Eosinophilic Airway Inflammation and Airway Hyperresponsiveness According to Aeroallergen Sensitization Pattern in Patients With Lower Airway Symptoms (original) (raw)
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Clinical <html_ent glyph="@amp;" ascii="&"/> Experimental Allergy, 2000
Background We investigated whether the association of allergy symptoms with sensitization to inhalant allergens depends on bronchial hyperresponsiveness, blood eosinophil count, or the degree and nature of sensitization. Methods Data on asthma and rhino-conjunctivitis symptoms were obtained from 1904 subjects from a random sample of the Dutch population, aged 20±70 years by the ECRHS questionnaire. Total IgE and speci®c IgE to four inhalant allergens were measured using CAP System. Bronchial hyperresponsiveness (BHR) was de®ned as PD 20 # 2 mg methacholine and`high eosinophil count' as an eosinophil count in the highest quartile. Results Forty-three percent of the subjects with speci®c IgE to inhalant allergens was asymptomatic. These subjects had a lower degree of sensitization than symptomatic sensitized subjects and had`normal' prevalences of BHR and`high eosinophil count'. Logistic regression showed that the presence of BHR increased the risk of having symptoms for subjects who were sensitized to indoor allergens. Low levels of speci®c IgE to indoor allergens were only associated with symptoms when BHR was present. Sensitization to outdoor allergens was associated with symptoms at all levels of speci®c IgE, independently of BHR or eosinophils. Conclusion Our epidemiological data suggest that whether low levels of speci®c IgE to indoor allergens lead to allergic symptoms is probably determined by the concurrent existence of in¯ammation of the airways.
Is allergic sensitization relevant in severe asthma? Which allergens may be culprit?
The World Allergy Organization journal, 2017
Severe asthma is a major health concern. The allergic (IgE-mediated) form of asthma is well known from a pathogenic viewpoint. We searched the available literature to identify which allergens are most frequently associated with severe, refractory or life threatening asthma. According to the results, molds, pet dander, cockroach and ragweed were more frequently responsible for severe asthma. Thunderstorm asthma, in addition, represents a special association between allergic sensitization and an external climatic factor. A detailed knowledge of the most harmful allergens is mandatory for an appropriate diagnostic and preventive approach.
Asthma and Lung Biology [Working Title]
Eosinophilic asthma is known as a main phenotype of asthma classified on the basis of immune cells involved in inflammatory response in the respiratory airway. Eosinophilic asthma can be related to increased severity of asthma, allergic sensitization, adult onset, and increased resistance to corticosteroids. The prevalence of eosinophilic asthma is 32-40% among asthmatic patients. Different cells and cytokines are involved in its pathogenesis including eosinophil, mast cells, type 2 helper T cells, innate lymphoid cells, IL-4, IL-5, and IL-13. Eosinophil count in induced sputum and bronchoalveolar lavage is the yardstick for recognizing and distinguishing eosinophilic asthma from non-eosinophilic asthma, while various tests which are noninvasive such as fractional exhaled nitric oxide and periostin are arising as possible substitutes. Novel and advanced therapies new and advanced therapies and more convenient biological drugs, Leads to high requirement for particular endotype-and phenotype-related treatment plans. Identification and knowledge of the specific pathophysiology of eosinophilic asthma have great association with disease management and chances for better patient prognosis.
Clinical <html_ent glyph="@amp;" ascii="&"/> Experimental Allergy, 2006
Background Patients with atopic dermatitis (AD) often have symptoms suggestive of asthma or rhinitis. The prevalence and signs of respiratory disease in AD patients have been studied to a limited extent. Objectives To assess the prevalence and clustering of respiratory symptoms, bronchial hyperresponsiveness (BHR), and eosinophilic airway inflammation in patients with moderate-tosevere AD. Methods Eighty-six consecutive patients with moderate-to-severe AD and 49 randomly selected control subjects without AD were studied by questionnaire, flow volume spirometry, histamine challenge to detect BHR, induced sputum test to detect eosinophilic airway inflammation, and skin prick tests (SPTs) and total serum immunoglobulin (Ig)E measurements to detect atopy. Results The patients with AD showed increased risk of physician-diagnosed asthma (36% vs. 2%, odds ratio (OR) 10.1, confidence interval (CI) 1.3-79.7, P = 0.03), physician-diagnosed allergic rhinitis (AR) (45% vs. 6%, OR 4.5, CI 1.2-16.7, P = 0.02), BHR (51% vs. 10%, OR 5.5, CI 1.5-20.1, P = 0.01), and sputum eosinophilia (81% vs. 11%, OR 76.1, CI 9.3-623.5, P o 0.0001) compared with the control subjects. In AD patients, elevated s-IgE and positive SPTs were associated with the occurrence of physician-diagnosed asthma and AR, BHR, and the presence of sputum eosinophilia. Conclusions BHR and eosinophilic airway inflammation are more common in patients with AD than in control subjects. The highest prevalences were seen in patients with AD who were SPT positive and had high IgE levels. Longitudinal studies are needed to assess the outcome of patients with signs of airway disease, in order to identify those who need early initiation of asthma treatment.
Thorax, 2005
Background: The effect of exposure to allergens not causing sensitisation in atopic asthmatic subjects has not previously been studied. A study was undertaken to assess the degree of asthma severity (measured by spirometry, airway reactivity and exhaled nitric oxide) in atopic asthmatic patients not sensitised to the domestic allergen to which they were exposed. Methods: Dust samples were collected from the living room carpet and mattress in the homes of 248 subjects and dust mite, cat and dog allergen concentrations were measured. Spirometry, non-specific bronchial reactivity (BR), and exhaled nitric oxide (eNO) were ascertained. Patients' sensitisation status was assessed by skin prick testing. Results: Adult atopic asthmatics not sensitised to mite but exposed to high levels of mite allergen had significantly more severe BR than subjects not exposed to high levels of mite (PD 20 , geometric mean (GM) 0.21 mg (95% CI 0.09 to 0.47) v 0.86 mg (95% CI 0.44 to 1.67), mean ratio difference 4.1 (95% CI 1.5 to 11.4), p = 0.008). Subjects not sensitised but exposed to high levels of dog allergen also had significantly more severe BR than subjects not exposed (PD 20 GM 0.16 v 0.52 mg, mean ratio difference 3.3 (95% CI 1.2 to 9.2), p = 0.01). The differences in BR between these groups were still significant after adjusting for confounding factors. This effect of greater airway reactivity was not seen in subjects exposed but not sensitised to cat allergens. Conclusion: Atopic asthmatic subjects who are exposed to high levels of dust mite or dog allergens but not sensitised to these allergens have evidence of increased airway reactivity.
Journal of Allergy and Clinical Immunology, 1994
Nonspecific airway hyperresponsiveness is a fundamental characteristic of patients with asthma and can be influenced by several stimuli. In nine patients with asthma and an isolated allergy to house dust mite, the variation of natural evposure to the house dust mite allergen Der p Z and the corresponding changes in nonspecific airway hyperresponsiveness were followed up for I year. The concentration of Der p I in floor dust from living rooms and bedrooms (as a measure of eaposure) reached maximum levels in late summer and the beginning of autumn (August to October), whereas the lowest levels were found during the months of March to May (ADer p I = +2.31 p&m and-1.33 ~/gm respectively, both compared with the year average). Airway hyperresponsiveness (as measured by the provocative concentration of histamine causing a 20% fall in forced eqiratory volume in I second [PC,$ threshold) also showed a seasonal variation, with most severe hyperresponsiveness during the months of August to November; almost the same period in which the exposure to house dust mite allergens reached maximal levels (APC*, histamine =-1.47 mglml in November vs + 1.79 mglml in March, both compared with the year average). Our results support the view that seasonal changes of exposure to environmental allergens such as house dust mite allergens will have an effect on the level of airway hyperresponsiveness in patients with allergic asthma. (J ALLERGY C~uvIhf~uNoL 1994;93:470-5.
American Journal of Respiratory Cell and Molecular Biology, 1999
Nonspecific airway hyperresponsiveness (AHR) is a hallmark of human asthma. Both airway eosinophilia and high serum levels of total and antigen-specific immunoglobulin E (IgE) are associated with AHR. It is unclear, however, whether either eosinophilia or increased IgE levels contribute directly to, or predict, the development of AHR. Investigations conducted with various murine models of asthma and different mouse strains have resulted in conflicting evidence about the roles that IgE and airway eosinophilia play in the manifestation of AHR. We show that systemic priming with ovalbumin (OVA) in alum, followed by a single day of OVA aerosol challenge, is sufficient to induce AHR, as measured by increased pulmonary resistance in response to intravenously delivered methacholine in BALB/c, but not C57BL/6 or B 6 D 2 F1, mice. This was observed despite the fact that OVA-challenged BALB/c mice had less airway eosinophilia and smaller increases in total IgE than either C57BL/6 or B 6 D 2 F1 mice, and had less pulmonary inflammation and OVA-specific IgE than B 6 D 2 F1 mice. We conclude that airway eosinophilia, pulmonary inflammation, and high serum levels of total or OVA-specific IgE are all insufficient to induce AHR in C57BL/6 and B 6 D 2 F1 mice, whereas BALB/c mice demonstrate AHR in the absence of airway eosinophilia. These data confirm that the development of AHR is genetically determined, not only in naive mice, but also in actively immunized ones, and cannot be predicted by levels of airway eosinophilia, pulmonary inflammation, total IgE, or antigen-specific IgE. . 1999. Dissociation of airway hyperresponsiveness from immunoglobulin E and airway eosinophilia in a murine model of allergic asthma. Am. J. Respir. Cell Mol.
Allergologia et Immunopathologia, 2014
Background: Allergic rhinitis and asthma due to mite sensitisation are diseases which are frequently associated and characterised by persistent inflammation. In the present study, we aimed to investigate the relationship between nasal airflows and nasal eosinophils in patients with asthma and/or rhinitis due to house dust mite sensitisation. Methods: Twenty-four children with both rhinitis and asthma (R + A), 13 children with rhinitis and no asthma (R) and 10 non-allergic healthy children were evaluated prospectively. The patients belonging to the first two groups had moderate-severe grade of nasal obstruction. Total nasal symptom scores, peak nasal inspiratory flows (PNIFs) obtained by anterior rhinomanometry, skin prick tests, nasal eosinophils and FEV1 values were all assessed. Results: Percentages of nasal eosinophils and PNIFs in patients with R + A and R (r = −0.415, p = 0.04) were found to be statistically significant and to have an inverse correlation. Skin prick tests were also significantly correlated with nasal eosinophils and PNIFs (r = 0.372, p = 0.01 and r = −0.306, p = 0.04, respectively). Both PNIFs and nasal eosinophils of patients with R + A were significantly correlated with FEV1 values (r = −0.641, p = 0.001 and r = 0.548, p = 0.007, respectively). Conclusion: In this study, a close relationship was demonstrated between eosinophil infiltration and nasal airflows in children having asthma and/or rhinitis monosensitised to mites. Additionally, the significant association found between FEV1 values and nasal eosinophils or PNIFs supported the close link of upper and lower airways.
Allergy, 2000
Comparison of allergen-induced changes in bronchial hyperresponsiveness and airway in¯ammation between mildly allergic asthma patients and allergic rhinitis patients Bronchial eosinophilic in¯ammation and bronchial hyperresponsiveness (BHR) are the main features of allergic asthma (AA), but they have also been demonstrated in allergic rhinitis (AR), suggesting a continuity between both diseases. In spite of not fully reproducing natural allergenic exposure, the allergen bronchial provocation test (A-BPT) has provided important knowledge of the pathophysiology of AA. Our aim was to verify the existence of a behavior of AA and AR airways different from the allergen bronchial challenge-induced airway eosinophilic in¯ammation and BHR changes. We studied a group of 31 mild and short-evolution AA and 15 AR patients, sensitized to Dermatophagoides pteronyssinus. The A-BPT was performed with a partially biologically standardized D. pteronyssinus extract, and known quantities of Der p 1 were inhaled. Peripheral blood (eosinophils and ECP) and induced sputum (percentage cell counts, ECP, albumin, tryptase, and interleukin [IL]-5) were analyzed, before and 24 h after A-BPT. Methacholine BHR, assessed before and 32 h after the A-BPT, was de®ned by M-PD 20 values and, when possible, by maximal response plateau (MRP). The A-BPT was well tolerated by all the patients. AA presented a lower Der p 1 PD 20 and a higher occurrence of latephase responses (LPR). M-PD 20 values decreased in AA, but not in AR, patients. MRP values increased in both groups. Eosinophils numbers and ECP levels increased in blood and sputum from both AA and AR, but only the absolute increment of sputum ECP levels was higher in AA than AR patients (P=0.025). The A-BPT induced no change in sputum albumin, tryptase, or IL-5 values. We conclude as follows: