Immediate Hypersensitivity Research Articles

Estimating emissions from open burning of municipal solid waste in municipalities of Nepal

Open burning of municipal solid waste (MSW) is a poorly-characterized and frequently-underestimated source of air pollution in developing countries. This paper estimates the quantity of MSW that was burned in five erstwhile municipalities of the Kathmandu valley, Nepal. A household survey, a transect walk survey, an experiment to measure the fraction of waste that is combustible, a survey on fraction of population burning waste outside their houses, and a survey of the fraction of MSW burned at dump sites were performed in this study, whereas burning/oxidation efficiency, municipal populations, MSW generation rates, and emission factors were derived from the literature. The total mass of MSW burned during 2016 is estimated to be 7400 tons (i.e., 20 tons/day), which was of 3% of the total MSW generated in the valley municipalities that year. This exceeds Government estimates by a factor of three. Multiplying the burned MSW mass by emission factors, the air pollutant emissions are estimated as PM2.5 55 tons (OC 42 tons and EC 1.4 tons), PM10 60 tons, BC 25 tons, CO2 11,900 tons, CH4 30 tons, SO2 5.0 tons, NOx 19.2 tons, CO 630 tons, NMVOC 112 tons, and NH3 5.7 tons per year. Open burning of MSW can trigger health impacts such as acute and chronic respiratory disease, heart diseases, and allergic hypersensitivity, in addition to impacts on local climate. Improved waste-segregation practices at the source and waste-collection systems throughout the valley are needed to mitigate this pollution source and its effects.

Assessment of otological and audiological status in patients of allergic rhinitis

<p class="abstract"><strong>Background:</strong> Allergic rhinitis (AR) is a type-I hypersensitivity reaction of the nasal mucosa to the airborne allergens, primarily mediated by immunoglobulin E (IgE) characterized by nasal obstruction, watery rhinorrhea, sneezing and itching at the nose, palate and nasopharyngeal region. Various studies have been done to study the relationship between middle ear afflictions and allergic rhinitis and majority of them incriminate nasal allergies as a probable factor to the development of otitis media.</p><p class="abstract"><strong>Methods:</strong> A total of 70 patients, affected by allergic rhinitis, were recruited for the study after fulfilling the inclusion and exclusion criteria. Complete audiological work up including tympanometry studies was performed. Patients’ data was then compiled and analyzed using statistical analyses. </p><p class="abstract"><strong>Results:</strong> It was observed that disease is more common in age group of 21 to 30 years. 63% patient had perennial allergic rhinitis and rest 37% had seasonal allergic rhinitis. Otoscopic examination of the participants revealed that abnormal tympanic membrane findings such as retracted, congested, bulged and dull TM is more common in PAR than SAR. Hearing impairment is more common in PAR than SAR. Tympanometry study showed that in PAR ‘B’ type of tympanogram was found in 20% cases and ‘C’ type curve was found in 19% cases while in SAR these value were 4% and 8% respectively.</p><p class="abstract"><strong>Conclusions:</strong> Allergic rhinitis whether seasonal or perennial adversely affect the eustachian tube functions which in turn may lead to increased incidence of middle ear effusion and otitis media. Diagnosis and proper management of allergic rhinitis is the key to avoid these middle ear diseases.</p>

Epigenome-wide association study of total serum immunoglobulin E in children: a life course approach

BackgroundIgE-mediated sensitization may be epigenetically programmed in utero, but early childhood environment may further alter complex traits and disease phenotypes through epigenetic plasticity. However, the epigenomic footprint underpinning IgE-mediated type-I hypersensitivity has not been well-understood, especially under a longitudinal early-childhood life-course framework.MethodsWe used epigenome-wide DNA methylation (IlluminaHumanMethylation450 BeadChip) in cord blood and mid-childhood peripheral blood to investigate pre- and post-natal methylation marks associated with mid-childhood (age 6.7–10.2) total serum IgE levels in 217 mother-child pairs in Project Viva—a prospective longitudinal pre-birth cohort in eastern Massachusetts, USA. We identified methylation sites associated with IgE using covariate-adjusted robust linear regressions.ResultsNineteen methylation marks in cord blood were associated with IgE in mid-childhood (FDR < 0.05) in genes implicated in cell signaling, growth, and development. Among these, two methylation sites (C7orf50, ZAR1) remained robust after the adjustment for the change in DNA methylation from birth to mid-childhood (FDR < 0.05). An analysis of the change in methylation between cord blood and mid-childhood DNA (Δ-DNAm) identified 395 methylation marks in 272 genes associated with mid-childhood IgE (FDR < 0.05), with multiple sites located within ACOT7 (4 sites), EPX (5 sites), EVL (3 sites), KSR1 (4 sites), ZFPM1 (3 sites), and ZNF862 (3 sites). Several of these methylation loci were previously associated with asthma (ADAM19, EPX, IL4, IL5RA, and PRG2).ConclusionThis study identified fetally programmed and mid-childhood methylation signals associated with mid-childhood IgE. Epigenetic priming during fetal development and early childhood likely plays an important role in IgE-mediated type-I hypersensitivity.

Aspergillus fumigatus-sensitive IgE is associated with bronchial hypersensitivity in a murine model of neutrophilic airway inflammation

Neutrophils are the predominant inflammatory cells that infiltrate airways during acute exacerbation of asthma. The importance of A.fumigatus sensitization, and IgE response in the airways in patients with acute asthma is unclear. Rockefeller (RK) mice were sensitized with A.fumigatus extract protein. The animals were subsequently challenged with different degrees of A.fumigatus contamination in the cage bedding. All groups of mice were euthanized to obtain bronchoalveolar lavage fluid (BALF) for cytological and Elisa assays, and lung tissue for histological analysis. Moreover, several bioassays were conducted to determine whether BALF IgE antibodies can activate mast cells. In this study, we demonstrated that exposure of sensitized mice to a known concentration of A.fumigatus conidia produces bronchial hyperreactivity with marked neutrophilic bronchial infiltration and increased BALF IgE, capable of triggering mast cell degranulation. This study suggests that IgE may play a role in bronchial hyperreactivity associated to A.fumigatus exposure in mice. Mice sensitized and challenged with this fungus showed characteristics of severe asthma, with an increase of BALF neutrophils, histological changes consistent with severe asthma and an increase of IgE capable of triggering typeI hypersensitivity.

Calls to Poison Centers for hookah smoking exposures

Over the past decade, smoking behaviors have changed in the US. Hookah or waterpipe smoking is increasing, especially among youth and young adults. Social media sites describe the “hookah high” or “buzz”, which may be related to nicotine, carbon monoxide, or other inhalants in hookah smoke. Most important is the risk of carbon monoxide poisoning. Case reports include a high number of victims presenting with loss of consciousness from either syncope or seizures. Anaphylaxis and a very rare respiratory hypersensitivity reaction, acute eosinophilic pneumonia, have also been reported from hookah smoking in previously healthy young adults. This article provides background information on hookah smoking, describes hookah-induced acute injuries that could precipitate poison center calls, and offers suggestions for exposure characterization.

Bronchiolitis: A Practical Approach for the General Radiologist.

Radiologists consciously or unconsciously encounter bronchiolitis on images frequently. The purpose of this article is to simplify the concept of bronchiolitis to facilitate the formulation of a succinct and accurate differential diagnosis and suggest potential causes for the imaging findings. Direct and indirect signs of bronchiolitis that are seen on computed tomographic images are detailed. The most common causes of bronchiolitis are covered, including several distinct entities to be considered in specific clinical scenarios. In order of prevalence, the top two causes of bronchiolitis are infection and aspiration. Less common entities include respiratory bronchiolitis and hypersensitivity pneumonitis, which tend to manifest with ground-glass centrilobular nodules. Some types of bronchiolitis affect specific ethnic groups or are associated with a characteristic clinical history. For example, diffuse panbronchiolitis typically affects Japanese subjects. Constrictive bronchiolitis should be considered in lung transplant recipients with ongoing rejection. Given the high frequency of bronchiolitis, radiologists should develop a systematic approach to both cellular and constrictive bronchiolitis. Recognition of specific clinical or imaging characteristics may be sufficient for providing a relevant differential diagnosis. ©RSNA, 2017.

Improving Allergen Prediction in Main Crops Using a Weighted Integrative Method.

As a public health problem, food allergy is frequently caused by food allergy proteins, which trigger a type-I hypersensitivity reaction in the immune system of atopic individuals. The food allergens in our daily lives are mainly from crops including rice, wheat, soybean and maize. However, allergens in these main crops are far from fully uncovered. Although some bioinformatics tools or methods predicting the potential allergenicity of proteins have been proposed, each method has their limitation. In this paper, we built a novel algorithm PREALW, which integrated PREAL, FAO/WHO criteria and motif-based method by a weighted average score, to benefit the advantages of different methods. Our results illustrated PREALW has better performance significantly in the crops' allergen prediction. This integrative allergen prediction algorithm could be useful for critical food safety matters. The PREALW could be accessed at http://lilab.life.sjtu.edu.cn:8080/prealw .

Respiratory hypersensitivity reactions to NSAIDs in Europe: the global allergy and asthma network (GA2 LEN) survey.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most prevalent drugs inducing hypersensitivity reactions. The aim of this analysis was to estimate the prevalence of NSAID-induced respiratory symptoms in population across Europe and to assess its association with upper and lower respiratory tract disorders. The GA2 LEN survey was conducted in 22 centers in 15 European countries. Each of 19 centers selected random samples of 5000 adults aged 15-74 from their general population, and in three centers (Athens, Munich, Oslo), a younger population was sampled. Questionnaires including questions about age, gender, presence of symptoms of asthma, allergic rhinitis, chronic rhinosinusitis, smoking status, and history of NSAID-induced hypersensitivity reactions were sent to participants by mail. Totally, 62 737 participants completed the questionnaires. The mean prevalence of NSAID-induced dyspnea was 1.9% and was highest in the three Polish centers [Katowice (4.9%), Krakow (4.8%), and Lodz (4.4%)] and lowest in Skopje, (0.9%), Amsterdam (1.1%), and Umea (1.2%). In multivariate analysis, the prevalence of respiratory reactions to NSAIDs was higher in participants with chronic rhinosinusitis symptoms (Odds Ratio 2.12; 95%CI 1.78-2.74), asthma symptoms in last 12 months (2.7; 2.18-3.35), hospitalization due to asthma (1.53; 1.22-1.99), and adults vs children (1.53; 1.24-1.89), but was not associated with allergic rhinitis. Our study documented significant variation between European countries in the prevalence of NSAID-induced respiratory hypersensitivity reactions, and association with chronic airway diseases, but also with environmental factors.

Food Allergy and Intolerance : Distinction, Definitions and Delimitation

Immunologically mediated hypersensitivity to foods is defined as food allergy, mainly due to immunglobulins of classE (IgE) triggering immediate reactions (typeI hypersensitivity) with possible involvement of mucosa, skin, airways, intestinal tract, and the vascular system. Primary food allergy is based on (early) IgE sensitization against animal (e. g., cow's milk, hen's eggs) or plant proteins (e. g. peanut, hazelnut or wheat). In the case of secondary food allergies, IgE against pollen proteins (e. g., birch) reacts to structurally related food proteins (with cross-reactions to stone and pit fruits). Non-immunological food intolerance reactions are mostly based on carbohydrate malassimilation (e. g., lactose intolerance, fructose malabsorption) and are rarely due to pseudo-allergies (e. g., flavors, dyes, preservatives) primarily in patients with chronic urticaria. Common intestinal symptoms are mainly due to functional disorders (e. g., irritable bowel disease), rarely because of inflammatory intestinal diseases (e. g., celiac disease). Histamine intolerance, gluten hypersensitivity, and so-called food typeIII hypersensitivities are controversial diagnoses. The aforementioned disease entities/models are of variable importance for the affected individuals, the public health system, and society in general.

Histone Modifications in a Mouse Model of Early Adversities and Panic Disorder: Role for Asic1 and Neurodevelopmental Genes.

Hyperventilation following transient, CO2-induced acidosis is ubiquitous in mammals and heritable. In humans, respiratory and emotional hypersensitivity to CO2 marks separation anxiety and panic disorders, and is enhanced by early-life adversities. Mice exposed to the repeated cross-fostering paradigm (RCF) of interference with maternal environment show heightened separation anxiety and hyperventilation to 6% CO2-enriched air. Gene-environment interactions affect CO2 hypersensitivity in both humans and mice. We therefore hypothesised that epigenetic modifications and increased expression of genes involved in pH-detection could explain these relationships. Medullae oblongata of RCF- and normally-reared female outbred mice were assessed by ChIP-seq for H3Ac, H3K4me3, H3K27me3 histone modifications, and by SAGE for differential gene expression. Integration of multiple experiments by network analysis revealed an active component of 148 genes pointing to the mTOR signalling pathway and nociception. Among these genes, Asic1 showed heightened mRNA expression, coherent with RCF-mice’s respiratory hypersensitivity to CO2 and altered nociception. Functional enrichment and mRNA transcript analyses yielded a consistent picture of enhancement for several genes affecting chemoception, neurodevelopment, and emotionality. Particularly, results with Asic1 support recent human findings with panic and CO2 responses, and provide new perspectives on how early adversities and genes interplay to affect key components of panic and related disorders.

Exposure and Health Effects of Fungi on Humans

Fungi are ubiquitous microorganisms that are present in outdoor and indoor environments. Previous research has found relationships between environmental fungal exposures and human health effects. We reviewed recent articles focused on fungal exposure and dampness as risk factors for respiratory disease development, symptoms, and hypersensitivity. In particular, we reviewed the evidence suggesting that early exposure to dampness or fungi is associated with the development of asthma and increased asthma morbidity. Although outdoor exposure to high concentrations of spores can cause health effects such as asthma attacks in association with thunderstorms, most people appear to be relatively unaffected unless they are sensitized to specific genera. Indoor exposure and dampness, however, appears to be associated with an increased risk of developing asthma in young children and asthma morbidity in individuals who have asthma. These are important issues because they provide a rationale for interventions that might be considered for homes and buildings in which there is increased fungal exposure. In addition to rhinitis and asthma, fungus exposure is associated with a number of other illnesses including allergic bronchopulmonary mycoses, allergic fungal sinusitis, and hypersensitivity pneumonitis. Additional research is necessary to establish causality and evaluate interventions for fungal- and dampness-related health effects.

Management of tinea corporis, tinea cruris, and tinea pedis: A comprehensive review.

The prevalence of superficial mycotic infection worldwide is 20–25% of which dermatophytes are the most common agents. Recent developments in understanding the pathophysiology of dermatophytosis have confirmed the central role of cell-mediated immunity in countering these infections. Hence, a lack of delayed hypersensitivity reaction in presence of a positive immediate hypersensitivity (IH) response to trichophytin antigen points toward the chronicity of disease. Diagnosis, though essentially clinical should be confirmed by laboratory-based investigations. Several new techniques such as polymerase chain reaction (PCR) and mass spectroscopy can help to identify the different dermatophyte strains. Management involves the use of topical antifungals in limited disease, and oral therapy is usually reserved for more extensive cases. The last few years have seen a significant rise in the incidence of chronic dermatophyte infections of skin which have proven difficult to treat. However, due to the lack of updated national or international guidelines on the management of tinea corporis, cruris, and pedis, treatment with systemic antifungals is often empirical. The present review aims to revisit this important topic and will detail the recent advances in the pathophysiology and management of tinea corporis, tinea cruris, and tinea pedia while highlighting the lack of clarity of certain management issues.

Chemical determinants of occupational hypersensitivity pneumonitis

Workplace inhalational exposures to low molecular weight (LMW) chemicals cause hypersensitivity pneumonitis (HP) as well as the more common manifestation of respiratory hypersensitivity, occupational asthma (OA). To explore whether chemical causation of HP is associated with different structural and physico-chemical determinants from OA. Chemical causes of human cases of HP and OA were identified from searches of peer-reviewed literature up to the end of 2011. Each chemical was categorized according to whether or not it had been the attributed cause of at least one case of HP. The predicted asthma hazard was determined for each chemical using a previously developed quantitative structure-activity relationship (QSAR) model. The chemicals in both sets were independently and 'blindly' analysed by an expert in mech anistic chemistry for a qualitative prediction of protein cross-linking potential and determination of lipophilicity (log K ow). Ten HP-causing chemicals were identified and had a higher median QSAR predicted asthma hazard than the control group of 101 OA-causing chemicals (P < 0.01). Nine of 10 HP-causing chemicals were predicted to be protein cross-linkers compared with 24/92 controls (P < 0.001). The distributions of log K ow indicated higher values for the HP list (median 3.47) compared with controls (median 0.81) (P < 0.05). These findings suggest that chemicals capable of causing HP tend to have higher predicted asthma hazard, are more lipophilic and are more likely to be protein cross-linkers than those causing OA.

Bronchial asthma: the possible role of the chemical mediators of immediate hypersensitivity in the pathogenesis of subacute chronic disease.

Bronchial asthma: the possible role of the chemical mediators of immediate hypersensitivity in the pathogenesis of subacute chronic disease.

Thresholds in chemical respiratory sensitisation

There is a continuing interest in determining whether it is possible to identify thresholds for chemical allergy. Here allergic sensitisation of the respiratory tract by chemicals is considered in this context. This is an important occupational health problem, being associated with rhinitis and asthma, and in addition provides toxicologists and risk assessors with a number of challenges. In common with all forms of allergic disease chemical respiratory allergy develops in two phases. In the first (induction) phase exposure to a chemical allergen (by an appropriate route of exposure) causes immunological priming and sensitisation of the respiratory tract. The second (elicitation) phase is triggered if a sensitised subject is exposed subsequently to the same chemical allergen via inhalation. A secondary immune response will be provoked in the respiratory tract resulting in inflammation and the signs and symptoms of a respiratory hypersensitivity reaction. In this article attention has focused on the identification of threshold values during the acquisition of sensitisation. Current mechanistic understanding of allergy is such that it can be assumed that the development of sensitisation (and also the elicitation of an allergic reaction) is a threshold phenomenon; there will be levels of exposure below which sensitisation will not be acquired. That is, all immune responses, including allergic sensitisation, have threshold requirement for the availability of antigen/allergen, below which a response will fail to develop. The issue addressed here is whether there are methods available or clinical/epidemiological data that permit the identification of such thresholds. This document reviews briefly relevant human studies of occupational asthma, and experimental models that have been developed (or are being developed) for the identification and characterisation of chemical respiratory allergens. The main conclusion drawn is that although there is evidence that the acquisition of sensitisation to chemical respiratory allergens is a dose-related phenomenon, and that thresholds exist, it is frequently difficult to define accurate numerical values for threshold exposure levels. Nevertheless, based on occupational exposure data it may sometimes be possible to derive levels of exposure in the workplace, which are safe. An additional observation is the lack currently of suitable experimental methods for both routine hazard characterisation and the measurement of thresholds, and that such methods are still some way off. Given the current trajectory of toxicology, and the move towards the use of non-animal in vitro and/or in silico) methods, there is a need to consider the development of alternative approaches for the identification and characterisation of respiratory sensitisation hazards, and for risk assessment.

Management of patients with nonaspirin-exacerbated respiratory disease aspirin hypersensitivity reactions.

Because of widespread use, nonsteroidal anti-inflammatory drugs (NSAIDs) are the second most common cause of all adverse drug reactions, with hypersensitivity reported in ∼1% of the population. NSAID hypersensitivity can be categorized into five types by the underlying disease, symptoms of reaction, and timing of reaction. These include rhinitis and asthma induced by NSAIDs (also known as aspirin-exacerbated respiratory disease), NSAID-exacerbated cutaneous disease (NECD), urticaria or angioedema induced by multiple NSAIDs, single NSAID-induced reactions, and delayed NSAID reactions. NECD occurs in one-third of patients with chronic urticaria who develop an exacerbation of their urticaria, sometimes with angioedema, typically beginning 30-90 minutes after ingestion of NSAIDs that inhibit cyclooxygenase (COX)-1. In urticaria or angioedema induced by multiple NSAIDs, patients without underlying disease develop urticaria or angioedema 30-90 minutes after ingestion of COX-1-inhibiting NSAIDs including aspirin. Single NSAID-induced reactions are immediate and specific to a single NSAID and are thought to occur because of an IgE-mediated reaction against a specific epitope of the NSAID. Delayed NSAID reactions occur days to weeks after initiating an NSAID. These are T-cell mediated and not amenable to desensitization or rechallenge. Classifying the type of NSAID hypersensitivity is important because many patients with a prior history of urticaria or angioedema induced by multiple NSAIDs will often tolerate aspirin test dose. This would allow the use of an aspirin for primary or secondary prevention in patients with coronary artery disease despite a presumed history of NSAID hypersensitivity.

IL-4 and IL-5 Secretions Predominate in the Airways of Wistar Rats Exposed to toluene Diisocyanate Vapor

Objectives We established a Wistar rat model of asthma caused by TDI exposure, and investigated the relationship between TDI exposure concentrations and respiratory hypersensitivity, airway inflamm...

Protective immunotherapy against seasonal allergy in horses (834.2)

The study objective was to evaluate the effectiveness of active and passive immunotherapy in horses affected with recurrent airway obstruction (RAO), using a newly developed peptide and antibodies to the peptide. This peptide is part of an endogenous protein and has a sequence homology to some common environmental allergens. RAO is a type‐I immediate hypersensitivity response involving reaginic antibodies (IgE and IgG), and is a model for human asthma. Our hypothesis is that a protective immune response to asthma can be induced by active vaccination or by passive immunotherapy. Five RAO‐affected horses with a history of seasonal RAO, transpulmonary pressure &gt;15 cm of H2O, and a clinical score (CS) of 5 and above were selected. Either of the two doses of the antibody, 0.1 mg/kg or 0.2 mg/kg, was administered subcutaneously to 2 horses each. A third dose 0.3 mg/kg was given to the fifth horse. The peptide (0.1 mg/kg) was used to vaccinate two additional RAO‐horses. After closely watching them for 2 days, they were returned to the pasture. Blood samples were collected on day 0 (pre‐immune sample), day 1 and every 7th day for two months along with clinical scores. A dose related decrease in CS was observed in horses that received antibodies. The serum antibody titer was below detection levels by ELISA. The vaccinated horses showed significant protective antibody titer when the season arrived. The study suggests that protective immunotherapy early in the season has some therapeutic potential for RAO‐affected horses.Grant Funding Source: Supported by EHSP, LSU‐SVM

IL-4 and IL-5 Secretions Predominate in the Airways of Wistar Rats Exposed to Toluene Diisocyanate Vapor

ObjectivesWe established a Wistar rat model of asthma caused by toluene diisocyanate (TDI) exposure, and investigated the relationship between TDI exposure concentrations and respiratory hypersensitivity, airway inflammation, and cytokine secretions in animals, to better understand the mechanism of TDI induced occupational asthma.MethodsWistar rats were exposed to two different concentrations of TDI vapor four hours a day for five consecutive days. Bronchoalveolar lavage (BAL) was performed, and differential leucocytes from the BAL fluid were analyzed. Lung histopathological examination was carried out to investigate the inflammatory status in the airways. Production of cytokines interleukin (IL)-4 and IL-5 productions in the BAL fluid in vivo was determined with enzyme-linked immunosorbent assay kits.ResultsThe TDI-exposed rats exhibited greater airway hypersensitivity symptoms than the control rats. The BAL differential cell count and lung histopathological examination demonstrated that inflammation reactions were present in both the central and peripheral airways, characterized with marked infiltration of eosinophils in the TDI-exposed rats. The cytokine assay showed that IL-4 and IL-5 were predominantly produced in the BAL fluid in vivo.ConclusionsThese findings imply that TDI exposure concentrations may greatly affect the occurrence and extent of inflammatory events and that Th2 type cytokines may play an important role in the immunopathogenesis of TDI-induced occupational respiratory hypersensitivity.

Immunity in dermatophyte infection

Immune responses to dermatophyte infection include both innate and adaptive immune response,and the adaptive immune response involves both humoral and cellular immune response.Both keratinocytes,which express a variety of pattern recognition receptors,and neutrophils,which exert antifungal activity inside and outside cells via phagocytosis and oxidization products (such as superoxide anion) in respiration burst,are involved in the innate immune response.The predominance of cellular or humoral immune response determines the clinical manifestations and outcomes of dermatophyte infection,which may spontaneously heal or become chronic.The currently accepted view is that cell-mediated immune response is responsible for the control of dermatophytosis.Moreover,Trichophyton may serve as an antigen with distinct immune capabilities to induce immediate hypersensitivity (IH) or delayed-type hypersensitivity (DTH) in different individuals. Key words: Dermatomycoses; Immunity ; Infection