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Background: Physical exercise is often recommended as additional treatment for people suffering from allergic rhinitis and/or asthma, but less is known about the specific effects of recreational winter outdoor exercise on allergic airway inflammation. Methods: We performed a longitudinal, randomized controlled intervention study to investigate the effects of recreational winter exercise on allergic airway inflammation, quality of life, spirometry and cardiorespiratory fitness in adults suffering from allergic rhinitis and/or asthma. The exercise group participated in a ten-day winter sports program. The control group did not receive any intervention. Results: A significant improvement of fractional oral exhaled nitric oxide (FeNO; p = 0.008, day 10) and a significant decrease in FeNO after a single 4 h hiking tour (p < 0.001, time effect) were observed for the exercise group. The nasal eosinophilic cell count revealed a short-term reduction (p = 0.021, treatment effect) in the exercise group and for the visual analogue scale sustainable improvements in allergic symptoms (p < 0.001, day 60) were found. No adverse effects of outdoor winter exercise were observed. Conclusion: Recreational winter exercise at moderately cold temperatures reduces allergic airway inflammation measured as FeNO, nasal eosinophilic cell count and induces sustainable improvements in allergic symptoms.

Background Epidemiological and experimental studies suggest that exposure to ultrafine particles (UFP) might aggravate the allergic inflammation of the lung in asthmatics. Methods We exposed 12 allergic asthmatics in two subgroups in a double-blinded randomized cross-over design, first to freshly generated ultrafine carbon particles (64 μg/m 3 ; 6.1 ± 0.4 × 10 5 particles/cm 3 for 2 h) and then to filtered air or vice versa with a 28-day recovery period in-between. Eighteen hours after each exposure, grass pollen was instilled into a lung lobe via bronchoscopy. Another 24 hours later, inflammatory cells were collected by means of bronchoalveolar lavage (BAL). (Trial registration: NCT00527462) Results For the entire study group, inhalation of UFP by itself had no significant effect on the allergen induced inflammatory response measured with total cell count as compared to exposure with filtered air (p = 0.188). However, the subgroup of subjects, which inhaled UFP during the first exposure, exhibited a significant increase in total BAL cells (p = 0.021), eosinophils (p = 0.031) and monocytes (p = 0.013) after filtered air exposure and subsequent allergen challenge 28 days later. Additionally, the potential of BAL cells to generate oxidant radicals was significantly elevated at that time point. The subgroup that was exposed first to filtered air and 28 days later to UFP did not reveal differences between sessions. Conclusions Our data demonstrate that pre-allergen exposure to UFP had no acute effect on the allergic inflammation. However, the subgroup analysis lead to the speculation that inhaled UFP particles might have a long-term effect on the inflammatory course in asthmatic patients. This should be reconfirmed in further studies with an appropriate study design and sufficient number of subjects.

Abstract Rationale Secondhand tobacco smoke (SHS) and traffic-related air pollutants are associated with asthma and allergy. Diesel exhaust particles (DEPs) and SHS can interact with allergens in exacerbating allergic airway diseases through generation of reactive oxygen species. Glutathione S-transferases (GSTs) metabolize reactive oxygen species and detoxify electrophilic xenobiotics present in SHS and DEPs. Objectives We tested the hypotheses that functional GSTM1-null genotype and GSTP1 codon 105 variants (Ile105 and Val105) are determinants of allergic responses to SHS, and that responses to SHS and DEPs are correlated. Methods and Measurements In a randomized, placebo-controlled crossover trial, 19 ragweed allergen–sensitive subjects who had previously participated in a DEP trial were challenged intranasally with allergen after having been exposed to either clean air or SHS at separate visits. Nasal allergen–specific IgE, histamine, IL-4, and IFN-γ levels were measured before and after allergen challenge. Main Results Individuals with GSTM1-null or GSTP1 Ile105 genotypes showed larger nasal responses to allergens with SHS compared with clean air. GSTM1-null subjects had a larger increase in IgE than GSTM1-present subjects (median, 173.3 vs. 46.7 U/ml; p = 0.03), and the Ile105 GSTP1 genotype subjects had increased histamine (median, 10.2 vs. 4.6 nM; p = 0.01) after SHS plus allergen challenge. Responses to SHS and DEPs were correlated. Enhancement of IgE and histamine was greatest in the subjects with both the GSTM1-null and GSTP1 Ile/Ile genotypes. Conclusions GSTM1 and GSTP1 are important cytoprotective factors that reduce SHS and DEP exacerbation of allergic responses.

Background Previous studies have shown that routine heated humidifier (HH) do not provide any benefit during continuous positive airway pressure (CPAP) titration if there are no significant naso-pharyngeal symptoms. In clinical practice, nasal diseases and upper airway symptoms are very common. This study investigates the effects of HH during CPAP titration in subjects with or without naso-pharyngeal symptoms. Methods Fifty-two patients who received polysomnography with CPAP titration were randomly assigned to HH and non-HH groups. Their nasal cavity, pharynx, and naso-pharynx were evaluated before CPAP titration, and a questionnaire on subjective sensation, including naso-pharyngeal symptoms, willingness to further use CPAP, and sleep improvement, was used. Objective (e.g., leak, apnea–hypopnea index (AHI) reduction, and optimal CPAP pressure level) and subjective data were analyzed between the two groups. Results In subjective sensation, the HH group did not have any benefit in further willingness to use CPAP and in sleep improvement, but had improved naso-pharyngeal symptoms ( p  = 0.043). There were no significant differences in leak, AHI reduction, and optimal CPAP pressure, even in patients with significant naso-pharyngeal symptoms. Conclusion Routine use of HH is not necessary during CPAP titration regardless of naso-pharyngeal symptoms.

ObjectivesTo determine the response of nebulized magnesium sulfate on the lung function of children with bronchial hyperresponsiveness.MethodsEighty-four children with asthma were divided into three groups randomly: magnesium sulfate (M), albuterol (A), and a combination of magnesium sulfate and albuterol (M + A). All patients were nebulized with acetylcholine, and then treated as designed. Lung function was compared between the three groups.ResultsForced expiratory volume in first second (FEV1) significantly improved in all the three groups but it was better in (A) and (M + A) compared to (M) at 10 min and 20 min [10 min: 1.26 L ± 0.53 (A) vs. 1.10 L ± 0.27 (M), 1.35 L ± 0.59 (M + A) vs. 1.10 L ± 0.27 (M), p < 0.05; 20 min: 1.32 L ± 0.61 (A) vs. 1.17 L ± 0.30 (M), 1.42 L ± 0.59 (M + A) vs. 1.17 L ± 0.30 (M), p < 0.05]. Variation of FEV1, as absolute value at 10 min or 20 min over post-Ach FEV1 was significantly different in (A) or (M + A) compared to (M).ConclusionsNebulized albuterol and magnesium sulfate + albuterol can more effectively improve FEV1 in children with bronchial hyperresponsiveness than nebulized magnesium sulfate at 10 min and 20 min after inhalation. It is further suggested that addition of magnesium sulfate to albuterol does not result in additional benefit.

Background: Subjects with allergic asthma develop isolated late asthmatic reactions after inhalation of allergen-derived T cell peptides. Animal experiments have shown that airway hyperresponsiveness (AHR) is CD4+ cell-dependent. It is hypothesised that peptide inhalation produces increases in non-specific AHR and a T cell-dominant bronchial mucosal inflammatory response. Methods: Bronchoscopy, with bronchial biopsies and bronchoalveolar lavage (BAL), was performed in 24 subjects with cat allergy 6 h after aerosol inhalation of short overlapping peptides derived from Fel d 1, the major cat allergen. Biopsy specimens and BAL fluid were studied using immunohistochemistry and ELISA. Results: Twelve of the 24 subjects developed an isolated late asthmatic reaction without a preceding early (mast cell/histamine-dependent) reaction characteristic of whole allergen inhalation. These responders had significant between-group differences (responders vs non-responders) in the changes (peptide vs diluent) in AHR (p = 0.007) and bronchial mucosal CD3+ (p = 0.005), CD4+ (p = 0.006) and thymus- and activation-regulated chemokine (TARC)+ (p = 0.003) but not CD8+ or CD25+ cells or eosinophils, basophils, mast cells and macrophages. The between-group difference for neutrophils was p = 0.05 but with a non-significant within-group value (peptide vs diluent, responders, p = 0.11). In BAL fluid there was a significant between-group difference in TARC (p = 0.02) but not in histamine, tryptase, basogranulin, C3a or C5a, leukotrienes C4/D4/E4, prostaglandins D2 or F2α. Conclusions: Direct activation of allergen-specific airway T cells by peptide inhalation in patients with atopic asthma leads to increased AHR with local increases in CD3+ and CD4+ cells and TARC but no significant changes in eosinophils or basophil/mast cell products. These findings support previous animal experiments which showed a CD4+ dependence for AHR.

The pathogenesis of asthma includes a complex interplay among airway inflammation, hyperresponsiveness, and remodeling. Current evidence suggests that airway structural cells, including bronchial smooth muscle cells, myofibroblasts, fibroblasts, and epithelial cells, mediate all three aspects of asthma pathogenesis. Although studies show a connection between airway remodeling and changes in bronchomotor tone, the relationship between the two remains unclear. Transforming growth factor β1 (TGF-β1), a growth factor elevated in the airway of patients with asthma, plays a role in airway remodeling and in the shortening of various airway structural cells. However, the role of TGF-β1 in mediating airway hyperresponsiveness remains unclear. In this review, we summarize the literature addressing the role of TGF-β1 in airway remodeling and shortening. Through our review, we aim to further elucidate the role of TGF-β1 in asthma pathogenesis and the link between airway remodeling and airway hyperresponsiveness in asthma and to define TGF-β1 as a potential therapeutic target for reducing asthma morbidity and mortality.

Inflammation is a stereotypical physiological response to infections and tissue injury; it initiates pathogen killing as well as tissue repair processes and helps to restore homeostasis at infected or damaged sites. Acute inflammatory reactions are usually self-limiting and resolve rapidly, due to the involvement of negative feedback mechanisms. Thus, regulated inflammatory responses are essential to remain healthy and maintain homeostasis. However, inflammatory responses that fail to regulate themselves can become chronic and contribute to the perpetuation and progression of disease. Characteristics typical of chronic inflammatory responses underlying the pathophysiology of several disorders include loss of barrier function, responsiveness to a normally benign stimulus, infiltration of inflammatory cells into compartments where they are not normally found in such high numbers, and overproduction of oxidants, cytokines, chemokines, eicosanoids and matrix metalloproteinases. The levels of these mediators amplify the inflammatory response, are destructive and contribute to the clinical symptoms. Various dietary components including long chain ω-3 fatty acids, antioxidant vitamins, plant flavonoids, prebiotics and probiotics have the potential to modulate predisposition to chronic inflammatory conditions and may have a role in their therapy. These components act through a variety of mechanisms including decreasing inflammatory mediator production through effects on cell signaling and gene expression (ω-3 fatty acids, vitamin E, plant flavonoids), reducing the production of damaging oxidants (vitamin E and other antioxidants), and promoting gut barrier function and anti-inflammatory responses (prebiotics and probiotics). However, in general really strong evidence of benefit to human health through anti-inflammatory actions is lacking for most of these dietary components. Thus, further studies addressing efficacy in humans linked to studies providing greater understanding of the mechanisms of action involved are required.

Asthma, accompanied by lung inflammation, bronchoconstriction and airway hyper-responsiveness, is a significant public health burden. Here we report that Mas-related G protein-coupled receptors (Mrgprs) are expressed in a subset of vagal sensory neurons innervating the airway and mediates cholinergic bronchoconstriction and airway hyper-responsiveness. These findings provide insights into the neural mechanisms underlying the pathogenesis of asthma.

Background: The use of anti-allergic mattress covers in patients with asthma can result in a large reduction in the level of house dust mite allergen in dust samples. Apart from a reduction in histamine induced bronchial hyperresponsiveness, there are few data on the effect of mattress covers on clinical efficacy and quality of life in patients with moderate to severe asthma. Methods: Thirty patients with asthma and house dust mite allergy were studied in a randomised, double blind, placebo controlled study. Before and after using anti-allergic covers for 1 year, dust was collected from the mattresses to determine concentrations of Dermatophagoides pteronyssinus (Der p 1), and bronchial hyperresponsiveness and quality of life were measured. The patients scored their symptoms (lungs and nose), morning and evening peak flow values, and rescue medication for 14 days before and after the intervention period. Results: There was a significant reduction in the concentration of Der p 1 in the dust collected from the mattresses in the actively treated group after 1 year compared with before treatment; no change was found in the placebo group. In both the actively treated and placebo groups there was no significant improvement in PC20 histamine. Quality of life improved similarly in both groups. The symptom score of the lower airways did not significantly change in either group. A significant decrease in nasal symptom score was seen in the actively treated group compared with before treatment, but there was no significant difference between the groups. No changes in morning and evening peak flow values, peak flow variability, nor in the use of rescue medication were found in either group. Conclusion: The use of anti-allergic mattress covers results in significant reductions in Der p 1 concentrations in carpet-free bedrooms. However, in patients with moderate to severe asthma, airways hyperresponsiveness and clinical parameters are not affected by this effective allergen avoidance.