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PubMed1997

High prevalence of allergic sensitization in children with habitual snoring and obstructive sleep apnea.

STUDY OBJECTIVE: To determine whether allergic sensitization occurs frequently in children with habitual snoring and whether allergy predicts the occurrence of obstructive sleep apnea syndrome (OSAS) in snoring children. DESIGN: Prospective study of 39 children with habitual snoring who were referred for polysomnography. SETTING: Pediatric pulmonary sleep disorders clinic in a tertiary referral center. MEASUREMENTS: Subjects underwent a complete history and physical examination. To assess for the presence of allergic sensitization, a multiantigen radioallergosorbent test (RAST) was performed on serum samples. Subjects then underwent nocturnal polysomnography to determine the presence and severity of OSAS. RESULTS: Fourteen subjects (36%) demonstrated sensitivity to allergens; this is higher than expected for the general pediatric population. The frequency of OSAS was increased in subjects with positive RAST results compared to those with negative RAST results (57% vs 40%; chi 2 = 9.11; p < 0.01). CONCLUSION: Allergy is frequently present in pediatric patients with habitual snoring. Furthermore, the presence of allergy is associated with an increased risk of OSAS in this population.

Child↗
PubMed2001

Allergic sensitization and diet: ecological analysis in selected European cities.

It has been postulated that the prevalence of atopic diseases and their increase over time are associated with regional differences in diet and trends. The results of an ecological correlation study comparing the mean daily intake of selected dietary constituents and the prevalence of allergic sensitization in adults in Europe is presented. Prevalence data from the European Community Respiratory Health Survey (ECRHS) were used. For eight out of 37 ECRHS centres (including 3,872 subjects), comparable dietary data could be obtained. The effect for each dietary constituent was modelled using logistic regression analyses with a term for over dispersion. Inverse associations between the prevalence of allergic sensitization and the energy adjusted intake of fruit were found (odds ratio (OR) = 0.68, p = 0.034). Furthermore OR for energy adjusted intake of vitamin A (OR = 0.73, p = 0.057), vitamin C (OR = 0.83, p = 0.338) and riboflavin (OR = 0.72, p = 0.077) were consistently < 1, but confidence intervals were wider. Daily intake of monounsaturated fatty acids (energy adjusted) was positively associated with sensitization prevalence (OR = 1.59, p = 0.035). These results support the hypothesis that a high intake of monounsaturated fatty acids might promote the development of allergic sensitization.

Antioxidants↗
PubMed2000

Respiratory syncytial virus (RSV)-induced airway hyperresponsiveness in allergically sensitized mice is inhibited by live RSV and exacerbated by formalin-inactivated RSV.

Respiratory syncytial virus (RSV)-induced disease is associated with recurrent episodes of wheezing in children, and an effective vaccine currently is not available. The use of 2 immunizations (a formalin-inactivated, alum-precipitated RSV vaccine [FI-RSV] given intramuscularly and live RSV given intranasally [LVIN]), with a control immunization, were compared in a well-characterized model of RSV challenge, with or without concomitant allergic sensitization with ovalbumin. FI-RSV caused a significant increase in airway hyperresponsiveness in mice after RSV infection during allergic sensitization, and this was associated with an increase in type 2 cytokine production. In contrast, immunization with LVIN did not change type 2 cytokine production and protected against RSV-induced airway hyperresponsiveness in the setting of allergic sensitization. This study suggests that immune modulation with RSV vaccination can have profound effects on RSV-induced airway disease and that prevention of airway hyperresponsiveness is an important end point in vaccine development.

Administration, Intranasal↗
PubMed1992

SO2-induced enhancement of inhalative allergic sensitization: inhibition by anti-inflammatory treatment.

Epidemiological studies have shown a relationship between air pollution and allergic airway disease. In a previous study we have found that exposure to SO2 enhances allergic sensitization to inhaled ovalbumin (OA) in the guinea pig. We have now investigated the influence of pre-treatment with anti-inflammatory drugs on SO2-induced enhancement of allergic sensitization in this model. Four groups of 6 guinea pigs each were exposed to 5 ppm SO2 on 5 consecutive days over 8 h per day with intermittent inhalation of OA, while the air-control group was exposed to clean air and OA. During the period of SO2 exposure and sensitization three experimental groups were treated with indomethacin (group I), methylprednisolone (group M) and nebulized nedocromil sodium (group N), while the control group remained untreated. Guinea pigs were investigated for sensitization to OA by specific bronchial provocation tests using body plethysmographic measurement of compressed air (CA) and by measurement of specific antibody response in serum. While in the SO2-exposed control group 5 of 6 animals reacted to specific bronchial provocation testing (CA median 0.15 ml, range 0-0.175 ml), only 1 animal was sensitized in group M (CA 0 ml, 0-0.125, p < 0.05), whereas no bronchial reactions were seen in groups I and N (CA 0 ml, 0-0.05, p < 0.025). Specific IgG antibody titres increased in the control group (median 43 EU-->85 EU), but not in the treatment groups (medians group I 35 EU-->35 EU, group M 30-->35 EU, group N 64-->50 EU).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1996

Parainfluenza-3-virus infection enhances allergic sensitization in the guinea-pig.

BACKGROUND: Viral respiratory tract infections have been previously considered to be associated with induction of allergic sensitization. OBJECTIVE AND METHODS: In order to investigate this relationship in an animal model, guinea-pigs were inoculated intranasally with Parainfluenza-3-(PI-3) virus (n = 16) or virus-free culture medium (controls, n = 12), sensitized at day 4 with inhaled ovalbumin (OA) and challenged 3 weeks later with inhaled OA using specific bronchial provocation testing with body plethysmographic measurement of compressed air (CA). Furthermore, specific anti-OA-IgG1-antibodies in serum before challenge were determined by enzyme linked immunosorbent assay (ELISA). For investigation of airway epithelium permeability horseradish peroxidase (HRP) was inhaled at day 4 after inoculation by six animals, and HRP serum concentrations were determined by a direct ELISA 30 min after inhalation. RESULTS: PI-3 infected animals were found to be significantly more sensitized to OA compared with controls, with higher CA values (P < 0.001) on specific bronchial provocation and with increased specific anti-OA-IgG1 titers. Serum-HRP concentrations were about 20 times higher in the infected animals compared with controls. PI-3 infected and sham-infected animals had comparable bronchial reactions on specific provocation with OA when sensitized systemically. CONCLUSIONS: We conclude that viral respiratory tract infection with PI-3 virus enhances inhalative allergic sensitization in the guinea-pig. Increased mucosal permeability to antigens may be an important pathophysiological mechanism.

Adjuvants, Immunologic↗
PubMed1997

Association between pronounced IgA response in RSV bronchiolitis and development of allergic sensitization.

Forty-five children who had been hospitalized with bronchiolitis caused by respiratory syncytial virus (RSV) at a mean age of 4 months, and 90 matched control children, were tested for occurrence of RSV antibodies at one year of age. Of the children who had suffered from bronchiolitis, forty had demonstrable IgG antibodies, whereas the remaining five only had IgA antibodies against RSV. In the control group, 42% were RSV seropositive. The anti-RSV IgA antibody titres tended to be higher in patients with bronchiolitis than in controls and a larger proportion of the seropositive children in the former than in the latter group had demonstrable IgG antibodies. These findings suggest that RSV infections causing bronchiolitis are more often associated with a strong antibody response than are mild cases of the infection. Follow-up of the children at 3 years of age showed that allergic sensitization and development of asthma had occurred much more frequently in children with past RSV bronchiolitis than in controls. Children with past RSV bronchiolitis who later developed allergic sensitization had elevated RSV IgA antibody titres at one year of age more frequently than children with past RSV-bronchiolitis, who were not sensitized (p = 0.015). No significant differences regarding IgG antibody titres were observed. Since IgA, similarly as IgE, antibody formation is strongly Th2 cell dependent, the results are compatible with other findings suggesting that RSV has an unusual propensity to activate the Th2 cell system. This may contribute to the pathological picture of bronchiolitis in small children and at the same time render the infected child predisposed for later development of allergic sensitization. RSV bronchiolitis may thus be an important risk factor for later development of atopic disease although it cannot be excluded that the bronchiolitis simply serves as a marker that predict later development of atopy.

Antibodies, Viral↗
PubMed2006

Adult obesity, farm childhood, and their effect on allergic sensitization.

BACKGROUND: Obesity as well as a reduced microbial exposure, 2 markers of Western lifestyle, might be associated with an increased risk of allergic sensitization. OBJECTIVE: We aimed to analyze the interplay of these markers of Western lifestyle on allergic sensitization. METHODS: A questionnaire survey was completed by rural adults (18-45 years). Clinical assessments included those of sensitization (specific IgE) against inhalant allergens and body mass index (BMI). Subjects were grouped on the basis of their recent BMI (obesity: BMI > or =30 kg/m2) and whether they had regular farm contact during the first 3 years of life (farm subjects). Nonobese nonfarm subjects served as the reference group. Overall, 1861 subjects were included in the analyses. RESULTS: Compared with nonobese nonfarm subjects, nonobese farm subjects showed a decreased odds ratio for sensitization (odds ratio, 0.6; 95% CI, 0.5-0.8). This decrease was not observed in obese subjects (obese nonfarm subjects: 1.2, 0.8-1.9; obese farm subjects: 1.0, 0.6-1.6). Associations were similar for symptoms of allergic rhinitis. CONCLUSION: Obesity, as a risk factor for respiratory allergies per se, might diminish or even cancel the protective effect of a farm childhood. CLINICAL IMPLICATIONS: The high prevalence of respiratory allergies in inner-city societies despite lower levels of hygiene might be explained by obesity.

Adolescent↗
PubMed1999

Effect of respiratory syncytial virus on subsequent allergic sensitization to ovalbumin in guinea-pigs.

Children with acute respiratory syncytial virus (RSV) bronchiolitis often develop recurrent wheezing, asthma and allergic sensitization, but the role of RSV in the pathogenesis of these sequelae is unclear. This study examined whether RSV infection potentiates subsequent allergic sensitization, airway hyperresponsiveness (AHR) and airway inflammation induced by repeated exposures to aerosolized ovalbumin (OA) in guinea-pigs. Guinea-pigs received either RSV or sham inoculum, followed by exposures to OA- or saline-containing aerosols to form the following groups: 1) noninfected, nonsensitized controls (sham/saline group); 2) RSV-infected, nonsensitized animals (RSV/ saline group); 3) noninfected, OA-sensitized animals (sham/OA group); 4) RSV infection and first OA exposure on the same day (RSV/OA group), and 5) RSV infection six days prior to first OA exposure (RSV6/OA group). Three days after the final aerosol exposure, circulating OA-specific immunoglobulin (Ig)G1 antibody titres and AHR to inhalation acetylcholine challenge were measured and morphometry performed to evaluate allergic inflammation of the airways. OA-exposed animals developed OA-specific IgG1 antibodies, AHR and airway eosinophilia (sham/OA, RSV/OA and RSV6/OA groups. RSV infection alone induced significant AHR and airway eosinophilia (RSV/saline group). RSV infection, and concomitant exposure to OA (RSV/OA group) enhanced OA-specific IgG1 antibodies, but not airway eosinophilia or AHR. Such increases were not observed in the RSV6/OA group. In conclusion, respiratory syncytial virus potentiates the production of ovalbumin-specific immunoglobulin G1 antibodies in guinea-pigs, but circulating titres of these antibodies do not reflect the extent of airway hyperresponsiveness or airway inflammation. In addition, respiratory syncytial virus infection alone can produce slight increases in airway hyperresponsiveness that are associated with increased numbers of eosinophils in the airways.

Allergens↗
PubMed1998

BCG infection suppresses allergic sensitization and development of increased airway reactivity in an animal model.

BACKGROUND: Epidemiologic studies suggest an inverse correlation between infections and development of atopy. The purpose of this study was to test the hypothesis whether a preexisting Th1-type immune response elicited by BCG immunization could suppress allergic sensitization and airway hyperreactivity in an animal model. METHODS: BALB/c mice were immunized with BCG and/or sensitized to ovalbumin. RESULTS: BCG immunization alone resulted in cutaneous type-IV hypersensitivity reactions to tuberculin and granulomatous lesions in the liver. Splenic mononuclear cells (MNCs) produced increased levels of IFN-gamma after activation by Concanavalin A (ConA). Ovalbumin sensitization alone resulted in increased production of IL-4 after activation by ConA. Ovalbumin-sensitized animals also demonstrated markedly elevated anti-ovalbumin IgE/IgG1 serum antibody titers and increased airway reactivity after allergen challenges by means of the airways. BCG immunization 14 days before the start of ovalbumin sensitization markedly hindered the development of allergic responses as indicated by (1) increased IFN-gamma and normalized IL-4 and IL-10 production by splenic MNCs after activation with ConA, (2) a reduced proliferation rate of splenic MNCs after ovalbumin restimulation, (3) partial prevention of ovalbumin-specific IgE/IgG1 serum antibody titers but elevated (nonallergic) anti-ovalbumin IgG2a serum antibody titers, (4) prevention of airway responsiveness, (5) reduced eosinophilic influx into the airway lumen, and (6) reduced levels of IL-4 and IL-5 in broncho alveolar lavage fluids. CONCLUSION: In this model BCG immunization established a Th1-type immune response that hinders allergic sensitization and the development of increased airway reactivity.

Animals↗
PubMed2005

House dust mite facilitates ovalbumin-specific allergic sensitization and airway inflammation.

RATIONALE: Mouse models of allergic airway disease have greatly contributed to our understanding of disease induction and pathogenesis. Although these models typically investigate responses to a single antigen or allergen, humans are frequently exposed to a myriad of allergens, each with distinct antigenic potential. OBJECTIVES: Given that airway exposure to ovalbumin (OVA), a prototypic innocuous antigen, induces inhalation tolerance, we wished to investigate how this response would be altered if OVA were encountered concurrently with a house dust mite extract (HDM), which we have recently shown is capable of eliciting a robust allergic airway inflammatory response that is mediated, at least in part, by granulocyte-macrophage colony-stimulating factor. METHODS: Balb/c mice were exposed daily to HDM (intranasally) followed immediately by exposure to aerosolized OVA for 5 weeks. To allow the inflammatory response elicited by HDM to subside fully, mice were then allowed to rest, unexposed, for 8 weeks, at which time they were rechallenged with aerosolized OVA for 3 consecutive days. MEASUREMENTS AND MAIN RESULTS: At this time, we observed a robust eosinophilic inflammatory response in the lung that was associated with an increase in bronchial hyperreactivity. Moreover, we documented significantly elevated serum levels of OVA-specific IgE and IgG(1) and increased production of the Th2 cytokines interleukin 4 (IL-4), IL-5, and IL-13 by splenocytes stimulated in vitro with OVA. CONCLUSION: Our data demonstrate the potential of a potent allergen such as HDM to establish a lung microenvironment that fosters the development of allergic sensitization to otherwise weak or innocuous antigens, such as OVA.

Animals↗
PubMed1998

Ascaris-specific IgE and allergic sensitization in a cohort of school children in the former East Germany.

BACKGROUND: Helminthic infections induce an IL-4-dependent polyclonal stimulation of IgE synthetization. It is still unclear, however, what role helminths play in allergic sensitization. OBJECTIVE: We sought to determine the relationship between Ascaris-specific IgE and allergic sensitization in a nontropical country. METHODS: In 2 consecutive cross-sectional surveys in 1992-1993 and 1995-1996, data from school entrants (age range, 5 to 7 years), third graders (age range, 8 to 10 years), and sixth graders (age range, 11 to 14 years) were collected. The 2 younger groups were reexamined in the second survey. Data for about 2300 children, including a cohort of 700 subjects, were analyzed. Ascaris IgE and total and specific IgE to inhalant allergens were measured, and skin prick tests were performed. Information about asthma and allergic rhinitis was collected by a questionnaire. RESULTS: Children who were Ascaris-IgE seropositive (>0.35 IU/mL) in both surveys had 10-fold higher levels of total IgE (451 IU/mL vs 45 IU/mL, P < .001) and higher prevalence rates of allergen-specific IgE seropositivity (56.3% vs 26.6%, P < .001). They also had a higher prevalence of allergic rhinitis (12.6% vs 3.7%, P < .001) and asthma (5.7% vs 1.6%, P < .05). In subjects who were Ascaris-seronegative in the first survey but seropositive in the second survey, total and specific IgE increased markedly. Sensitization to Dermatophagoides pteronyssinus increased nearly 3-fold in this group. In contrast, in children who became Ascaris-seronegative, total and specific IgE decreased. CONCLUSIONS: Contact with low doses of helminthic antigen is associated with an increase of total and specific IgE production. Helminthic infections in East German children are not the cause for a low prevalence of allergies in the former East Germany.

Adolescent↗
PubMed1999

The association between pre- and postnatal tobacco smoke exposure and allergic sensitization during early childhood. Multicentre Allergy Study Group, Germany.

AIM: of our study was to investigate the effect of pre- and postnatal passive tobacco smoke exposure on the incidence of allergic sensitization. PATIENTS AND METHODS: Specific sensitization to food, outdoor and indoor allergens was determined in 342 children at the age of 1, 2 and 3 years. Parents were asked about their smoking habit at the birth of their children, at 18 months and 3 years of age. RESULTS: Multivariate regression analysis indicated, that during the first 3 years of life, pre- and postnatally exposed children had a significantly higher risk for sensitization to food allergens compared to children never exposed to tobacco smoke (OR 2.2, 95% CI 1.1-4.2; P = 0.02). With respect to inhalant allergens no significant influence of tobacco smoke exposure on specific sensitization could be demonstrated. CONCLUSION: During early childhood both pre- and postnatal tobacco smoke exposure has an adjuvant effect on allergic sensitization to food allergens.

Child, Preschool↗
PubMed2001

Does the sibling effect have its origin in utero? Investigating birth order, cord blood immunoglobulin E concentration, and allergic sensitization at age 4 years.

There is a great body of evidence that siblings have a protective effect against atopic manifestations such as hay fever, atopic eczema, allergic sensitization, or asthma. Factors that may explain this association remain largely unknown. One hypothesis is that siblings promote early infections in childhood, and repeated infections protect against atopic disorders. Another hypothesis, the potential in utero programming, has been neglected. The authors investigated if cord blood immunoglobulin E (IgE) is dependent upon birth order and if both are associated with an increased incidence of allergic sensitization (skin prick test) at the age of 4 years in a cohort of 981 newborns recruited between January 1989 and February 1990 on the Isle of Wight, England. The authors found that IgE is reduced with increasing birth order (first child: odds ratio (OR) = 1; second child: OR = 0.78, 95% confidence interval (CI): 0.57, 1.05; third child: OR = 0.59, 95% CI: 0.41, 0.83). Cord IgE, but not birth order, is a significant predictor of skin prick test positivity at age 4 (IgE below detection limit: OR = 1; IgE of 0.2-<0.5 kilounits/liter: OR = 1.11, 95% CI: 0.73, 1.68; IgE of >or=0.5 kilounits/liter: OR = 2.63, 95% CI: 1.62, 4.29). The findings suggest that cord IgE is reduced in pregnancies with higher order, indicating that the sibling effect may have its origin in utero.

Birth Order↗
PubMed2005

Epicutaneous exposure to peanut protein prevents oral tolerance and enhances allergic sensitization.

BACKGROUND: Food allergies are an important cause of life-threatening hypersensitivity reactions. Oral tolerance can be considered the default immune response to dietary antigens, with immune deviation resulting in allergic sensitization. However, primary sensitization to food allergens may not solely be through the gastrointestinal mucosa, as strong T-helper type 2 (Th2)-biased immunity can result from exposure to protein allergens on barrier-disrupted skin. OBJECTIVE: The purpose of this study was to examine whether exposure to allergens through the skin may interfere with the normal development of oral tolerance and promote allergic sensitization to food proteins. METHODS: Female BALB/c mice were exposed epicutaneously to peanut protein and induction of systemic oral tolerance through high dose feeds of peanut protein was subsequently assessed. Other mice were rendered tolerant prior to epicutaneous peanut exposure. Sensitivity to peanut was determined by assessing delayed-type hypersensitivity, proliferative, cytokine and antibody responses. RESULTS: Epicutaneous exposure to peanut protein induced potent Th2-type immunity with high levels of IL-4 and serum IgE. Primary skin exposure prevented the subsequent induction of oral tolerance to peanut in an antigen-specific manner. Upon oral challenge, mice became further sensitized and developed strong peanut-specific IL-4 and IgE responses. Furthermore, animals with existing tolerance to peanut were partly sensitized following epicutaneous exposure. CONCLUSION: Epicutaneous exposure to peanut protein can prevent induction of oral tolerance, and may even modify existing tolerance to peanut. Epidermal exposure to protein allergens selectively drives Th2-type responses, and as such may promote sensitization to food proteins upon gastrointestinal exposure.

Administration, Cutaneous↗
PubMed1981

Allergic sensitivity confirmed by the release of histamine from small blood samples.

An enzymatic-isotopic microassay that can measure picogram amounts of histamine in 20 microliter samples of plasma has been used to confirm diagnosis of allergic sensitivity to extracts of house dust mite, cat dander, grass, plantain, Cladosporium mould and bee sting venom by the skin test procedure. Multiple assays for allergic histamine release can be performed on minimal blood samples resulting in a qualitative and quantitative prediction of allergic sensitivity from an in vitro biochemical procedure.

Animals↗
PubMed2002

Siberian hamster: a new indoor source of allergic sensitization and respiratory disease.

BACKGROUND: The identification of 'unknown' allergic sensitizations may determine the prognosis and treatment of patients with respiratory airway disease. Currently, the presence in homes of 'exotic' animals as pets is increasing. In this article the Siberian hamster or dwarf hamster (Phodopus sungorus) was identified as a new indoor source of aeroallergens and respiratory disease. METHODS: The subjects were six outpatients who were treated for asthma and rhinitis. Siberian hamster hair extract was prepared with a standard wt/vol method, and patients were skin-prick tested with the extract. Serum-specific immunoglobulin (Ig)E against the Siberian hamster, common hamster (Cricetus cricetus) and golden hamster (Mesocricetus auratus) was determined. IgE-immunoblotting was also performed for all six sera. Specific bronchial challenge was carried out with the Siberian hamster extract. RESULTS: Skin prick tests (SPT) with the Siberian hamster extract, and specific IgE-antibodies against Siberian hamster, were strongly positive in all six patients. Determinations of specific IgE-antibodies against C. cricetus and M. auratus were negative in all patients. IgE-immunoblotting of the sera revealed two IgE-binding fractions (MW 18 and 32 kDa) in five of the six sera. Specific bronchial provocation tests resulted in early asthmatic responses in the two patients who were challenged. CONCLUSIONS: The present study reveals the Siberian hamster to be able to induce both sensitization and disease, and this species of hamster should be taken into consideration as a cause of respiratory disease in exposed subjects. A noteworthy finding was the lack of sensitization in our patients to common hamster allergens (M. auratus and C. cricetus) that are usually tested when hamster allergy is suspected.

Adult↗
PubMed1995

The central rôle of T-cells in allergic sensitization and IgE regulation.

The atopic phenotype develops on the basis of a genetic predisposition. Several candidate genes and chromosomal regions have been recently identified that may play a rôle in the development of allergic sensitization and total IgE production, including genes encoding MHC and T-cell receptor (TCR) molecules, cytokines and others. Genetic predisposition triggers and immunological dysregulation which is controlled by CD4+ T-cells. (Specialized) antigen presenting cells process and present allergenic peptides (T-cell epitopes) on MHC class II molecules to T-cells that recognize MHC plus peptide using the TCR. Cognate and non-cognate interaction results in T-cell activation. Selective stimulation of the allergen specific T-cells is the result of allergen-specific sensitization. These T-cells are characterized by (simultaneous) production of IL-3, IL-4, IL-5 (and may be IL-13). These cytokines control the production of IgE by B cells and play a critical rôle in the activation and differentiation of effector cells of the allergic response (such as eosinophils and mast cells). In addition to MHC-TCR interaction and cytokine production, ligation of CD40 and CD40L represents an additional requirement for the production of functional IgE molecules. Immediate hypersensitivity responses are characterized by an early phase response (triggered by many mediators released from effector cells following allergen exposure, IgE cross-linking and activation of signal transduction pathways) and a late phase response that is mediated to a large extend by the influx of T-cells and effector cells into the site of allergic inflammation. Deliniation of the immunological mechanisms that result in allergic sensitization will contribute to the development of specific immunomodulatory strategies aimed to prevent the development of allergies.

Animals↗