Literature DB >> 18201436

Cytokine expression in peripheral blood lymphocytes before and after aspirin desensitization in aspirin-exacerbated respiratory disease.

Goutam P Shome1, James Tarbox, Michael Shearer, Ronald Kennedy.   

Abstract

Aspirin intolerance is the hallmark of aspirin-exacerbated respiratory disease (AERD). Overproduction of cysteinyl-leukotrienes (Cys-LTs) has been implicated as major mediators of AERD; however, the LT receptor antagonist montelukast is only partially effective in inhibiting aspirin responses. Several studies have documented the importance of cytokine production by T lymphocytes in asthma. Peripheral blood lymphocyte (PBL) cytokine expression and its relation to aspirin desensitization in aspirin-sensitive patients with asthma have not been studied. This study was performed to examine PBL cytokine expression in aspirin-sensitive patients who have asthma before and after aspirin desensitization. A 42-year-old white woman with a history of severe asthma, nasal polyps, aspirin sensitivity, and chronic sinusitis was treated with aspirin desensitization. Blood was taken before and after aspirin desensitization, and PBL cytokine expression was studied by flow cytometry. Aspirin desensitization differentially affects interferon (IFN) gamma expression. This effect results in an increase in IFN-gamma expression by CD4(+) lymphocytes and a decrease in IFN-gamma expression by CD8(+) lymphocytes. Aspirin desensitization in an aspirin-sensitive patient with asthma resulted in an increase in IFN-gamma expression by CD4(+) lymphocytes and a decrease in IFN-gamma expression by CD8(+) lymphocytes, the significance of which needs additional investigation.

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Year:  2007        PMID: 18201436     DOI: 10.2500/aap.2007.28.3052

Source DB:  PubMed          Journal:  Allergy Asthma Proc        ISSN: 1088-5412            Impact factor:   2.587


  7 in total

1.  Prominent role of IFN-γ in patients with aspirin-exacerbated respiratory disease.

Authors:  John W Steinke; Lixia Liu; Phillip Huyett; Julie Negri; Spencer C Payne; Larry Borish
Journal:  J Allergy Clin Immunol       Date:  2013-06-24       Impact factor: 10.793

Review 2.  Factors driving the aspirin exacerbated respiratory disease phenotype.

Authors:  John W Steinke; Larry Borish
Journal:  Am J Rhinol Allergy       Date:  2015 Jan-Feb       Impact factor: 2.467

Review 3.  Eosinophils and Mast Cells in Aspirin-Exacerbated Respiratory Disease.

Authors:  John W Steinke; Spencer C Payne; Larry Borish
Journal:  Immunol Allergy Clin North Am       Date:  2016-09-13       Impact factor: 3.479

4.  Cytokine expression before and after aspirin desensitization therapy in aspirin-exacerbated respiratory disease.

Authors:  Ayse Aktas; Emel Kurt; Zafer Gulbas
Journal:  Inflammation       Date:  2013-12       Impact factor: 4.092

5.  Subphenotypes of nonsteroidal antiinflammatory disease-exacerbated respiratory disease identified by latent class analysis.

Authors:  Natalia Celejewska-Wójcik; Krzysztof Wójcik; Maria Ignacak-Popiel; Adam Ćmiel; Katarzyna Tyrak; Anna Gielicz; Aleksander Kania; Paweł Nastałek; Marek Sanak; Lucyna Mastalerz
Journal:  Allergy       Date:  2020-01-28       Impact factor: 13.146

Review 6.  Aspirin-exacerbated respiratory disease: pathophysiological insights and clinical advances.

Authors:  John W Steinke; Jeff M Wilson
Journal:  J Asthma Allergy       Date:  2016-03-10

7.  Local and Systemic Production of Pro-Inflammatory Eicosanoids Is Inversely Related to Sensitization to Aeroallergens in Patients with Aspirin-Exacerbated Respiratory Disease.

Authors:  Daniel P Potaczek; Gabriela Trąd; Marek Sanak; Holger Garn; Lucyna Mastalerz
Journal:  J Pers Med       Date:  2022-03-11
  7 in total

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