Respiratory viruses and asthma

Rs, Peebles; Tv, Hartert

doi:10.1097/00063198-200001000-00003

Cited by 14 publications

(8 citation statements)

References 38 publications

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“…43, 44 It is conceivable that the downregulation of STAT1 phosphorylation in severe allergic asthmatic patients might render them more susceptible to certain infections. Although we have shown that STAT1 signaling was impaired in all memory CD4 + T cells of allergic asthmatic patients, an actual link between the downregulation of STAT1 phosphorylation and susceptibility to atypical mycobacterial or viral respiratory infection requires further study.…”

Section: Discussionmentioning

confidence: 99%

IL-4 confers resistance to IL-27–mediated suppression on CD4+ T cells by impairing signal transducer and activator of transcription 1 signaling

Chen

Wang

Erekosima

et al. 2013

Journal of Allergy and Clinical Immunology

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Background Th2 cells play a critical role in the pathogenesis of allergic asthma. Established Th2 cells have been shown to resist reprogramming into Th1 cells. The inherent stability of Th2 cells poses a significant barrier to treating allergic diseases. Objective We sought to understand the mechanisms by which CD4+ T cells from asthmatic patients resist the IL-27-mediated inhibition. Methods We isolated and cultured CD4+ T cells from both healthy individuals and allergic asthmatic patients in order to test whether IL-27 can inhibit IL-4 production by the cultured CD4+ T cells using ELISA. Culturing conditions that resulted in resistance to IL-27 were determined using both murine and human CD4+ T cell culture systems. STAT1 phosphorylation was analyzed by Western blot and flow cytometry. Suppressor of cytokine signaling (Socs) mRNA expression was measured by quantitative PCR. The small interfering RNA method was used to knockdown the expression of Socs3 mRNA. Main Results We demonstrated that CD4+ T cells from asthmatic patients resisted the suppression of IL-4 production mediated by IL-27. We observed that repeated exposure to Th2-inducing conditions rendered healthy human CD4+ T cells resistant to IL-27-mediated inhibition. Using an in vitro murine culture system, we further demonstrated that repeated or higher doses of IL-4 stimulation, but not IL-2 stimulation, upregulated Socs3 mRNA expression and impaired IL-27-induced STAT1 phosphorylation. The Knockdown of Socs3 mRNA expression restored IL-27-induced STAT1 phosphorylation and IL-27-mediated inhibition of IL-4-production. Conclusions Our findings demonstrate that differentiated Th2 cells can resist IL-27-induced reprogramming toward Th1 cells by downregulating STAT1 phosphorylation and likely explain why the CD4+ T cells of asthmatic patients are resistant to IL-27-mediated inhibition.

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Section: Discussionmentioning

confidence: 99%

IL-4 confers resistance to IL-27–mediated suppression on CD4+ T cells by impairing signal transducer and activator of transcription 1 signaling

Chen

Wang

Erekosima

et al. 2013

Journal of Allergy and Clinical Immunology

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“…12,17 We have argued that RRVD is caused by immunopathologic inflammatory responses directed at virus persisting in synovial macrophages. 1,18 -20 A number of virusmediated immune pathologies are currently treated with steroids; these include croup in children, 21 virus-induced asthma flares, 22 Bell palsy, 23 viral encephalitis, 24 and hepatitis C virus arthritis. 25 Although RRVD can be severe and debilitating at onset, the disease progressively resolves within 3 to 6 months, there is no discernible articular damage, and there is no evidence of RRVD leading to autoimmune arthritis.…”

Section: Discussionmentioning

confidence: 99%

Corticosteroid Therapy in an Alphaviral Arthritis

Mylonas¹,

Harley²,

Purdie³

et al. 2004

JCR: Journal of Clinical Rheumatology

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“…It is possible that the serotype of RV involved may be important and some strains such as RV16 are particularly associated with reduced lung function and increased AHR and symptoms of asthma and rhinitis (Peebles & Hartert, 2000).…”

Section: Decreased Lung Function/ahr Several Investigatorsmentioning

confidence: 99%

Understanding the mechanisms of viral induced asthma: New therapeutic directions

Hansbro

Horvat

Wark

2008

Pharmacology & Therapeutics

114

113

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Asthma is a common and debilitating disease that has substantially increased in prevalence in Western Societies in the last 2 decades. Respiratory tract infections by respiratory syncytial virus (RSV) and rhinovirus (RV) are widely implicated as common causes of the induction and exacerbation of asthma. These infections in early life are associated with the induction of wheeze that may progress to the development of asthma. Infections may also promote airway inflammation and enhance T helper type 2 lymphocyte (Th2 cell) responses that result in exacerbations of established asthma. The mechanisms of how RSV and RV induce and exacerbate asthma are currently being elucidated by clinical studies, in vitro work with human cells and animal models of disease. This research has led to many potential therapeutic strategies and, although none are yet part of clinical practise, they show much promise for the prevention and treatment of viral disease and subsequent asthma.

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Respiratory viruses and asthma

Cited by 14 publications

References 38 publications

IL-4 confers resistance to IL-27–mediated suppression on CD4+ T cells by impairing signal transducer and activator of transcription 1 signaling

IL-4 confers resistance to IL-27–mediated suppression on CD4+ T cells by impairing signal transducer and activator of transcription 1 signaling

Corticosteroid Therapy in an Alphaviral Arthritis

Understanding the mechanisms of viral induced asthma: New therapeutic directions

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