BACKGROUND: Rhinoviruses (RVs) are the most frequent precipitants of the common cold and asthma exacerbations, but little is known about the immune response to these viruses and its potential implications in the pathogenesis of asthma. METHODS: Peripheral blood mononuclear cells (PBMC) from patients with atopic asthma and normal subjects were exposed to live or inactivated RV preparations. Levels of interferon (IFN)gamma and interleukins IL-12, IL-10, IL-4, IL-5 and IL-13 were evaluated in the culture supernatants with specific immunoassays. RESULTS: Exposure of PBMC to RVs induced the production of IFNgamma, IL-12, IL-10, and IL-13. Cells from asthmatic subjects produced significantly lower levels of IFNgamma and IL-12 and higher levels of IL-10 than normal subjects. IL-4 was induced only in the asthmatic group, while the IFNgamma/IL-4 ratio was more than three times lower in the asthmatic group. CONCLUSIONS: This evidence suggests that the immune response to RVs is not uniquely of a type 1 phenotype, as previously suggested. The type 1 response is defective in atopic asthmatic individuals, with a shift towards a type 2 phenotype in a way similar, but not identical, to their aberrant response to allergens. A defective type 1 immune response to RVs may be implicated in the pathogenesis of virus induced exacerbations of asthma.
BACKGROUND: Rhinoviruses (RVs) are the most frequent precipitants of the common cold and asthma exacerbations, but little is known about the immune response to these viruses and its potential implications in the pathogenesis of asthma. METHODS: Peripheral blood mononuclear cells (PBMC) from patients with atopic asthma and normal subjects were exposed to live or inactivated RV preparations. Levels of interferon (IFN)gamma and interleukins IL-12, IL-10, IL-4, IL-5 and IL-13 were evaluated in the culture supernatants with specific immunoassays. RESULTS: Exposure of PBMC to RVs induced the production of IFNgamma, IL-12, IL-10, and IL-13. Cells from asthmatic subjects produced significantly lower levels of IFNgamma and IL-12 and higher levels of IL-10 than normal subjects. IL-4 was induced only in the asthmatic group, while the IFNgamma/IL-4 ratio was more than three times lower in the asthmatic group. CONCLUSIONS: This evidence suggests that the immune response to RVs is not uniquely of a type 1 phenotype, as previously suggested. The type 1 response is defective in atopic asthmatic individuals, with a shift towards a type 2 phenotype in a way similar, but not identical, to their aberrant response to allergens. A defective type 1 immune response to RVs may be implicated in the pathogenesis of virus induced exacerbations of asthma.
Authors: T H Harju; M Leinonen; J Nokso-Koivisto; T Korhonen; R Räty; Q He; T Hovi; J Mertsola; A Bloigu; P Rytilä; P Saikku Journal: Thorax Date: 2006-03-03 Impact factor: 9.139
Authors: Vasile Laza-Stanca; Luminita A Stanciu; Simon D Message; Michael R Edwards; James E Gern; Sebastian L Johnston Journal: J Virol Date: 2006-08 Impact factor: 5.103
Authors: A Głobińska; M Pawełczyk; A Piechota-Polańczyk; A Olszewska-Ziąber; S Moskwa; A Mikołajczyk; A Jabłońska; P K Zakrzewski; M Brauncajs; M Jarzębska; S Taka; N G Papadopoulos; M L Kowalski Journal: Clin Exp Immunol Date: 2016-11-14 Impact factor: 4.330
Authors: Tuomas Jartti; Maria Paul-Anttila; Pasi Lehtinen; Vilhelmiina Parikka; Tytti Vuorinen; Olli Simell; Olli Ruuskanen Journal: Respir Res Date: 2009-09-25