Frequency, Severity and Duration of Rhinovirus Infections in Asthmatic and Non Asthmatic Individuals; A Longitudinal Cohort Study
Imperial College London, Londinium, England, United Kingdom The Lancet
(Impact Factor: 45.22).
04/2002; 359(9309):831-4. DOI: 10.1016/S0140-6736(02)07953-9
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.
Available from: sciencedirect.com
- "Dodatkowo jasne jest, że istotną rolę w odpowiedzi na infekcje dróg oddechowych odgrywa indywidualna podatność osobnicza. Pacjenci z astmą mają zmienioną nabłonkową odpowiedź immunologiczną na rinowirusy  i w związku z tym są bardziej podatni na infekcje dolnych dróg oddechowych . Ponadto nadreaktywność dróg oddechowych jest typową cechą dzieci astmatycznych i stwierdzono, że dzieci, u których później rozwinie się astma, wykazują zwiększoną odpowiedź oskrzelową, zanim przejdą jakąkolwiek infekcję dolnych dróg oddechowych  . "
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ABSTRACT: Infekcje dolnego odcinka dróg oddechowych w pierwszych latach życia wiążą się z wystąpieniem astmy w późniejszym okresie. Obserwacja ta doprowadziła do badań nad potencjalną rolą przyczynową w rozwoju astmy specyficznych wirusów odpowiedzialnych za infekcje dróg oddechowych, takich jak rinowirusy i wirus RSV. Ponieważ jednak liczne wirusy i bakterie wywołują podobne objawy ze strony układu oddechowego, to możliwe, że istotnymi czynnikami rozwoju astmy są istniejąca wrażliwość na infekcje oraz nadmierna reakcja na taki bodziec, a nie sam czynnik wywołujący infekcję.
Available from: Olivia Larsson
- "Bacterial infections, such as Streptococcus pneumoniae, Haemophilius influenzae and Moraxella cattarhalis are also present during asthma exacerbations and have been shown to be both triggers of the exacerbation or play an opportunistic role following viral infection . Moreover, microbial exacerbations have been shown not only to extend the period of illness, but also increase the respiratory symptoms, such as airway hyperresponsiveness (AHR) , , . Despite the breadth of epidemiological studies in this area, the mechanisms behind these phenomena are still poorly understood. "
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ABSTRACT: It is well-established that bacterial and viral infections have an exacerbating effect on allergic asthma, particularly aggravating respiratory symptoms, such as airway hyperresponsiveness (AHR). The mechanism by which these infections alter AHR is unclear, but some studies suggest that Toll-like receptors (TLRs) play a role. In this study, we investigated the impact of TLR3 and TLR4 ligands on AHR and airway inflammation in a model of pre-established allergic inflammation. Female BALB/c mice were sensitised and challenged intranasally (i.n.) with either PBS or ovalbumin (OVA) and subsequently i.n. challenged with poly (I:C) (TLR3) or LPS (TLR4) for four consecutive days. The response to methacholine was measured in vivo; cellular and inflammatory mediators were measured in blood, lung tissue and broncheoalveolar lavage fluid (BALF). OVA challenge resulted in an increase in AHR to methacholine, as well as increased airway eosinophilia and TH2 cytokine production. Subsequent challenge with TLR agonists resulted in a significant increase in AHR, but decreased TLR-specific cellular inflammation and production of immune mediators. Particularly evident was a decline in LPS-induced neutrophilia and neutrophil-associated cytokines following LPS and poly (I:C) treatment. The present data indicates that TLRs may play a pivotal role in AHR in response to microbial infection in allergic lung inflammation. These data also demonstrate that aggravated AHR occurs in the absence of an exacerbation in airway inflammation and that allergic inflammation impedes a subsequent inflammatory response to TLRs. These results may parallel clinical signs of microbial asthma exacerbation, including an extended duration of illness and increased respiratory symptoms.
Available from: Suraj George
- "Reports indicate that majority of the viral respiratory tract infections caused by human rhinoviruses are associated with asthma exacerbations (Busse et al., 2010). However, studies also indicate that asthmatic individuals do not necessarily develop frequent episodes of cold, and the severity and duration are not enhanced by respiratory allergies or asthma (Doyle et al., 1992; Corne et al., 2002). "
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ABSTRACT: Indukantha Ghritha (IG), a polyherbal drug used for centuries in Ayurveda, is claimed to be successful in the treatment of respiratory diseases and as a rejuvenating drug. To date, little is known about the immunomodulatory role of IG in recurrent upper respiratory tract infections (RURIs). This study was designed to scientifically validate and evaluate the immunological response mechanisms in patients with RURI. Primarily, immunological functioning of the lymphocyte subsets, Th1 and Th2 cytokines, and immunoglobulins was evaluated before and after administration of IG in patients (n = 48) and normal subjects (n = 25) for a period of 28 days. Flow cytometry revealed a significant increase in the CD3+, CD4+ T cells and CD56+ natural killer cells with a concomitant reduction of percentage of B cells during IG treatment. Increased Th1 cytokines, IL-2 and IFN-γ, and decreased Th2 cytokine, IL-4, were also observed with IG treatment. IgG was markedly decreased, and IgM was increased with no changes in IgA. Assessment of liver and kidney functions and cholesterol levels was within normal limits in patients administered IG, which reinforces its drug utility as a non-toxic polyherbal drug. Overall, IG provides symptomatic relief by functioning as a potent immunostimulator that can induce type 1 and decrease type 2 immune responses thereby maintaining immunological homeostasis in RURI patients. Copyright © 2014 John Wiley & Sons, Ltd.
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