Frequency, severity, and duration of rhinovirus infections in asthmatic and non-asthmatic individuals: A longitudinal cohort study

ArticleinThe Lancet 359(9309):831-4 · April 2002with24 Reads
DOI: 10.1016/S0140-6736(02)07953-9 · Source: PubMed
Rhinovirus infections cause exacerbations of asthma. We postulated that people with asthma are more susceptible to rhinovirus infection than people without the disease and compared the susceptibility of these groups. We recruited 76 cohabiting couples. One person in every couple had atopic asthma and one was healthy. Participants completed daily diary cards of upper-respiratory-tract (URT) and lower-respiratory-tract (LRT) symptoms and measured peak expiratory flow twice daily. Every 2 weeks nasal aspirates were taken and examined for rhinovirus. Mixed models were used to compare risks of infection between groups. We also compared the severity and duration of infections. We analysed 753 samples. Rhinovirus was detected in 10.1% (38/378) of samples from participants with asthma and 8.5% (32/375) of samples from healthy participants. After adjustment for confounding factors, asthma did not significantly increase risk of infection (odds ratio 1.15, 95% CI 0.71-1.87). Groups did not differ in frequency, severity, or duration of URT infections or symptoms associated with rhinovirus infection. First rhinovirus infection was associated more frequently with LRT infection in participants with asthma than in healthy individuals (12 of 28 infections vs four of 23, respectively, p=0.051). Symptoms of LRT associated with rhinovirus infection were significantly more severe (p=0.001) and longer-lasting in participants with asthma than in healthy participants (p=0.005). People with atopic asthma are not at greater risk of rhinovirus infection than healthy individuals but suffer from more frequent LRT infections and have more severe and longer-lasting LRT symptoms.
    • "In two third of the cases with proven virus, rhinoviruses are detected. In asthmatics , the up-regulation of ICAM-1 on epithelial cells, a receptor that is used by 90% of the rhinoviruses, might be responsible for the higher sensitivity especially of atopic patients with more frequent infections and more severe and longer lasting symptoms [134]. In vitro studies reveal that rhinoviruses replicate more efficiently in primary bronchial epithelial cells of asthmatics than healthy people. "
    [Show abstract] [Hide abstract] ABSTRACT: Research in immunology has brought great progress in knowledge of inflammatory processes in the last 2 decades, which also has an impact on the upper airways. Our understanding of the pathophysiology of chronic rhinosinusitis developed from a rather mechanistic point of view with a focus on narrow clefts and mucociliary clearance to the appreciation of a complex network of immunological pathways forming the basis of disease. We today differentiate various forms of inflammation, we start to understand complex immune-regulatory networks and the reasons for their failure, and have already developed innovative approaches for therapy for the most severely ill subjects. Due to this new knowledge in inflammation and remodeling processes within mucosal tissue, specifically on the key driving factors, new diagnostic tools and therapeutic approaches for chronic rhinosinusitis have developed; the differentiation of endotypes based on pathophysiological principles will be crucial for the use of innovative therapies, mostly humanized monoclonal antibodies. Several hundred of those antibodies are currently developed for various indications and will impact our specialty as well as pneumology to a great extent.
    Full-text · Article · Dec 2015
    • "In addition, it has been demonstrated that rhinovirus-induced infection in atopic subjects heightened susceptibility to the detrimental effects of colds both concerning immunological and clinical aspects[17]. Another study reported that atopic asthmatics suffer from more frequent lowerrespiratory-tract infections and have more severe and persistent lower-respiratory-tract symptoms than normal subjects[18]. Thus, a relevant link between RI and AR exists as underlined by several studies1920212223242526Allergen-specific immunotherapy exerts profound effects on immune response, mainly concerning the balance between Th1 and Th2 cells. "
    [Show abstract] [Hide abstract] ABSTRACT: Aim: Allergic inflammation may promote respiratory infections (RI). House dust mite (HDM) sensitization is common in childhood. Allergen immunotherapy may cure allergy as it restores a physiological immune and clinical tolerance toward the causal allergen and exerts anti- inflammatory activity. This study retrospectively investigated whether 3 year high-dose HDM- sublingual immunotherapy (SLIT) could affect respiratory infections in children with allergic rhinitis. Methods: Globally, 33 HDM allergic children (18 males, mean age 9.3 years) were subdivided in 2 groups: 20 treated with symptomatic drugs alone (Group 1) and 13 by high-dose SLIT, titrated in mcg of major allergens (Group 2) for 3 years. Results: SLIT-treated children had significantly (p=0.01) less RI episodes (3.6) than symptomatically-treated children (5.4). In addition, SLIT-treated children had less fever (p<0.01) and took fewer medications, such as antibiotics (p<0.05) and fever-reducers (p<0.01), than symptomatically-treated children. Conclusion: This preliminary study suggests that high-dose 3-year SLIT might lessen RI in allergic children.
    Article · Nov 2015
    • "Haemophilius influenza), respectively. As a consequence of respiratory infections patients with allergic asthma generally suffer from prolonged and more severe symptoms than patients without established allergy [7, 8]. The mechanistic interplay between on-going allergy inflammation, microbial infections and TLR activation is complex and still poorly understood. "
    [Show abstract] [Hide abstract] ABSTRACT: Viral infections are a common cause of asthma exacerbation. These maladies are sometimes complicated by bacterial infections. Toll-like receptors (TLRs) are in the forefront of our microbial defence, with TLR3 responding to viral and TLR4 to bacterial stimulation. The present study was designed to evaluate the effect of concomitant TLR3 and TLR4 stimulation in a murine model of allergic asthma. BALB/c mice were stimulated intranasally with a combination of poly(I:C) and LPS activating TLR3 and TLR4, respectively. This resulted in the development of airway hyperresponsiveness (AHR) in the proximal part of the lung, along with signs of neutrophilic inflammation. Analysis of the bronchioalveolar lavage fluid (BALF) revealed a marked increase in TNFα. In contrast, the allergic airway inflammation induced by ovalbumin administration to sensitized mice caused AHR in the whole lung along with an increase in eosinophils and lymphocytes in the BALF and lung. When poly(I:C) + LPS were given to mice with an ongoing allergic airway inflammation induced by ovalbumin, the AHR was further increased in the peripheral lung and neutrophils appeared together with eosinophils and lymphocytes in the BALF and lung. Treatment with the TNFα-blocking antibody infliximab blunted the AHR increase, without affecting the cells influx in BALF. To conclude; a combined TLR3- and TLR4-stimulation, representing a concomitant viral and bacterial infection, causes an AHR that is further exaggerated during an ongoing allergic inflammation. The airway stabilizing effect of infliximab indicates the possible future use of TNFα blockade in treatment of microbial induced exacerbations of allergic asthma.
    Full-text · Article · Oct 2015
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