Symptoms Of Allergic Asthma Research Articles

Birch pollen-associated peanut allergies in children

Panallergens show structural similarities, and they are responsible for many cross-reactions between pollen and plant food sources. The aim of the present study was to investigate IgE reactivity to peanut allergen components in children with birch pollen allergy. Patients experienced symptoms of allergic asthma, allergic rhinitis, and urticaria, and they underwent a complete diagnostic evaluation, including skin prick test (SPT), specific IgE (sIgE) to birch pollen allergen (t3), peanut allergen (f13). In addition, measurement of sIgE to the major birch allergen components, Betula verrucosa (Bet v1, Bet v2), and to peanut allergen components, Arachis hypogaea (genuine componens: Ara h1, Ara h2, Ara h3, and cross-reactive Ara h8) was performed, by using a microarray technique (component resolved diagnosis, CRD). SPT to birch extract was positive in all children, and SPT to peanut extract was positive in 51 % of them. sIgE to both allergens was increased in 39 % of children, 55 % of them had increased sIgE (t3), and one child had increased sIgE (f13). CRD results confirmed that some children were sensitized to Bet v1 only, and some children to genuine Ara h only. Bet v1/Ara h8 cross-reactivity was found in 16 % of children. Results of the present study reveal that SPT, sIgE, and CRD may detect sensitization and co-sensitization with birch and peanut allergens/allergen components, and CRD may help to differentiate sensitization to genuine peanut components from sensitization to peanut cross-reactive component in birch-sensitive children. Diagnostic approach has to be individualized for each patient.

Associations between Quantitative Measures of Fungi in Home Floor Dust and Lung Function among Older Adults with Chronic Respiratory Disease: A Pilot Study

Objective. Many fungi may cause allergic reactions and increase asthma symptoms prevalence and severity. One susceptible, vulnerable population subgroup of increasing size in industrialized countries and of public health concern who spends the majority of their time at home is older adults. Older adults diagnosed with chronic obstructive pulmonary disease (COPD) are at risk of exposure to fungi. Currently, species identification is based on observation of microscopic and macroscopic morphologies, which may underestimate concentrations compared to quantitative polymerase chain reaction (qPCR)-based measurements which are toxicologically more relevant to exposure science. Methods. This article analyzes quantitative indoor exposure data on fungi in floor dust (cells/cm2 floor) by real-time qPCR-based detection with quantitative outcome data via field spirometry in a pilot community-based study in Visalia, Tulare County, California, between July 2009 and January 2010. Subjects (n = 9, five females, four males) were Caucasian, English-speaking, nonsmoking older adults with doctor-diagnosed asthma and/or COPD. Results. While certain results did not reach statistical significance (p ≤ .10) due to sample size—overall and by gender—we found consistent trends and statistically significant associations for total fungal DNA (summer data) with forced vital capacity and forced expiratory volume in 1 second. Conclusions. The results of this pilot study are novel and suggest adverse effects of exposure inside homes to certain fungal species. This pilot study supports the need for larger prospective epidemiologic studies of older adults with asthma and/or chronic bronchitis based on quantitative environmental and clinical measures.

Calcitriol Decreases Expression of Importin α3 and Attenuates RelA Translocation in Human Bronchial Smooth Muscle Cells

A potent immunomodulatory role of Vitamin D in both innate and adaptive immunity has recently been appreciated. In allergic asthma, activation of NF-кB induces transcription of various cytokines and chemokines involved in allergic airway inflammation. The nuclear import of activated NF-кB p50/RelA subunit is dependent on importin α3 (KPNA4) and importin α4 (KPNA3). In this study, we examined the role of importin α3 in immunomodulatory effect of calcitriol in human bronchial smooth muscle cells (HBSMCs). Cultured HBSMCs were stimulated with calcitriol in the presence and absence of cytokines, TNF-α, IL-1β, and IL-10. The mRNA transcripts of importin α3 and α4 were analyzed using qPCR while protein expression of importin α3, α4 and nuclear RelA was analyzed by immunoblotting. Calcitriol significantly decreased mRNA and protein expression of importin α3 as well as nuclear protein expression of NF-кB p65 (RelA). The decreased activation of RelA by calcitriol was confirmed by decreased release of RelA-inducible molecules, including IL-5, IL-6 and IL-8, by HBSMCs upon calcitriol treatment. Calcitriol attenuated the effect of TNF-α and IL-1β to upregulate mRNA and protein expression of importin α3. IL-10 significantly decreased the TNF-α induced expression of importin α3 and this effect was further potentiated by calcitriol. These data suggest that under inflammatory conditions, calcitriol decreases the expression of importin α3 resulting in decreased nuclear import of activated RelA. This could be a novel mechanism by which calcitriol could exert its immunomodulatory effects to reduce allergic airway inflammation and thus may alleviate the symptoms in allergic asthma.

Presentation of atopic disease in a large cohort of pediatric liver transplant recipients

Atopic disease occurs in solid organ transplant recipients with an increasingly recognized frequency. The time course for the development of these atopic diseases in liver transplantation has not been described. The objective was to characterize the atopic manifestations of children receiving chronic immunosuppression after orthotopic liver transplantation (OLT). Chart review and follow-up questionnaire were utilized for 176 OLT pediatric recipients at a single institution for manifestations of allergic disease. Atopic disease was present in 25 (14.2%) patients. Median age at transplant was 16 months with a median follow-up of 63 months. Food allergy and non-food related atopic symptoms presented at a median of 11.5 (IQR, 6-28) and 19 (IQR, 5-41) months post-transplantation, respectively. The median age at transplant of the non-atopic children was 72 months, higher than patients with atopy (p < 0.001). Food allergy and atopic skin disease symptoms were present in 40% and 56% of cases, respectively. Asthma, allergic rhinitis, or both were found in 66% of cases. The onset of symptoms of food allergy and eczema (median, 12 months post-transplantation) preceded symptoms of allergic rhinitis and asthma. (median of 27 and 30 months post-transplantation, respectively). Atopy occurs in ∼14% of pediatric liver transplant recipients, with manifestations including food allergy, eczema, allergic rhinitis, and asthma.

Short-term roxithromycin treatment attenuates airway inflammation via MAPK/NF-κB activation in a mouse model of allergic asthma

We investigated whether roxithromycin reduces ovalbumin-specific allergic asthma symptoms in mice, and we further investigated the inhibitory mechanism of roxithromycin in ovalbumin-specific allergic asthma. Mice were divided into five groups (n=10 for each): control group, roxithromycin-treated groups (5, 20 and 40mg/kg) and ovalbumin-challenged group. We measured the recruitment of inflammatory cells into the bronchoalveolar lavage fluid (BALF) or the lung tissues by Kwik-Diff and hematoxylin and eosin (H&E) staining, goblet cell hyperplasia by alcian blue-periodic acid-Schiff (AB-PAS) staining, airway hyperresponsiveness (AHR) by whole-body plethysmograph chamber, cytokine and immunoglobulin E (IgE) levels by ELISA, and the activation of mitogen-activated protein (MAP) kinases and nuclear factor-kappa B (NF-κB) in the lung tissues by Western blotting. Treatment with roxithromycin resulted in fewer inflammatory cells in the BALF and peribronchial areas, and decreased AHR, goblet cell hyperplasia, IgE levels and inflammatory cytokines, as well as MAP kinases and NF-κB activation, which are increased in lung tissues of mice with ovalbumin-induced allergic asthma. Our data suggest that oral administration of roxithromycin suppresses ovalbumin-induced airway inflammation and AHR by regulating the inflammatory cytokines via MAP kinases/NF-κB pathway in inflammatory cells. Based on these results, we suggest that roxithromycin may be used as a therapeutic agent for allergy-induced asthma.

Oral administration of allergen extracts from mugwort pollen desensitizes specific allergen-induced allergy in mice

Clinically, sublingual immunotherapy (SLIT) using allergen extracts effectively alleviates the symptoms of allergic rhinitis and asthma. We hypothesized that oral administration of a high-dose of allergen extracts imitates SLIT, which may prevent IgE-related responses in allergic diseases. In the present study, we investigated the effects of oral administration of allergen extracts from mugwort pollen (MP) on allergen-induced inflammation and airway hyperresponsiveness (AHR) in an allergic mouse model. After administration of MPdrop containing Art v 1 and Art v 4 extracts derived from MP specifically in MP-sensitized mice, the effects of MPdrop on AHR, inflammatory cell accumulation, cytokine production in the bronchoalveolar lavage fluid and lung tissue, and serum IgE and IgG levels were investigated. The results indicated that MPdrop not only prevented the AHR in response to methacholine in a dose-dependent manner but also significantly reduced the total serum and allergen-specific IgE levels. All of the maximal effects were achieved at a dose of 100μg/(kgd) and were comparable to the effects of dexamethasone at a dose of 0.5mg/(kgd). Furthermore, oral administration of MPdrop dose-dependently elevated allergen-specific serum IgG2a levels, reduced total and allergen-specific IgE levels and normalized the imbalance between the Th1 cytokine IL-12 and Th2 cytokines IL-4 and IL-5. Finally, oral administration of MPdrop significantly reduced goblet cell hyperplasia and eosinophilia in the MP-sensitized allergic mouse model. These data suggest that MPdrop effectively improves specific allergen-induced inflammation and AHR in MP-sensitized and -challenged mice and provides the rationale for clinical use of MPdrop in the specific allergen-induced asthma.

PA01.09. Efficacy of ayurvedic formulations in allergic asthma patients with special reference to elevation of TIgE

Purpose: Allergic Asthma Tamaka swasa is one of the most distressing common diseases that affect a sizable number of world populations. Internal and external allergens such as environmental change, pollutants and unsuitable foods are believed to be the predisposing factors which sensitize the immune system of the body and trigger production of the antibody Immunoglobulin E. These result in sneezing, running nose, irritation of eyes, inflammation of bronchial mucosa and wheezing. Ayurvedic formulations such as Dasamoolakatuthrayam kwatha, Vyoshadi vatakam, Swasanandam gutika and Swasa kalpa are widely used by Ayurvedic physicians and clinically proven to have anti allergic effect. They relieve bronco spasm, airway block, sneezing and running nose. Current study was aimed at proving the efficacy of these formulations in Allergic Asthma. Method: Patients diagnosed with Allergic Asthma were chosen for clinical study. A total of 38 patients of either sex ranging from the age of 4 to 48 were selected for the study. All the patients were tested for their blood level TIgE. Most of them were found to have elevated blood level TIgE. Every patient was given Dasamoolakatuthrayam kwatha, Vyoshadi vatakam, Swasanandam gutika and Swasa kalpa orally for 6 8 weeks and the progress was observed. The observations were recorded based on subjective and objective methods. Result: It was construed from the results that the trial medicines had significantanti allergic, expectorant, bronco dilatation and overall reduction in the symptoms of Allergic Asthma in the analyzed patients. By the end of 8 weeks 16 out of 38 patients had significant recovery from the symptoms, 18 had good control of the ailment while the rest 4 displayed poor progress. Conclusion: The study vividly fortified the therapeutic efficacy of the trial drugs in the management of Allergic Asthma. Besides relieving the symptoms, the drugs significantly reduced the elevated TIgE in the blood.

Validation of a Phage Display and Computational Algorithm by Mapping a Conformational Epitope of Bla g 2

Background: Bla g 2, one of the major cockroach allergens, induces a strong IgE response against conformational epitopes, and on reexposure, sensitized individuals often display symptoms of allergic rhinitis and asthma. The aim of the current study was to perform a test of the efficacy of a modified phage display screening, characterization of selected phages and an automated algorithm, EpiSearch, in locating an important conformational epitope. Methods: The monoclonal antibody 7C11, which partially inhibits the binding of patient IgE antibodies to Bla g 2, was used to screen a random peptide phage library. After 3 rounds of panning, 32 phage clones were isolated and the amino acid sequences of their peptides were determined. The relative affinity and specificity of the binding of these peptides to 7C11 were tested in ELISAs. The amino acid composition of these peptides was then matched with clusters of residues on the surface of the 3-dimensional (3D) structure of Bla g 2, using our EpiSearch algorithm. Results: The amino acid sequences of the peptides on selected phages differed at only one position, occupied by 1 of 2 negatively charged residues. The two 12-mer sequences bound to 7C11 with similar avidity and specificity. There was good concordance between the residues in the 3D clusters identified from our phage display/computational method with the co-crystal structural analysis. Conclusion: Conformational epitopes may be mapped through screening of clones from random peptide phage display libraries and EpiSearch.

Serum TARC and CTACK concentrations in children with atopic dermatitis, allergic asthma, and urticaria

Thymus and activation-regulated chemokine (TARC/CCL17) and cutaneous T cell-attracting chemokine (CTACK/CCL27) belong to the CC chemokine family, which plays an important role in immune-inflammatory processes. It has been demonstrated that serum concentrations of TARC and CTACK are increased in patients with various allergic diseases. To compare serum TARC and CTACK concentrations between children with different clinical manifestation of mast cell-dependent diseases, such as atopic allergy and urticaria. A total of 87 children including 26 with mild to severe atopic dermatitis (AD), 43 children with controlled allergic asthma symptoms (treated and untreated with anti-inflammatory drugs), and 18 children with urticaria were recruited into the study. The control group consisted of 31 healthy non-atopic children. Serum concentrations of TARC and CTACK were significantly higher in children with AD than in healthy controls. No significant differences in serum concentrations of the chemokines between asthmatics, urticaria patients, and healthy controls were found. The severity of AD symptoms significantly correlated with serum CTACK and TARC concentrations. These findings, in conjunction with earlier data, indicate that differences may exist in circulating concentrations of TARC and CTACK, between patients with atopic allergy and urticaria.

Current Prospective of Aldose Reductase Inhibition in the Therapy of Allergic Airway Inflammation in Asthma

The prevalence of asthma and costs of its care have been continuously increasing, but novel therapeutic options to treat this inflammatory disease have not been brought to the US market. Current therapies such as inhaled steroids, long-acting beta-agonist bronchodilators, antihistamines and immunomodulators may control the symptoms of allergic asthma but fail to modify the underlying disease. Excessive use of steroids and other immunosuppresents alter the patient's quality of life, produce undesirable toxicities, and increase the risk of other pathologies such as diabetes. Hence novel therapeutic options to manage asthma are desirable. In the present review, we have discussed the role of the polyol pathway enzyme aldose reductase (AR) in the amplification of allergic airway inflammation. Recent studies have indicated that AR inhibition prevents the NF-κB-dependent generation of pro-inflammatory cytokines and chemokines in mouse models of allergic airway inflammation indicating the potential use of AR inhibition as a novel tool to control allergic responses. Since orally available AR inhibitors have already undergone phase III clinical trials for diabetic neuropathy and appear to have a manageable side effects profile, they could be readily developed as potential new drugs for the treatment of asthma and related complications.

Particulate allergens potentiate allergic asthma in mice through sustained IgE-mediated mast cell activation.

Allergic asthma is characterized by airway hyperresponsiveness, inflammation, and a cellular infiltrate dominated by eosinophils. Numerous epidemiological studies have related the exacerbation of allergic asthma with an increase in ambient inhalable particulate matter from air pollutants. This is because inhalable particles efficiently deliver airborne allergens deep into the airways, where they can aggravate allergic asthma symptoms. However, the cellular mechanisms by which inhalable particulate allergens (pAgs) potentiate asthmatic symptoms remain unknown, in part because most in vivo and in vitro studies exploring the pathogenesis of allergic asthma use soluble allergens (sAgs). Using a mouse model of allergic asthma, we found that, compared with their sAg counterparts, pAgs triggered markedly heightened airway hyperresponsiveness and pulmonary eosinophilia in allergen-sensitized mice. Mast cells (MCs) were implicated in this divergent response, as the differences in airway inflammatory responses provoked by the physical nature of the allergens were attenuated in MC-deficient mice. The pAgs were found to mediate MC-dependent responses by enhancing retention of pAg/IgE/FcεRI complexes within lipid raft–enriched, CD63(+) endocytic compartments, which prolonged IgE/FcεRI-initiated signaling and resulted in heightened cytokine responses. These results reveal how the physical attributes of allergens can co-opt MC endocytic circuitry and signaling responses to aggravate pathological responses of allergic asthma in mice.

Anti-inflammatory effects of ivermectin in mouse model of allergic asthma

Asthma is an inflammatory disease of the lungs that is characterised by increased inflammatory cell infiltration into the airways and poor respiratory function. Ivermectin is a semi-synthetic derivative of a family of macrocyclic lactones that shows broad-spectrum anti-parasitic activity. This drug has been shown to possess anti-inflammatory activity, but whether it can be used in asthma treatment has not yet been investigated. In this study, we aimed to investigate the inhibitory effects of ivermectin on allergic asthma symptoms in mice. We used a mouse asthma model, in which allergic airway inflammation and airway remodelling were induced by ovalbumin (OVA) sensitisation and challenge. Ivermectin or PBS treatment was administered 1 h before OVA challenge. Ivermectin at 2 mg/kg significantly diminished recruitment of immune cells, production of cytokines in the bronchoalveolar lavage fluids and secretion of OVA-specific IgE and IgG1 in the serum. Histological studies indicated that ivermectin suppressed mucus hypersecretion by goblet cells in the airway. This is the first study to demonstrate that ivermectin is an effective suppressor of inflammation and may be efficacious in the treatment of non-infectious airway inflammatory diseases such as allergic asthma.

Neutralisation of Interleukin-13 in Mice Prevents Airway Pathology Caused by Chronic Exposure to House Dust Mite

BackgroundRepeated exposure to inhaled allergen can cause airway inflammation, remodeling and dysfunction that manifests as the symptoms of allergic asthma. We have investigated the role of the cytokine interleukin-13 (IL-13) in the generation and persistence of airway cellular inflammation, bronchial remodeling and deterioration in airway function in a model of allergic asthma caused by chronic exposure to the aeroallergen House Dust Mite (HDM).Methodology/Principal FindingsMice were exposed to HDM via the intranasal route for 4 consecutive days per week for up to 8 consecutive weeks. Mice were treated either prophylactically or therapeutically with a potent neutralising anti-IL-13 monoclonal antibody (mAb) administered subcutaneously (s.c.). Airway cellular inflammation was assessed by flow cytometry, peribronchial collagen deposition by histocytochemistry and airway hyperreactivity (AHR) by invasive measurement of lung resistance (RL) and dynamic compliance (Cdyn). Both prophylactic and therapeutic treatment with an anti-IL-13 mAb significantly inhibited (P<0.05) the generation and maintenance of chronic HDM-induced airway cellular inflammation, peribronchial collagen deposition, epithelial goblet cell upregulation. AHR to inhaled methacholine was reversed by prophylactic but not therapeutic treatment with anti-IL-13 mAb. Both prophylactic and therapeutic treatment with anti-IL-13 mAb significantly reversed (P<0.05) the increase in baseline RL and the decrease in baseline Cdyn caused by chronic exposure to inhaled HDM.Conclusions/SignificanceThese data demonstrate that in a model of allergic lung disease driven by chronic exposure to a clinically relevant aeroallergen, IL-13 plays a significant role in the generation and persistence of airway inflammation, remodeling and dysfunction.

Prevalence of Chronic Nasal Symptoms in West Sweden: Risk Factors and Relation to Self-Reported Allergic Rhinitis and Lower Respiratory Symptoms

Background: There are few population-based studies on chronic nasal symptoms and little is known about their prevalence and determinants, or their association with allergic rhinitis and asthma. Methods: A questionnaire focused on respiratory symptoms and conditions was mailed in 2008 to 30,000 randomly selected subjects aged 16–75 years in West Sweden, 29,218 could be traced and 18,087 (62%) responded. The questionnaire included questions on self-reported allergic rhinitis, asthma, lower respiratory and nasal symptoms and possible determinants. Results: Nasal congestion was reported by 14.9% and runny nose by 13.1% of subjects. In total, 19.8% had chronic nasal symptoms. Subjects with chronic nasal symptoms had considerably more symptoms from the lower airways compared with nonrhinitic subjects and vice versa. Forty-seven percent of the subjects with chronic nasal symptoms had concurrent self-reported allergic rhinitis. Several hereditary and environmental factors were associated with chronic rhinitis, including family history of asthma [odds ratio (OR) 1.27; 95% confidence interval 1.07–1.50], family history of allergy (OR 1.74; 1.57–1.92) and current smoking (OR 1.39; 1.25–1.54). Further, chronic nasal symptoms were increasingly prevalent with an increasing degree of urbanization. Conclusion: The prevalence of chronic nasal symptoms in West Sweden was found to be high and strongly associated both with self-reported allergic rhinitis and symptoms from the lower airways. Moreover, several risk factors were identified for chronic nasal symptoms, including family history of allergy and asthma and smoking.

The costs and consequences of omalizumab in uncontrolled asthma from a USA payer perspective

Omalizumab, an anti-immunoglobulin E antibody, reduces exacerbations and symptoms in uncontrolled allergic asthma. The study objective was to estimate the costs and consequences of omalizumab compared to usual care from a US payer perspective. We estimated payer costs, quality-adjusted survival (QALYs), and the incremental cost-effectiveness ratio (ICER) of omalizumab compared to usual care using a state-transition simulation model that included sensitivity analyses. Every 2 weeks, patients could transition between chronic asthma and exacerbation health states. The best available evidence informed the clinical and cost input estimates. Five years of omalizumab treatment followed by usual care was assumed to estimate a lifetime horizon. Omalizumab responders (60.5% of treated) were modeled as a separate scenario where nonresponders reverted back to usual care after 16 weeks of active treatment. The mean lifetime discounted costs and QALYs were $83,400 and 13.87 for usual care and $174,500 and 14.19 for omalizumab plus usual care resulting in $287 200/QALY (95% interval: $219,300, $557, 900). The ICER was $172 300/QALY when comparing omalizumab to usual care in the responder scenario. One-way sensitivity analyses indicated that the results were sensitive to the difference in treatment-specific utilities for the chronic state, exacerbation-associated mortality, omalizumab price, exacerbation rates, and response definition. The results suggest that adding omalizumab to usual care improves QALYs at an increase in direct medical costs. The cost-effectiveness of omalizumab is similar to other chronic disease biologics. The value increases when omalizumab response is used to guide long-term treatment.

The absence of the VPAC 2 receptor does not protect mice from Aspergillus induced allergic asthma

Allergic asthma is a T H2-mediated disease marked by airway inflammation, increased mucus production, and elevated serum IgE in response to allergen provocation. Among its ascribed functions, the neuropeptide vasoactive intestinal peptide (VIP) is believed to promote a T H2 phenotype when signaling through its VPAC 2 receptor. In this study, we assessed the requirement for the VIP/VPAC 2 axis in initiating the allergic pulmonary phenotype in a murine model of fungal allergic asthma. C57BL/6 wild-type (WT) and VPAC 2 knock-out (KO) mice were sensitized with Aspergillus fumigatus antigen and challenged with an aerosol of live conidia to induce allergic airways disease. WT and KO mice exhibited similar peribronchovascular inflammation, increased number of goblet cells, and elevated serum IgE. However, the absence of VPAC 2 receptor resulted in a marked enhancement of MUC5AC mRNA with an associated increase in goblet cells and a reduction in eosinophils in the airway lumen at day 3 when VIP mRNA was undetectable in the KO lung. Sustained elevation of serum IgE was noted in KO mice at day 14, while the level in WT mice declined at this time point. These data suggest that the absence of VPAC 2 does not protect mice from developing the signs and symptoms of allergic asthma.

A standardized aqueous extract of Anoectochilus formosanus modulated airway hyperresponsiveness in an OVA-inhaled murine model

Anoectochilus formosanus HAYATA, a Chinese herb, is a valued folk medicine for fever, pain, and diseases of the lung and liver. Allergic asthma is characterized by increased serum IgE level and inflammation of the airways with high levels of interleukin (IL)-4 and IL-5 in bronchoalveolar lavage fluids (BALF). Constriction of airway smooth muscle and development of airway hyperresponsiveness (AHR) are the most important symptoms of allergic asthma. In our previous study, a standardized aqueous extract of A. formosanus (SAEAF) was used to modulate innate immunity of normal mice. In this study, airway inflammatory infiltrations, including T cell differentiation, cytokine modulation, allergic antibodies estimation, pulmonary pathology, and enhanced pause (Penh) of AHR were used to evaluate SAEAF treatment of an ovalbumin (OVA)-inhaled airway allergic murine model. The resulting cytokine profiles demonstrated that SAEAF can significantly reduce Th2 polarization after administration of SAEAF in OVA inhalation. These results also suggest that SAEAF modulates cytokine secretion in allergic asthma. Modulated natural T regulatory cells (CD25+/CD4+, Treg) were also shown to increase immuno-suppression in the allergic lung inflammation and further down-regulate airway inflammatory infiltration in eosinophils and macrophages. Finally, decreased airway anti-OVA IgE secretion and reduced AHR were observed. Our results indicate that the administration of SAEAF can modulate cytokines and T cell subpopulation by regulating inflammatory cell infiltration and modulating the allergic response.

Stability evaluation of house dust mite vaccines for sublingual immunotherapy

Allergen-specific immunotherapy with house dust mite (HDM) allergen extracts can effectively alleviate the symptoms of allergic rhinitis and asthma. The efficacy of the immunotherapeutic treatment is highly dependent on the quality of house dust mite vaccines. This study was performed to assess the stability of house dust mite allergen vaccines prepared for sublingual immunotherapy. Lyophilized Dermatophagoides pteronyssinus (Dpt) mite bodies were the starting material for the production of sublingual vaccines in four therapeutic concentrations. The stability of the extract for vaccine production, which was stored below 4 ?C for one month, showed consistence in the protein profile in SDS PAGE. ELISA-inhibition showed that the potencies of Dpt vaccines during a 12 month period were to 65-80 % preserved at all analyzed therapeutic concentrations. This study showed that glycerinated Dpt vaccines stored at 4?C preserved their IgE-binding potential during a 12 month period, implying their suitability for sublingual immunotherapeutic treatment of HDM allergy.

Concentration of IgE in children during ragweed pollination season

Genetic and environmental factors are responsible for running allergic diseases. The aim of this study was to compare the values of total- (t-IgE) and allergen-specific IgE (s-IgE) to Ambrosia artemisiifolia L. (Amb a) in children with sensitization to Amb a during ragweed pollination season, who experienced seasonal symptoms of allergic rhinitis (rhinorrhea, post-nasal drip, nasal congestion, itching, sneezing) and asthma (coughing, especially at night, wheezing, shortness of breath, chest tightness). Ragweed pollen grains were collected in Virovitica (rural area) and Zagreb (urban area)—cities with the same geographical width and elevation—during ragweed pollination seasons (July–October in 2006 and 2007), and their count was estimated. Concentration of t-IgE and s-IgE in pollination season was determined in serum of children with symptoms of allergic diseases. The total count of ragweed pollen grains (PG) differed significantly between Virovitica and Zagreb in both years, 2006. and 2007. In Virovitica it was significantly greater than in Zagreb. There was no statistically significant seasonal difference in both, t-IgE and s-IgE, respectively. No correlation was found between pollen grain count and the concentration of IgE’s. To clarify the induction of IgE synthesis in children with sensitization to Amb a, further studies are needed.

The frequency of self-reported allergic diseases in patients with crimean-congo haemorrhagic fever

Background Crimean-Congo haemorrhagic fever (CCHF) is an acute, tick-borne viral disease. In temperate areas, CCHF cases occur between spring and early autumn when tick activity is high. This period is also the pollen season during which symptoms of allergic diseases are exacerbated. Viruses induce inflammatory and antiviral responses by binding to specific receptors on the surface of airway epithelial cells, resulting in activation of innate immune responses; release of mediators such as cytokines and chemokines; and recruitment of neutrophils and mononuclear cells to the area. Aim We aimed to evaluate the frequency of self-reported allergic diseases and the effect on CCHF severity. Method Between June and August 2008, a questionnaire was applied to 114 CCHF (+) patients and 122 healthy control subjects, 16 to 88 years old who attended the Infectious Diseases clinic and were hospitalised with CCHF suspected, by face to face interview including history of allergic rhinitis (AR), asthma symptoms and nonspecific bronchial reactivity, doctor diagnosed AR and/or asthma, and familial allergic diseases history. Results According to PCR and/or enzyme-linked immunoassay (ELISA) results, 51.7% of patients (n=114) had CCHF. There was no significant relation between CCHF and history of AR, asthma symptoms and nonspecific bronchial reactivity, doctor diagnosed AR and/or asthma, and familial allergic diseases history. The severity of CCHF has not affected these parameters (p>.05). Of patients with positive CCHF test, 2.6% (n=3) and 3.5% (n=4) had doctor diagnosed AR and asthma, respectively. Conclusion Self-reported allergic diseases and CCHF are not related with each other.