Severe grape allergy has been linked to lipid transfer protein (LTP) sensitization. LTPs are known to be resistant to pepsin digestion, although the effect of gastroduodenal digestion on its allergenicity has not been reported.|We sought to investigate the effect of gastric and gastroduodenal digestion on the allergenic activity of grape LTP.|The proteolytic stability of grape LTP was investigated by using an in vitro model of gastrointestinal digestion. The allergenicity of LTP and its digesta was assessed in vitro by means of IgE immunoblotting, RASTs, and in vivo skin prick tests in the same patients with grape allergy.|Grape LTP was resistant to gastric digestion, and yielded a 6000-d relative molecular mass C-terminally trimmed fragment after duodenal digestion. This fragment retained the in vitro IgE reactivity of the intact protein. Inclusion of phosphatidylcholine during gastric digestion protected the LTP to a limited extent against digestion. Digestion did not affect the in vivo (skin prick test) biologic activity of LTP.|The allergenic activity of grape LTP was highly resistant to in vitro digestion. This property might facilitate sensitization through the gastrointestinal tract and might also potentiate the ability of LTPs to elicit severe allergic reactions in sensitized individuals.|Purified natural allergens will facilitate the development of component-resolved diagnostic approaches, including allergen chips. This study contributes to our understanding of the role digestion plays in symptom elicitation in true food allergy.

The role of respiratory viral infection in the development of asthma remains unclear. A number of factors play crucial roles, including the type of virus, the severity of the disease, the time of the infection, and, most important, the host predisposition. On the other hand, there is little doubt that a strong association exists between viral respiratory infections and induction of wheezing illnesses and asthma exacerbations. The underlying mechanisms, although not fully clarified, are likely to be multifactorial, involving inflammation of the bronchial mucosa, which interacts under certain circumstances with allergic inflammation. In addition, repetitive infections play an important role in perpetuating inflammation and airway hyperresponsiveness, especially in the presence of atopy, leading from childhood asthma to a more persistent asthma phenotype.

Rhinoviruses (RV), the major trigger of acute asthma exacerbations, are able to infect bronchial epithelium and induce production of pro-inflammatory, but also angiogenic and pro-fibrotic mediators. Fluticasone propionate (FP) and salmeterol (S) are clinically effective and act synergistically in controlling persistent asthma; however, their effect on virus-associated asthma is less clear.|The aim of this study was to assess the individual and combined effects of FP and S on RV-induced epithelial production of vascular endothelial growth factor (VEGF) and fibroblast growth factor-2 (FGF-2).|Bronchial epithelial cells (BEAS-2B) were exposed in vitro to RV and were subsequently treated with FP and S, at physiologically relevant concentrations, alone or in combination. VEGF and FGF-2 were measured in the supernatants of these cultures using ELISA.|FP was able to reduce RV-induced VEGF production in a dose-dependent manner. S also induced a smaller reduction; addition of both factors inhibited VEGF synergistically. FGF-2 production was not inhibited by either FP or S alone, but was significantly reduced when both substances were present in the culture.|This study demonstrates that FP and S may synergistically inhibit the production of angiogenic and/or pro-fibrotic factors that are induced after RV infection of BEAS-2B and are implicated in airway remodelling, suggesting that this combination may represent an important therapeutic option on virus-induced asthma.

Decisions regarding the introduction of influenza immunization in healthy children require an accurate evaluation of influenza disease burden not only in the inpatient but also in the outpatient setting. We prospectively examined the impact of virologically confirmed influenza in 1462 outpatient children (> or = 6 months to < 14 years) and their families, during two consecutive influenza seasons. Influenza was documented in 573/1462 (39%) outpatients with febrile respiratory illness and accounted for 13.5% of all outpatient visits during the 14 weeks of each season. Acute otitis media (AOM) was the most common complication (18.5%) and about 40% of influenza positive patients received antibiotics. AOM and antibiotic use were more common in children younger than 5 years of age who accounted for 58% of all patients. For each child sick with influenza a mean of 1.34 workdays were lost by the parents. Family members of influenza positive children were more likely to develop a secondary respiratory illness and to require medical visits and antibiotic prescriptions. Influenza is associated with a heavy morbidity burden in the community that may be reduced considerably with the implementation of immunization in children younger than 5 years of age.

The preventive use of medications has been proposed to be effective in the treatment of seasonal rhinitis.|To evaluate the efficacy and safety of mometasone furoate and nedocromil sodium nasal sprays as prophylactic treatment for moderate to severe seasonal allergic rhinitis (SAR).|Sixty-one patients were recruited from 3 referral allergy centers. Inclusion criteria were history of SAR for 2 years or longer, sensitization to relevant local pollen (grasses, Parietaria, and olive), and age older than 12 years.|An open-label, randomized, parallel-group, "real-life" study design was used. Patients received mometasone furoate nasal spray once daily or nedocromil sodium nasal spray 3 times daily starting 2 to 4 weeks before the pollen season and continuing for up to 4 months. Instructions regarding the use of additional medications were given. Diary cards recording symptoms, use of medication, and adverse events were kept by the patients.|All 61 patients completed the study. The prophylactic use of mometasone furoate vs nedocromil sodium led to significantly more days without symptoms (75.1% vs 54.5%; P < .001). The mometasone furoate group also had lower nasal symptom scores (mean, 1.4 vs 2.9; median, 0 vs 2; P < .001) and was more satisfied (93.1% vs 43.5%; P < .001). No serious adverse event was recorded, and there was no difference between the treatments in any adverse event.|Prophylactic administration of mometasone furoate before the pollen season is safe and may lead to improved control of SAR compared with the use of nedocromil sodium.

Human rhinoviruses, major precipitants of asthma exacerbations, infect the lower airway epithelium inducing inflammation. The possibility that viral infection may mediate angiogenesis, thus contributing to airway remodeling, has not been evaluated.|To investigate whether epithelial infection with rhinovirus mediates angiogenesis in vitro, evaluate possible modulation by an atopic environment, and confirm angiogenic factor induction after in vivo rhinovirus infection.|Bronchial epithelial cells were infected with rhinovirus and levels of vascular endothelial growth factor (VEGF), and angiopoietins were measured. The angiogenic effect of epithelial products was assessed in in vitro models of angiogenesis. PBMCs, obtained from patients with atopic asthma and normal controls, were exposed to rhinovirus; the ability of supernatants from these cultures differentially to affect rhinovirus-mediated epithelial VEGF production was evaluated. VEGF levels were measured in respiratory secretions from patients with asthma, before and during rhinovirus-induced exacerbations.|Epithelial infection with rhinovirus specifically stimulated mRNA expression and release of VEGF, but not angiopoietins, in a time-dependent and dose-dependent manner. Supernatants from these cultures were able to induce angiogenesis in vitro, significantly inhibited by a neutralizing anti-VEGF antibody. When bronchial cells were exposed to supernatants of rhinovirus-infected mononuclear cells from normal subjects or atopic patients with asthma, VEGF induction was significantly higher under the influence of the atopic environment. VEGF was elevated during rhinovirus-associated asthma exacerbations.|Rhinovirus infection, a frequent event, induces VEGF production in bronchial epithelial cells and human airways, an effect enhanced in an atopic environment. Rhinovirus-associated, VEGF-mediated angiogenesis may contribute to airway remodeling in asthma.

Epidemiological evidence examining the role of atopy and/or allergy in the pathogenesis of otitis media with effusion (OME) is inconclusive. The aim of this study was to assess any increased risk for OME attributable to allergy-related factors, in a well-characterized population using a case-control design and multivariate analysis.|Eighty-eight 1-7-year-old children with OME, diagnosed by clinical and tympanometric evaluation and 80 matched controls were enrolled. A standardized questionnaire was completed, in order to assess factors related to OME and allergy-related symptoms and diagnoses using strict clinical definitions. Specific IgE was measured by skin-prick tests and/or CAP-FEIA.|The patient and control groups were well matched. Factors conferring increased risk for OME in the univariate analysis included IgE sensitization, dyspnea, wheezing, asthma, paroxysmal sneezing, rhinitis, eczema, 'any allergic disease,' family history of otitis media, and family history of allergy. After multivariate analysis IgE sensitization, wheezing, nasal obstruction, family history of otitis, and child-care attendance remained as independent risk factors for development of OME.|IgE sensitization and respiratory allergy symptoms are independent risk factors for the development of OME, suggesting that both immunological and mechanical pathways may contribute to the development of the disease. Otitis heritability provides additional risk, as well as frequent exposure to viral upper respiratory tract infections in children attending daycare. Treatment and/or prevention of OME using anti-allergic medications should be further examined.

Frequent viral upper respiratory tract infections (URTI) are considered to be risk factors for otitis media with effusion (OME). Atopy has also been associated with both OME and viral infections. The aim of this study was to evaluate the presence of viruses in middle ear effusions (MEE) in children 2-7 yr old with OME, and to determine risk factors for virus detection in the MEE. MEE samples, collected at the time of myringotomy from 37 children with OME were assessed. Physical examination, skin prick tests and a standardized questionnaire on OME and allergy were also performed. Viral RNA was detected by the use of reverse transcription PCR (RT-PCR). Fifteen samples (40.5%) were positive for rhinovirus (RV). One enterovirus and no other respiratory viruses were detected. Two out of five (40%), 3/7 (43%) and 10/25 (40%) were positive for RV in acute, subacute and chronic cases, respectively. Children with frequent episodes of OM, with early onset of OM (<2 yr old), and a positive family history of allergy had a statistically increased risk of RV detection. The two groups were comparable with respect to all other parameters examined. RV is the predominant virus recovered by RT-PCR in the middle ear cavity of children with asymptomatic OME, especially those with a history of longstanding OME or repeated episodes, or children with a family history of allergy. Interactions between allergy and RV infections are likely to predispose to middle ear disease.