|
|||||
|
|
Systemic expression of inflammatory mediators in patients with chronic rhinosinusitis and nasal polyps with and without Aspirin Exacerbated Respiratory Disease |
|
| Institution: | 1. Upper Airways Research Laboratory, Dept. of Otorhinolaryngology, Ghent University Hospital, Belgium;2. Dept. of Otorhinolaryngology, Head and Neck Surgery, Federal University of São Paulo, São Paulo, Brazil;3. Out-patient Allergy Clinic, Medex, Bielsko-Bia?a, Poland;4. Dept. of Medicine, Jagiellonian University School of Medicine, Cracow, Poland;1. Department of Allergy and Clinical Immunology, Rasool-e-Akram Hospital, Iran University of Medical Sciences (IUMS), Tehran, Iran;2. Research Center for Immunodeficiency, Children''s Medical Center, Tehran University of Medical Sciences (TUMS), Tehran, Iran;3. Department of Internal Medicine, Division of Infectious Diseases and Clinical Immunology, National Research Institute of Tuberculosis and Lung Diseases, Masih-e-Daneshvari Hospital, Shaheed Beheshti University of Medical Sciences (SBUMS), Tehran, Iran;4. Division of Immunology, Boston Children''s Hospital, Harvard Medical School, Boston, MA, USA;5. Department of Infectious Diseases, Ali-Asghar Hospital, IUMS, Tehran, Iran;6. Research Center of Pediatric Infectious Diseases, Rasool-e-Akram Hospital, IUMS, Tehran, Iran;7. Department of Pediatric Oncology, Rasool-e-Akram Hospital, IUMS, Tehran, Iran;8. Digestive Oncology Research Center, Digestive Disease Research Institute, TUMS, Tehran, Iran;9. Department of Immunology, Mofid Children''s Hospital, SBUMS, Tehran, Iran;10. Research Center of Otolaryngology and Head & Neck Surgery, IUMS, Tehran, Iran;11. Department of Allergy and Clinical Immunology, Mofid Hospital, SBUMS, Tehran, Iran;12. Allergy Research Center, Shiraz University of Medical Sciences, Shiraz, Iran;13. Hematology Oncology and Stem Cell Transplantation Research Center, TUMS, Iran;14. Antimicrobial Resistance Research Center, Rasool-e-Akram Hospital, IUMS, Tehran, Iran;15. Molecular Immunology Research Center, and Department of Immunology, School of Medicine, TUMS, Tehran, Iran;p. Universal Scientific Education and Research Network (USERN), Tehran, Iran;1. Department of Otolaryngology–Head and Neck Surgery, Beijing TongRen Hospital, Capital Medical University, Beijing, China;3. Department of Allergy, Beijing TongRen Hospital, Capital Medical University, Beijing, China;2. Beijing Key Laboratory of Nasal Diseases, Beijing Institute of Otolaryngology, Beijing, China;4. Upper Airways Research Laboratory, Department of Oto-Rhino-Laryngology, Ghent University Hospital, Ghent, Belgium;1. Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, United Kingdom;2. Translational Gastroenterology Unit, Nuffield Department of Clinical Medicine, Experimental Medicine Division, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom;3. National Institute for Health Research, Musculoskeletal Biomedical Research Unit, Nuffield Orthopaedic Centre, University of Oxford, Oxford, United Kingdom;4. Merck Research Laboratories, Palo Alto, Calif;5. Merck Research Laboratories, Boston, Mass;6. Lycera Corp, Ann Arbor, Mich;7. Department of Chemistry, University of Michigan, Ann Arbor, Mich;8. Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, United Kingdom;1. Stroke Center, Neuroscience Center, Department of Neurology, the First Hospital of Jilin University, Chang Chun, Jilin 130021, China;2. Center for Neurovascular Ultrasound, Department of Neurology, the First Hospital of Jilin University, Chang Chun, Jilin 130021, China;3. Clinical Trail and Research Center for Stroke, Department of Neurology, the First Hospital of Jilin University, Chang Chun, Jilin 130021, China;4. Division of Clinical Research, the First Hospital of Jilin University, Chang Chun, Jilin 130021, China |
| Abstract: | BackgroundSystemic reactions are related to the pathogenesis of Aspirin Exacerbated Respiratory Disease (AERD). With this work we wanted to study the changes in the systemic levels of inflammatory mediators in both baseline and after oral aspirin challenge in patients with and without AERD.MethodsPatients with nasal polyposis and asthma with AERD (n = 20) and without (n = 18) were orally challenged with aspirin in a single-blind placebo controlled study. Serum samples and urine were collected before and 6 h after placebo and aspirin oral challenges. Serum levels of inflammatory mediators were assayed by using the Luminex technology and ELISA. The concentrations of 9-alpha, 11-beta prostaglandin F2, and leukotriene E4 (uLTE4) were measured in urine samples by ELISA. The expression of T-cell surface markers was analyzed in peripheral blood mononuclear cells isolated before and after the challenges.ResultsAERD patients showed significantly higher baseline levels of s-IL-5R-alpha, uLTE4 and percentage of CD4+CD25+CD127pos and CD4+CD45RA?CD45RO+ but decreased levels of TGF-β1 and number of CD4+CD25+CD127neg cells. Aspirin challenge induced the release of uLTE4, IL-6 and increased the number of CD4+CD45RA?CD45RO+ memory T-cells only in AERD patients but failed to reduce the levels of sCD40L as observed in non-AERD subjects. Further, IL-8 and sIL-5R-alpha levels directly correlated with the PD20ASA and the effects of aspirin on IL-6 and number of memory T-cells was more pronounced in subjects showing more strong reaction (bronchial and nasal).ConclusionsAERD patients have a differential baseline inflammatory pattern that supports the role inflammation as underlying mechanism of the disease. Systemic response to oral aspirin challenge was related to an increase in serum IL-6 and the number of circulating memory T-cells in AERD patients. |
| Keywords: | Aspirin Exacerbated Respiratory Disease Interleukin 6 Memory T-cells Oral aspirin challenge Systemic reaction after aspirin challenge Interleukin 8 IL-5 receptor alpha AERD"} {"#name":"keyword" "$":{"id":"k0060"} "$$":[{"#name":"text" "_":"Aspirin Exacerbated Respiratory Disease CD127"} {"#name":"keyword" "$":{"id":"k0070"} "$$":[{"#name":"text" "_":"Interleukin-7 receptor Cys-LTs"} {"#name":"keyword" "$":{"id":"k0080"} "$$":[{"#name":"text" "_":"cysteinyl leukotrienes ENA78/CXCL5"} {"#name":"keyword" "$":{"id":"k0090"} "$$":[{"#name":"text" "_":"C-X-C motif chemokine 5 or epithelial-derived neutrophil-activating peptide 78 Eotaxin/CCL11"} {"#name":"keyword" "$":{"id":"k0100"} "$$":[{"#name":"text" "_":"chemokine (C-C motif) ligand 11 or Eotaxin forced expiratory volume in one second IgE"} {"#name":"keyword" "$":{"id":"k0120"} "$$":[{"#name":"text" "_":"Immunoglobulin E IP10/CXCL10"} {"#name":"keyword" "$":{"id":"k0130"} "$$":[{"#name":"text" "_":"C-X-C motif chemokine 10 or Interferon gamma-induced protein 10 (IP10) ITAC/CXCCL11"} {"#name":"keyword" "$":{"id":"k0140"} "$$":[{"#name":"text" "_":"C-X-C motif chemokine 11 or Interferon-inducible T-cell alpha chemoattractant MCP1/CCL2"} {"#name":"keyword" "$":{"id":"k0170"} "$$":[{"#name":"text" "_":"chemokine (C-C motif) ligand 2 or monocyte chemotactic protein-1 MIP-1α/CCL3"} {"#name":"keyword" "$":{"id":"k0180"} "$$":[{"#name":"text" "_":"chemokine (C-C motif) ligand 3 or macrophage inflammatory protein-1 alpha MIP-1β/CCL4"} {"#name":"keyword" "$":{"id":"k0190"} "$$":[{"#name":"text" "_":"chemokine (C-C motif) ligand 4 or macrophage inflammatory protein-1beta S90k/MacBP"} {"#name":"keyword" "$":{"id":"k0210"} "$$":[{"#name":"text" "_":"soluble mac-2 binding protein sCD40L/sCD154"} {"#name":"keyword" "$":{"id":"k0220"} "$$":[{"#name":"text" "_":"soluble CD40 ligand s-IL-5Rα"} {"#name":"keyword" "$":{"id":"k0230"} "$$":[{"#name":"text" "_":"soluble Interleukin-5 receptor alpha subunit tumor growth factor beta 1 |
| 本文献已被 ScienceDirect 等数据库收录！ | |