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Background: Allergic disorders are characterized by type 2 helper T cell (Th2)-polarization, thus physiological type 1 helper T cell (Th1)-dependent mechanisms involved in fighting respiratory infections (RI) may be defective. It has previously been reported that allergic children have more numerous and severe RI than nonallergic ones.
Objective: The aim of the study was to evaluate the number and duration of RI in adult allergic and nonallergic subjects.
Methods: Six hundred and twenty-four subjects were studied; 202 of them were allergic (i.e. suffering from allergic rhinitis). The number of RI as well as the duration of the disease were recorded for 2 years.
Results: Allergic subjects showed a significantly higher rate of RI episodes [adjusted incidence rate ratio (IRR) = 2.16, 95% confidence interval (CI) 1.94–2.41, P < 0.001] than subjects without allergy. The number of mild RI episodes was slightly higher in allergic subjects (IRR = 1.68, 95% CI 1.50–1.89, P < 0.001), while the number of severe episodes was markedly higher (IRR = 15.71, 95% CI 10.35–23.84, P < 0.001) when compared with nonallergic subjects. Moreover, allergic patients showed a longer total duration of RI than nonallergic subjects, with a mean difference of 17.4 days (95% CI 15.5–19.4, P < 0.001).
Conclusions: This study provides evidence that adult allergic patients have more numerous and prolonged RI than nonallergic subjects.
Allergic disorders show an increasing worldwide prevalence (1). The immunopathology of allergic rhinitis and asthma shares common mechanisms characterized by type 2 helper T cell (Th2)-dependent inflammation (2). As a consequence of it, the atopic subject develops a typical Th2-polarization with a type 1 helper T cell (Th1)-response reduction (2). Interferon-gamma, typical Th1-derived cytokine, is deputized in fighting infections. Thus, it has been pointed out that allergic patients could present higher susceptibility to contract respiratory infections (RI) rather than nonallergic subjects (3). This hypothesis could be reinforced by the evidence that rhinovirus infections are very common (4). Indeed, there is a clear link among allergen exposure, intercellular adhesion molecule 1 (ICAM1) expression, allergic inflammation and RI. The main receptor for rhinovirus is the adhesion molecule ICAM1 (4), and ICAM1 expression on nasal epithelial cells is strictly related to allergen exposure in allergic subjects (3). In addition, treatment with drugs able to reduce ICAM1 expression has shown to be able to lower both the number and the severity of RI in allergic children (5).
Respiratory infections are frequent in general population and constitute a demanding challenge for physicians (6).
Very recently, it has been evidenced that allergic children have more numerous and severe respiratory infections than nonallergic children (7).
Therefore, this study was performed to evaluate the number and duration of RI in adult allergic and nonallergic subjects to confirm previous findings observed in children.
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Not unexpectedly, this study showed that RI is a rare event in this population of otherwise healthy Navy soldiers, with a mean rate of two episodes per soldier over the 2-year follow-up, and that severe RI is even less frequent (with a mean rate of one episode for every three soldiers over 2 years). Our results have also underlined another important aspect of the disease, showing that allergic subjects have more frequent and prolonged RI than nonallergic ones. We have observed a two-fold increase of RI risk in allergic subjects, and a duration almost 3 weeks longer of the symptoms than in nonallergic. This phenomenon is particularly evident for severe RI, with a 15-fold risk increase in allergic patients. It has to be explicitely stated that no relevant difference exists between subjects presenting with mono- vs polysensitization, neither for the rate of RI nor for their total duration. The duration of the study and the large sample size further support our conclusions.
A possible explanation for these findings is that allergic reaction is characterized by mucosal inflammation that predisposes to infection. In addition, allergic subjects express ICAM1, an adhesion molecule involved in inflammatory events as ligand of lymphocyte function-associated antigen-1, expressed on leukocytes. Intercellular adhesion molecule 1 is also the main receptor for rhinovirus (3). Moreover, allergic patients present a typical Th2-polarization with a consequent reduced Th1-response that is supposed to adequately fight infections mainly through Interferon gamma. Eventually, the impaired reparative events and recovery in allergic patients, may explain the prolonged duration of RI.
On the contrary, it should be considered that allergic patients may refer more often to the physician, may have nasal hyperreactivity, leading to prolonged and/or more obvious symptoms than normals, and at least some of the observed symptoms may not be colds but episodes of rhinitis that were misinterpreted by the patient/doctor. Moreover, we have to consider that an important drawback of this study is the absence of cultural, viral or bacterial, determination.
It is to underline that the relationship between allergy and RI is of considerable interest as there are few studies over this topic and findings are conflicting. In this regard, a study performed by Bardin demonstrated that experimental rhinovirus cold in atopic subjects heightened susceptibility to the detrimental effects of colds both concerning immunological and clinical aspects (9). Another study of the same group reported that atopic asthmatics are not at greater risk of rhinovirus infection when compared to healthy individuals; still, they suffer from more frequent lower-respiratory-tract infections and have more severe and longer-lasting lower-respiratory-tract symptoms (8). Moreover, Xepapadaki has recently evidenced that in asthmatic children the duration of airway hyperreactivity, evaluated by methacholine bronchial challenge, after a single natural cold was from 5 to 11 weeks (10). However, this study highlighted that an increased rate of symptomatic cold and asthma episodes in atopic children was associated with considerable cumulative prolongation of airway hyperreactivity. This event might help to explain the role of atopy as a risk factor for asthma persistence (10). Anyway, most of these previous studies focussed on asthma, rather than rhinitis and do not differentiate between the atopic element and the respiratory element, such as asthma.
In conclusions, this study provides evidence that allergic patients have more numerous and prolonged RI than nonallergic subjects. Therefore, it confirms previous findings and demonstrates that atopics are more susceptible than nonallergic subjects to present with RI. Further studies should be addressed in order to investigate if anti-allergic treatments could improve this feature.