarkers could predict overall survival Although greater expression of the T-cell checkpoint molecule þ (OS) in treatment-na€ve PDAC patients. CTLA-4 on CD8 T cells was associated with significantly Experimental Design: Peripheral blood was collected from 73 shorter OS (P ¼ 0.020; HR ¼ 1.53), the TIM3 molecule had þ patients presenting with previously untreated metastatic PDAC. a positive association with survival when expressed on CD4 Extensive immunologic profiling was conducted to assess rela- T cells (P ¼ 0.046; HR ¼ 0.62). tionships between OS and the level of soluble plasma biomarkers Conclusions: These data support the hypothesis that base- or detailed immune cell phenotypes as measured by flow line immune status predicts PDAC disease course and over- cytometry. -
Inflammation-Related Plasma and CSF Biomarkers for Multiple Sclerosis
Inflammation-related plasma and CSF biomarkers for multiple sclerosis Jesse Huanga, Mohsen Khademia, Lars Fuggerb,c, Örjan Lindhed, Lenka Novakovae, Markus Axelssone, Clas Malmeströme, Clara Constantinescue, Jan Lyckee, Fredrik Piehla, Tomas Olssona,1, and Ingrid Kockuma,1,2 aNeuroimmunology Unit, Center of Molecular Medicine, Department of Clinical Neuroscience, Karolinska University Hospital, Karolinska Institutet, SE-171 77 Stockholm, Sweden; bOxford Centre for Neuroinflammation, Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DU, United Kingdom; cNuffield Department of Clinical Neurosciences, Division of Clinical Neurology, University of Oxford, Oxford OX3 9DU, United Kingdom; dOlink Proteomics AB, SE-751 83 Uppsala, Sweden; and eDepartment of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, SE-413 45 Gothenburg, Sweden Edited by Tak W. Mak, University of Toronto, Toronto, ON, Canada, and approved April 10, 2020 (received for review July 26, 2019) Effective biomarkers for multiple sclerosis diagnosis, assessment bands are currently used to support diagnosis (10). In addition, of prognosis, and treatment responses, in particular those measur- there is a restricted set of CSF markers, including chemokine able in blood, are largely lacking. We have investigated a broad (C-X-C motif) ligand 13 (CXCL13), matrix metallopeptidase-9 set of protein biomarkers in cerebrospinal fluid (CSF) and plasma (MMP-9), and osteopontin (OPN), which have been associated using a highly sensitive proteomic immunoassay. Cases from two with inflammation, along with neurofilament light chains independent cohorts were compared with healthy controls and (NfL), a measure of neuron/axon damage (10–13). -
Changes in Multiple Cytokine Concentrations in the Aqueous
BJO Online First, published on August 1, 2017 as 10.1136/bjophthalmol-2017-310284 Clinical science Br J Ophthalmol: first published as 10.1136/bjophthalmol-2017-310284 on 1 August 2017. Downloaded from Changes in multiple cytokine concentrations in the aqueous humour of neovascular age-related macular degeneration after 2 months of ranibizumab therapy Shinichi Sakamoto,1 Hidenori Takahashi,1,2,3 Xue Tan,2 Yuji Inoue,1,2 Yoko Nomura,2 Yusuke Arai,1 Yujiro Fujino,3 Hidetoshi Kawashima,1 Yasuo Yanagi4,5,6 ► Additional material is ABSTRACT Previous investigations have reported that eyes published online only. To view Purpose To determine changes in multiple cytokine with AMD have elevated concentrations of many please visit the journal online (http:// dx. doi. org/ 10. 1136/ concentrations in the anterior chamber during the cytokines, such as interferon-γ-induced protein bjophthalmol- 2017- 310284). induction phase of ranibizumab treatment in patients 10 (IP-10), monocyte chemoattractant protein 1 with neovascular age-related macular degeneration (MCP-1), C reactive protein, intercellular adhesion 1 Department of Ophthalmology, (AMD). molecule 1 and vascular cell adhesion molecule Jichi Medical University, Methods This prospective study included 48 treatment- 1.2 3 These cytokines also modify the activity of Shimotsuke, Tochigi, Japan 2Department of Ophthalmology, naïve neovascular AMD eyes of 48 patients who received choroidal neovascularisation (CNV) in neovascular Graduate School of Medicine, three consecutive monthly injections of ranibizumab at AMD. MCP-1, the best-studied cytokine in exuda- The University of Tokyo, Bunkyo- the Japan Community Health Care Organization Tokyo tive AMD, recruits inflammatory monocytes to ku, Tokyo, Japan Shinjuku Medical Center between November 2010 and inflamed tissue. -
Functional Expression of CCL8 and Its Interaction with Chemokine Receptor CCR3 Baosheng Ge*, Jiqiang Li, Zhijin Wei, Tingting Sun, Yanzhuo Song and Naseer Ullah Khan
Ge et al. BMC Immunology (2017) 18:54 DOI 10.1186/s12865-017-0237-5 RESEARCH ARTICLE Open Access Functional expression of CCL8 and its interaction with chemokine receptor CCR3 Baosheng Ge*, Jiqiang Li, Zhijin Wei, Tingting Sun, Yanzhuo Song and Naseer Ullah Khan Abstract Background: Chemokines and their cognate receptors play important role in the control of leukocyte chemotaxis, HIV entry and other inflammatory diseases. Developing an effcient method to investigate the functional expression of chemokines and its interactions with specific receptors will be helpful to asses the structural and functional characteristics as well as the design of new approach to therapeutic intervention. Results: By making systematic optimization study of expression conditions, soluble and functional production of chemokine C-C motif ligand 8 (CCL8) in Escherichia coli (E. coli) has been achieved with approx. 1.5 mg protein/l culture. Quartz crystal microbalance (QCM) analysis exhibited that the purified CCL8 could bind with −7 C-C chemokine receptor type 3 (CCR3) with dissociation equilibrium constant (KD)as1.2×10 Minvitro. Obvious internalization of CCR3 in vivo could be detected in 1 h when exposed to 100 nM of CCL8. Compared with chemokine C-C motif ligand 11 (CCL11) and chemokine C-C motif ligand 24 (CCL24), a weaker chemotactic effect of CCR3 expressing cells was observed when induced by CCL8 with same concentration. Conclusion: This study delivers a simple and applicable way to produce functional chemokines in E. coli. The results clearly confirms that CCL8 can interact with chemokine receptor CCR3, therefore, it is promising area to develop drugs for the treatment of related diseases. -
Inflammation Stress-Induced Neutrophilic Lung CCL7 And
CCL7 and CXCL10 Orchestrate Oxidative Stress-Induced Neutrophilic Lung Inflammation1 Lidia Michalec,2* Barun K. Choudhury,2* Edward Postlethwait,† James S. Wild,* Rafeul Alam,* Michael Lett-Brown,* and Sanjiv Sur3* Oxidative stress from ozone (O3) exposure augments airway neutrophil recruitment and chemokine production. We and others have shown that severe and sudden asthma is associated with airway neutrophilia, and that O3 oxidative stress is likely to augment neutrophilic airway inflammation in severe asthma. However, very little is known about chemokines that orchestrate oxidative stress-induced neutrophilic airway inflammation in vivo. To identify these chemokines, three groups of BALB/c mice were exposed to sham air, 0.2 ppm O3, or 0.8 ppm O3 for 6 h. Compared with sham air, 0.8 ppm O3, but not 0.2 ppm O3, induced pronounced neutrophilic airway inflammation that peaked at 18 h postexposure. The 0.8 ppm O3 up-regulated lung mRNA of CXCL1,2,3 (mouse growth-related oncogene-␣ and macrophage-inflammatory protein-2), CXCL10 (IFN-␥-inducible protein-10), CCL3 (macrophage-inflammatory protein-1␣), CCL7 (monocyte chemoattractant protein-3), and CCL11 (eotaxin) at 0 h postexposure, and expression of CXCL10, CCL3, and CCL7 mRNA was sustained 18 h postexposure. O3 increased lung protein levels of CXCL10, CCL7, and CCR3 (CCL7R). The airway epithelium was identified as a source of CCL7. The role of up-regulated chemokines was determined by administering control IgG or IgG Abs against six murine chemokines before O3 exposure. As expected, anti-mouse growth-related oncogene-␣ inhibited neutrophil recruitment. Surprisingly, Abs to CCL7 and CXCL10 also decreased neutrophil recruitment by 63 and 72%, respectively. -
Mouse CCL11/Eotaxin Antibody Antigen Affinity-Purified Polyclonal Goat Igg Catalog Number: AF-420-NA
Mouse CCL11/Eotaxin Antibody Antigen Affinity-purified Polyclonal Goat IgG Catalog Number: AF-420-NA DESCRIPTION Species Reactivity Mouse Specificity Detects mouse CCL11/Eotaxin in ELISAs and Western blots. In Western blots, approximately 50% crossreactivity with recombinant human CCL11/Eotaxin and recombinant mouse (rm) MARC is observed, and less than 2% crossreactivity with rmJE is observed. Source Polyclonal Goat IgG Purification Antigen Affinitypurified Immunogen E. coliderived recombinant mouse CCL11/Eotaxin His24Pro97 Accession # P48298 Endotoxin Level <0.10 EU per 1 μg of the antibody by the LAL method. Formulation Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. See Certificate of Analysis for details. *Small pack size (SP) is supplied as a 0.2 μm filtered solution in PBS. APPLICATIONS Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website. Recommended Sample Concentration Western Blot 0.1 µg/mL Recombinant Mouse CCL11/Eotaxin (Catalog # 420ME) Immunohistochemistry 515 µg/mL Perfusion fixed frozen sections of mouse intestine Mouse CCL11/Eotaxin Sandwich Immunoassay Reagent ELISA Capture 0.20.8 µg/mL Mouse CCL11/Eotaxin Antibody (Catalog # AF420NA) ELISA Detection 0.10.4 µg/mL Mouse CCL11/Eotaxin Biotinylated Antibody (Catalog # BAF420) Standard Recombinant Mouse CCL11/Eotaxin (Catalog # 420ME) Neutralization Measured by its ability to neutralize CCL11/Eotaxininduced chemotaxis in the BaF3 mouse pro-B cell line transfected with mouse CCR3. The Neutralization Dose (ND50) is typically 0.10.5 µg/mL in the presence of 10 ng/mL Recombinant Mouse CCL11/Eotaxin. -
CCL-11 Or Eotaxin-1: an Immune Marker for Ageing and Accelerated Ageing in Neuro-Psychiatric Disorders
pharmaceuticals Review CCL-11 or Eotaxin-1: An Immune Marker for Ageing and Accelerated Ageing in Neuro-Psychiatric Disorders Mariya Ivanovska 1,2,3,* , Zakee Abdi 4, Marianna Murdjeva 1,2,3, Danielle Macedo 5,6 , Annabel Maes 7 and Michael Maes 8,9,10 1 Department of Microbiology and Immunology, Faculty of Pharmacy, Research Institute, Medical University-Plovdiv, 4002 Plovdiv, Bulgaria; [email protected] 2 Laboratory of Clinical Immunology, University Hospital “St. George”-Plovdiv, 4002 Plovdiv, Bulgaria 3 Division of Immunological Assessment of Post-Traumatic Stress Disorder, TCEMED, 4002 Plovdiv, Bulgaria 4 Medical Faculty, Medical University-Plovdiv, 4002 Plovdiv, sBulgaria; [email protected] 5 Neuropsychopharmacology Laboratory, Drug Research, and Development Center, Faculty of Medicine, Universidade Federal do Ceará, Fortaleza 60455-760, Brazil; [email protected] 6 National Institute for Translational Medicine (INCT-TM, CNPq), Ribeirão Preto 14000-000, Brazil 7 Janssen Pharmaceutica NV, 2340 Beerse, Belgium; [email protected] 8 Department of Psychiatry, Chulalongkorn University, Bangkok 10140, Thailand; [email protected] 9 TCEMED, Medical University-Plovdiv, 4002 Plovdiv, Bulgaria 10 IMPACT Strategic Research Center, Deakin University, Geelong 3220, Australia * Correspondence: [email protected]; Tel.: +359-897312847 Received: 7 August 2020; Accepted: 31 August 2020; Published: 2 September 2020 Abstract: Background: CCL-11 (eotaxin) is a chemokine with an important role in allergic conditions. Recent evidence indicates that CCL-11 plays a role in brain disorders as well. This paper reviews the associations between CCL-11 and aging, neurodegenerative, neuroinflammatory and neuropsychiatric disorders. Methods: Electronic databases were searched for original articles examining CCL-11 in neuropsychiatric disorders. -
AXIN1 in Plasma Or Serum Is a Potential New Biomarker for Endometriosis
Supplementary Materials AXIN1 in Plasma or Serum Is a Potential New Biomarker for Endometriosis Table S1. Inflammation-related proteins measured by Proximity Extension Assay. Protein Abbreviation Interleukin-8 IL-8 Vascular endothelial growth factor A VEGF-A Brain-derived neurotrophic factor BDNF Monocyte chemotactic protein 3 MCP-3 Glial cell line-derived neurotrophic factor hGDNF CUB domain-containing protein 1 CDCP1 Natural killer cell receptor 2B4 CD244 Interleukin-7 IL-7 Osteoprotegerin OPG Latency-associated peptide transforming growth factor beta 1 LAP TGF-beta-1 Urokinase-type plasminogen activator uPA Interleukin-6 IL-6 Interleukin-17C IL-17C Monocyte chemotactic protein 1 MCP-1 Interleukin-17A IL-17A C-X-C motif chemokine 11 CXCL11 Axin-1 AXIN1 TNF-related apoptosis-inducing ligand TRAIL Interleukin-20 receptor subunit alpha IL-20RA C-X-C motif chemokine 9 CXCL9 Cystatin D CST5 Interleukin-2 receptor subunit beta IL-2RB Interleukin-1 alpha IL-1 alpha Oncostatin-M OSM Interleukin-2 IL-2 C-X-C motif chemokine 1 CXCL1 Thymic stromal lymphopoietin TSLP C-C motif chemokine 4 CCL4 T cell surface glycoprotein CD6 isoform CD6 Stem cell factor SCF Interleukin-18 IL-18 Signaling lymphocytic activation molecule SLAMF1 Transforming growth factor alpha TGF-alpha Monocyte chemotactic protein 4 MCP-4 Eotaxin-1 CCL11 Tumor necrosis factor ligand superfamily member 14 TNFSF14 Fibroblast growth factor 23 FGF-23 Interleukin-10 receptor subunit alpha IL-10RA Fibroblast growth factor 5 FGF-5 Matrix metalloproteinase-1 MMP-1 Leukemia inhibitory factor -
The Role of Chemokines and Chemokine Receptors in Eosinophil Activation During Inflammatory Allergic Reactions
ChemokinesBrazilian Journal and ofeosinophil Medical andactivation Biological Research (2003) 36: 1455-1463 1455 ISSN 0100-879X Review The role of chemokines and chemokine receptors in eosinophil activation during inflammatory allergic reactions S.H.P. Oliveira1 1Departamento de Ciências Básicas, Faculdade de Odontologia de Araçatuba, and N.W. Lukacs2 Universidade Estadual Paulista, Araçatuba, SP, Brasil 2Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA Abstract Correspondence Chemokines are important chemotactic cytokines that play a funda- Key words S.H.P. Oliveira mental role in the trafficking of leukocytes to sites of inflammation. • Chemokines Departamento de Ciências Básicas They are also potent cell-activating factors, inducing cytokine and • Chemokine receptors Faculdade de Odontologia de histamine release and free radical production, a fact that makes them • Allergic inflammation Araçatuba particularly important in the pathogenesis of allergic inflammation. • Eosinophil Rua José Bonifácio, 1193 16015-050 Araçatuba, SP The action of chemokines is regulated at the level of agonist produc- Brasil tion and processing as well as at the level of receptor expression and Fax: +55-18-624-4890 coupling. Therefore, an analysis of the ligands must necessarily E-mail: [email protected] consider receptors. Eosinophils are target cells involved in the allergic inflammatory response since they are able to release a wide variety of Publication supported by FAPESP. mediators including CC and CXC chemokines and express their receptors. These mediators could damage the airway epithelial cells and might be important to stimulate other cells inducing an amplifica- Received May 8, 2003 tion of the allergic response. This review focuses on recently emerging Accepted July 4, 2003 data pertaining to the importance of chemokines and chemokine receptors in promoting eosinophil activation and migration during the allergic inflammatory process. -
Functioning As a Death Receptor for B Cells CCR3 Expression Induced By
CCR3 Expression Induced by IL-2 and IL-4 Functioning as a Death Receptor for B Cells Tan Jinquan, Henrik H. Jacobi, Chen Jing, Anders Millner, Eva Sten, Lars Hviid, Liu Anting, Lars P. Ryder, Christian This information is current as Glue, Per S. Skov, Elizabeth Jarman, Kasper Lamberth, of September 28, 2021. Hans-Jørgen Malling and Lars K. Poulsen J Immunol 2003; 171:1722-1731; ; doi: 10.4049/jimmunol.171.4.1722 http://www.jimmunol.org/content/171/4/1722 Downloaded from References This article cites 78 articles, 43 of which you can access for free at: http://www.jimmunol.org/content/171/4/1722.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 28, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2003 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology CCR3 Expression Induced by IL-2 and IL-4 Functioning as a Death Receptor for B Cells1 Tan Jinquan,2*† Henrik H. -
A Pathogenic and Clonally Expanded B Cell Transcriptome in Active Multiple Sclerosis
A pathogenic and clonally expanded B cell transcriptome in active multiple sclerosis Akshaya Ramesha,b,1, Ryan D. Schuberta,b,1, Ariele L. Greenfielda,b,2, Ravi Dandekara,b,2, Rita Loudermilka,b, Joseph J. Sabatino Jra,b, Matthew T. Koelzerc, Edwina B. Trana,b, Kanishka Koshala,b, Kicheol Kima,b, Anne-Katrin Pröbstela,b, Debarko Banerjia,b, University of California, San Francisco MS-EPIC Team3, Chu-Yueh Guoa,b, Ari J. Greena,b, Riley M. Bovea,b, Joseph L. DeRisid,e, Jeffrey M. Gelfanda,b, Bruce A. C. Creea,b, Scott S. Zamvila,b,f, Sergio E. Baranzinia,b, Stephen L. Hausera,b, and Michael R. Wilsona,b,4 aWeill Institute for Neurosciences, University of California, San Francisco, CA 94158; bDepartment of Neurology, University of California, San Francisco, CA 94158; cDepartment of Mathematics, University of California, Los Angeles, CA 90095; dChan Zuckerberg Biohub, San Francisco, CA 94158; eDepartment of Biochemistry and Biophysics, University of California, San Francisco, CA 94158; and fProgram in Immunology, University of California, San Francisco, CA 94143 Edited by Lawrence Steinman, Stanford University School of Medicine, Stanford, CA, and approved August 3, 2020 (received for review May 6, 2020) Central nervous system B cells have several potential roles in may not only shed light on disease pathogenesis but also po- multiple sclerosis (MS): secretors of proinflammatory cytokines tentially provide more disease-specific and safer therapeutic and chemokines, presenters of autoantigens to T cells, producers targets to guide development of the next-generation of B cell of pathogenic antibodies, and reservoirs for viruses that trigger therapeutics. demyelination.