Diminished IL-10 production in subjects with allergy after infection with influenza A virus

• Published in: Journal of allergy and clinical immunology 1999-06, Vol.103 (6), p.1045-1048
• Main Authors: Gentile, Deborah A., Patel, Asha, Ollila, Chad, Fireman, Philip, Zeevi, Adriana, Doyle, William J., Skoner, David P.
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Allergic diseases; Allergic rhinitis; asthma; Biological and medical sciences; Female; g-Interferon; Humans; IL-10; Immunopathology; influenza A; Influenza A virus; Influenza, Human - virology; Interferon-gamma - metabolism; Interleukin-10 - biosynthesis; Interleukin-4 - metabolism; Male; Medical sciences; Middle Aged; Respiratory and ent allergic diseases; Respiratory Hypersensitivity - virology; Respiratory Tract Infections - virology; T-Lymphocytes, Helper-Inducer - chemistry; Time Factors
• ISSN: 0091-6749; 1097-6825
• DOI: 10.1016/S0091-6749(99)70177-6

Background: Recent studies have documented a link between respiratory viral infections and the expression of asthma and other allergic disorders. Results from other studies have suggested that diminished production of IL-10, an anti-inflammatory cytokine, may contribute to the pathophysiologic features of these diseases. Objective: The objective of this study was to determine whether diminished IL-10 production and T H2 cytokine skewing occur in allergic, as compared with nonallergic, subjects after experimental infection with the influenza A virus. Methods: PBMCs were isolated from 11 subjects with allergy and 14 subjects with no allergy before and after influenza A infection and stimulated with either mitogen (PHA) or antigen (influenza A). Supernatants were assayed for IL-10, IL-4, and IFN-γ by ELISA. Results: PBMC IL-10 production was significantly diminished in subjects with allergy, as compared with subjects with no allergy, after experimental infection with influenza A virus. However, significant T H2 skewing and enhanced airway symptoms were not observed in these same subjects. Conclusions: These data provide further support that subjects with allergy have an intrinsic inability to upregulate IL-10 production in response to inflammatory stimuli and extend this observation to include respiratory viral infections. Future studies in this area could lead to a better understanding of the pathogenesis of asthma and other allergic disorders (J Allergy Clin Immunol 1999;103:1045-8.)