Cezmi Akdis

Last updated

Cezmi Akdis is a medical researcher in the field of immunology. He is director of the Swiss Institute of Allergy and Asthma Research (SIAF) in Davos, Switzerland and the editor in chief of the journal Allergy .

Contents

He has been a professor in University of Zürich Medical Faculty since 2006, and one of the directors of the Christine Kühne-Center for Allergy Research and Education in Davos, Switzerland.

Education

Akdis Received his medical degree from Uludag University Medical Faculty, Bursa, Turkey in 1985. He has specialized in infectious disease and clinical microbiology 1991 and in immunology at Uludag University in 1994, and further was named a Venia Legendi (Habilitation) at the University of Zürich 2001. [1]

Publications

Akdis has published more than 650 articles. [2] His current h-index is 140. [2] and he has received over 80,000 [2] citations. He has also been selected to the ISI Web of Science and has received the Thomson Reuters (Clarivate) Highly Cited Researcher in the field of immunology in 2017, 2018, 2019, 2020 and 2021. [3]

Academic history

Organizations

Contributions

Honors

Related Research Articles

<span class="mw-page-title-main">Rhinitis</span> Irritation and inflammation of the mucous membrane inside the nose

Rhinitis, also known as coryza, is irritation and inflammation of the mucous membrane inside the nose. Common symptoms are a stuffy nose, runny nose, sneezing, and post-nasal drip.

<span class="mw-page-title-main">Omalizumab</span> Monoclonal antibody medication

Omalizumab, sold under the brand name Xolair, is an injectable medication to treat severe persistent allergic forms of asthma, nasal polyps, urticaria (hives), and immunoglobulin E-mediated food allergy.

<span class="mw-page-title-main">Aspirin-exacerbated respiratory disease</span> Chronic inflammatory disease affecting the sinuses and lungs

Aspirin-exacerbated respiratory disease (AERD), also called NSAID-exacerbated respiratory disease (N-ERD) or historically aspirin-induced asthma and Samter's Triad, is a long-term disease defined by three simultaneous symptoms: asthma, chronic rhinosinusitis with nasal polyps, and intolerance of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs). Compared to aspirin tolerant patients, AERD patients' asthma and nasal polyps are generally more severe. Reduction or loss of the ability to smell is extremely common, occurring in more than 90% of people with the disease. AERD most commonly begins in early- to mid-adulthood and has no known cure. While NSAID intolerance is a defining feature of AERD, avoidance of NSAIDs does not affect the onset, development or perennial nature of the disease.

Acute severe asthma, also known as status asthmaticus, is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators (inhalers) and corticosteroids. Asthma is caused by multiple genes, some having protective effect, with each gene having its own tendency to be influenced by the environment although a genetic link leading to acute severe asthma is still unknown. Symptoms include chest tightness, rapidly progressive dyspnea, dry cough, use of accessory respiratory muscles, fast and/or labored breathing, and extreme wheezing. It is a life-threatening episode of airway obstruction and is considered a medical emergency. Complications include cardiac and/or respiratory arrest. The increasing prevalence of atopy and asthma remains unexplained but may be due to infection with respiratory viruses.

<span class="mw-page-title-main">Filaggrin</span>

Filaggrin is a filament-associated protein that binds to keratin fibers in epithelial cells. Ten to twelve filaggrin units are post-translationally hydrolyzed from a large profilaggrin precursor protein during terminal differentiation of epidermal cells. In humans, profilaggrin is encoded by the FLG gene, which is part of the S100 fused-type protein (SFTP) family within the epidermal differentiation complex on chromosome 1q21. In cetaceans and sirenians, the FLG family has lost its function, with the curious exception of manatees in the latter clade: manatees still retain some functional FLG genes.

<span class="mw-page-title-main">Milk allergy</span> Type of food allergy caused by milk

Milk allergy is an adverse immune reaction to one or more proteins in cow's milk. Symptoms may take hours to days to manifest, with symptoms including atopic dermatitis, inflammation of the esophagus, enteropathy involving the small intestine and proctocolitis involving the rectum and colon. However, rapid anaphylaxis is possible, a potentially life-threatening condition that requires treatment with epinephrine, among other measures.

<span class="mw-page-title-main">Eosinopenia</span> Medical condition

Eosinopenia is a condition where the number of eosinophils, a type of white blood cell, in circulating blood is lower than normal. Eosinophils are a type of granulocyte and consequently from the same cellular lineage as neutrophils, basophils, and mast cells. Along with the other granulocytes, eosinophils are part of the innate immune system and contribute to the defense of the body from pathogens. The most widely understood function of eosinophils is in association with allergy and parasitic disease processes, though their functions in other pathologies are the subject of ongoing research. The opposite phenomenon, in which the number of eosinophils present in the blood is higher than normal, is known as eosinophilia.

<span class="mw-page-title-main">Eosinophil cationic protein</span> Mammalian protein found in Homo sapiens

Eosinophil cationic protein (ECP) also known as ribonuclease 3 is a basic protein located in the eosinophil primary matrix. In humans, the eosinophil cationic protein is encoded by the RNASE3 gene.

<span class="mw-page-title-main">Cysteinyl leukotriene receptor 1</span> Protein-coding gene in humans

Cysteinyl leukotriene receptor 1, also termed CYSLTR1, is a receptor for cysteinyl leukotrienes (LT). CYSLTR1, by binding these cysteinyl LTs contributes to mediating various allergic and hypersensitivity reactions in humans as well as models of the reactions in other animals.

<span class="mw-page-title-main">Thymic stromal lymphopoietin</span> Cytokine, alarmin, and growth factor.

Thymic stromal lymphopoietin (TSLP) is an interleukin (IL)-2-like cytokine, alarmin, and growth factor involved in numerous physiological and pathological processes, primarily those of the immune system. It shares a common ancestor with IL-7.

<span class="mw-page-title-main">Intestinal epithelium</span> Single-cell layer lining the intestines

The intestinal epithelium is the single cell layer that forms the luminal surface (lining) of both the small and large intestine (colon) of the gastrointestinal tract. Composed of simple columnar epithelium its main functions are absorption, and secretion. Useful substances are absorbed into the body, and the entry of harmful substances is restricted. Secretions include mucins, and peptides.

<span class="mw-page-title-main">Dupilumab</span> Drug used to treat allergic diseases

Dupilumab, sold under the brand name Dupixent, is a monoclonal antibody blocking interleukin 4 and interleukin 13, used for allergic diseases such as atopic dermatitis (eczema), asthma and nasal polyps which result in chronic sinusitis. It is also used for the treatment of eosinophilic esophagitis and prurigo nodularis.

<span class="mw-page-title-main">Irwin McLean</span> Emeritus Professor of Genetic Medicine

(William Henry) Irwin McLean FRS FRSE FMedSci is Emeritus Professor of Genetic Medicine, at the School of Life Sciences, University of Dundee.

<span class="mw-page-title-main">Kari Nadeau</span> American Physician and scientist

Kari C. Nadeau is the Chair of the Department of Environmental Health at Harvard School of Public Health and John Rock Professor of Climate and Population Studies. She is adjunct professor at Stanford University in the Department of Pediatrics and the co-chair of the Medical Societies Consortium for Climate Change and Health. She practices Allergy, Asthma, Immunology in children and adults. She has published over 400+ papers, many in the field of climate change and health. Her team focuses on quantifying health outcomes of solutions as they pertain climate change mitigation and adaptation at the local, regional, country, and global levels. Dr. Nadeau, with a team of individuals and patients and families, has been able to help major progress and impact in the clinical fields of immunology, infection, asthma, and allergy. Dr. Nadeau is a member of the National Academy of Medicine and the U.S. EPA Children’s Health Protection Committee.

NSAIDhypersensitivity reactions encompass a broad range of allergic or allergic-like symptoms that occur within minutes to hours after ingesting aspirin or other NSAID nonsteroidal anti-inflammatory drugs. Hypersensitivity drug reactions differ from drug toxicity reactions in that drug toxicity reactions result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual. Hypersensitivity reactions are idiosyncratic reactions to a drug. Although the term NSAID was introduced to signal a comparatively low risk of adverse effects, NSAIDs do evoke a broad range of hypersensitivity syndromes. These syndromes have recently been classified by the European Academy of Allergy and Clinical Immunology Task Force on NSAIDs Hypersensitivity.

<span class="mw-page-title-main">Intestinal mucosal barrier</span>

The intestinal mucosal barrier, also referred to as intestinal barrier, refers to the property of the intestinal mucosa that ensures adequate containment of undesirable luminal contents within the intestine while preserving the ability to absorb nutrients. The separation it provides between the body and the gut prevents the uncontrolled translocation of luminal contents into the body proper. Its role in protecting the mucosal tissues and circulatory system from exposure to pro-inflammatory molecules, such as microorganisms, toxins, and antigens is vital for the maintenance of health and well-being. Intestinal mucosal barrier dysfunction has been implicated in numerous health conditions such as: food allergies, microbial infections, irritable bowel syndrome, inflammatory bowel disease, celiac disease, metabolic syndrome, non-alcoholic fatty liver disease, diabetes, and septic shock.

<span class="mw-page-title-main">Cadherin related family member 3</span> Protein-coding gene in the species Homo sapiens

Cadherin related family member 3 (CDHR3), also known as CDH28 or its abbreviation CDHR3, is a protein that in humans is encoded by the CDHR3 gene. The protein is predominately expressed in respiratory epithelium and the first notion of its clinical implications was from the discovery that genetic variation of CDHR3 is strongly associated to early severe asthma exacerbations in children. Subsequent studies have suggested that CDHR3 is a receptor for a subtype of rhinovirus.

Donna Elizabeth Davies is a British biochemist and professor of respiratory cell and molecular biology at the University of Southampton. In 2003, Davies was the co-founder of Synairgen, an interferon-beta drug designed to treat patients with asthma and chronic obstructive pulmonary disease.

Type 2 inflammation is a pattern of immune response. Its physiological function is to defend the body against helminths, but a dysregulation of the type 2 inflammatory response has been implicated in the pathophysiology of several diseases.

Asthma phenotyping and endotyping is a novel approach to asthma classification inspired by precision medicine. It seeks to separate the clinical presentations or clusters of signs and symptoms of asthma, known as asthma phenotypes, from their underlying etiologies or causes, known as asthma endotypes.

References

  1. 1 2 3 4 5 6 7 8 9 10 11 "Cezmi Akdis Short Biography" (PDF). SIAF. Retrieved 21 February 2020.
  2. 1 2 3 "Google Scholar". scholar.google.com. Retrieved 2020-02-16.
  3. "Thomson Reuters Highly Cited Researcher" . Retrieved 21 February 2020.
  4. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 "EAACI Awardees". EAACI. Retrieved 21 February 2020.
  5. "Senate". SAMWASSM. Retrieved 13 May 2022.
  6. "Allergy Editorial Board". Wiley Online Library. doi:10.1111/(ISSN)1398-9995 . Retrieved 21 February 2020.
  7. Akdis, Cezmi (1996). "Epitope-specific T cell tolerance to phospholipase A2 in bee venom immunotherapy and recovery by IL-2 and IL-15 in vitro". Journal of Clinical Investigation. 98 (7): 1676–83. doi:10.1172/JCI118963. PMC   507602 . PMID   8833918.
  8. Akdis, Cezmi (1998). "Role of interleukin 10 in specific immunotherapy". Journal of Clinical Investigation. 102 (1): 98–106. doi:10.1172/JCI2250. PMC   509070 . PMID   9649562.
  9. Jutel (2001). "Histamine regulates T-cell and antibody responses by differential expression of H1 and H2 receptors". Nature. 413 (6854): 420–5. Bibcode:2001Natur.413..420J. doi:10.1038/35096564. PMID   11574888.
  10. Trautmann (2000). "T cell-mediated Fas-induced keratinocyte apoptosis plays a key pathogenetic role in eczematous dermatitis". Journal of Clinical Investigation. 106 (1): 25–35. doi:10.1172/JCI9199. PMC   517909 . PMID   10880045.
  11. Deniz (2002). "Human NK1 and NK2 subsets determined by purification of IFN-gamma-secreting and IFN-gamma-nonsecreting NK cells". European Journal of Immunology. 32 (3): 879–84. doi:10.1002/1521-4141(200203)32:3<879::AID-IMMU879>3.0.CO;2-2. PMID   11870632.
  12. Truatmann (2002). "T cells and eosinophils cooperate in the induction of bronchial epithelial cell apoptosis in asthma". Journal of Allergy and Clinical Immunology. 109 (2): 329–37. doi: 10.1067/mai.2002.121460 . PMID   11842305.
  13. Basinski (2009). "Dual nature of T cell-epithelium interaction in chronic rhinosinusitis". Journal of Allergy and Clinical Immunology. 124 (1): 74–80.e1–8. doi:10.1016/j.jaci.2009.04.019. PMID   19523671.
  14. Deniz (2008). "Regulatory NK cells suppress antigen-specific T cell responses". Journal of Immunology. 180 (2): 850–7. doi: 10.4049/jimmunol.180.2.850 . PMID   18178824.
  15. Agache (2012). "Untangling asthma phenotypes and endotypes". Allergy. 67 (7): 835–46. doi: 10.1111/j.1398-9995.2012.02832.x . PMID   22594878.
  16. Lötvall (2011). "Asthma endotypes: a new approach to classification of disease entities within the asthma syndrome". Journal of Allergy and Clinical Immunology. 127 (2): 355–60. doi:10.1016/j.jaci.2010.11.037. PMID   21281866.
  17. Akdis, Cezmi (2013). "Endotypes and phenotypes of chronic rhinosinusitis: a PRACTALL document of the European Academy of Allergy and Clinical Immunology and the American Academy of Allergy, Asthma & Immunology". Journal of Allergy and Clinical Immunology. 131 (6): 1479–90. doi:10.1016/j.jaci.2013.02.036. PMC   4161279 . PMID   23587334.
  18. Akdis (2022). "The epithelial barrier hypothesis proposes a comprehensive understanding of the origins of allergic and other chronic noncommunicable diseases". Journal of Allergy and Clinical Immunology. 149 (1): 41–44. doi:10.1016/j.jaci.2021.11.010. PMID   34822880.
  19. Celebi Sozener (2022). "Epithelial barrier hypothesis: Effect of the external exposome on the microbiome and epithelial barriers in allergic disease" (PDF). Allergy. 75 (5): 1418–1449. doi: 10.1111/all.15240 . PMID   35108405.
  20. Wang (2019). "Laundry detergents and detergent residue after rinsing directly disrupt tight junction barrier integrity in human bronchial epithelial cells". Journal of Allergy and Clinical Immunology. 143 (5): 1892–1903. doi: 10.1016/j.jaci.2018.11.016 . PMID   30500342.
  21. Basinski. "Laundry detergents and detergent residue after rinsing directly disrupt tight junction barrier integrity in human bronchial epithelial cells". Journal of Allergy and Clinical Immunology. PMID   19523671.
  22. Sugita (2018). "Type 2 innate lymphoid cells disrupt bronchial epithelial barrier integrity by targeting tight junctions through IL-13 in asthmatic patients". Journal of Allergy and Clinical Immunology. 141 (1): 300–310.e11. doi: 10.1016/j.jaci.2017.02.038 . PMID   28392332.
  23. Xian (2016). "Anionic surfactants and commercial detergents decrease tight junction barrier integrity in human keratinocytes". Journal of Allergy and Clinical Immunology. 138 (3): 890–893.e9. doi: 10.1016/j.jaci.2016.07.003 . PMID   27596709.
  24. Wawrzyniak (2017). "Regulation of bronchial epithelial barrier integrity by type 2 cytokines and histone deacetylases in asthmatic patients" (PDF). Journal of Allergy and Clinical Immunology. 139 (1): 93–103. doi: 10.1016/j.jaci.2016.03.050 . PMID   27312821.
  25. Kubo (2015). "CpG-DNA enhances the tight junction integrity of the bronchial epithelial cell barrier". Journal of Allergy and Clinical Immunology. 136 (5): 1413–6.e1–8. doi: 10.1016/j.jaci.2015.05.006 . PMID   26100085.
  26. Soyka (2012). "Defective epithelial barrier in chronic rhinosinusitis: the regulation of tight junctions by IFN-γ and IL-4". Journal of Allergy and Clinical Immunology. 130 (5): 1087–1096.e10. doi: 10.1016/j.jaci.2012.05.052 . PMID   22840853.
  27. Sugita (2019). "Human type 2 innate lymphoid cells disrupt skin keratinocyte tight junction barrier by IL-13". Allergy. 74 (12): 2534–2537. doi:10.1111/all.13935. PMID   31166013.
  28. "Curriculum vitae Akdis, Cezmi A. Prof. Dr. med" (PDF). 18. Uludağ İç Hastalıkları Ulusal Kış Kongresi. Retrieved 10 May 2022.
  29. "Prof. Dr. Cezmi Akdis vom SIAF ist Träger des Erich Fuchs-Preises" (PDF). Academia Raetica. Retrieved 11 May 2022.
  30. "BUÜ Tıp Fakültesi'nden akademisyen çifte fahri profesörlük". Bursa Uludağ Üniversitesi Tıp Fakültesi. Retrieved 12 May 2022.