Eosinophilic Inflammation, Remodeling of Lower Airway, Bronchial Responsiveness and Cough Reflex Sensitivity in Non-Asthmatic Subjects with Nasal Allergy

Hara, Johsuke; Fujimura, Masaki; Myou, Shigeharu; Furusho, Shiho; Abo, Masahiro; Oribe, Yoshitaka; Ohkura, Noriyuki; Herai, Yoriko; Sone, Takashi; Waseda, Yuko; Yasui, Masahide; Kondo, Kazuo

doi:10.1159/000093711

Cited by 11 publications

(7 citation statements)

References 42 publications

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“…It has been reported that allergic rhinitis can cause asymptomatic lower airway eosinophilic inflammation and BHR . This eosinophilic inflammation was decreased with the avoidance of allergens, and BHR was reversible after corticosteroids treatment .…”

Section: Discussionmentioning

confidence: 98%

Eosinophilic airway inflammation is common in subacute cough following acute upper respiratory tract infection

et al. 2016

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Background and objective: Patients presenting with refractory postinfectious cough may respond to glucocorticosteroids but it is unclear whether airway eosinophilic inflammation exists in those patients. We aimed to determine the airway inflammation and causes of subacute cough following acute upper respiratory tract infection (AURTI). Methods: One hundred and sixteen patients with persistent cough lasting 3-8 weeks after upper respiratory tract infection were evaluated with differential cell count in induced sputum, spirometry and methacholine bronchial challenge testing. Results: In patients with subacute cough, sputum eosinophilia (median 8.5%,3.0-73.0%) was identified in 35 (33.6%) patients, 22 (18.5%) without bronchial hyperresponsiveness (BHR) were diagnosed as nonasthmatic eosinophilic bronchitis (NAEB), 13 (14.3%) of whom with BHR were diagnosed as cough variant asthma (CVA). Cough in patients with sputum eosinophilia improved after treatment with corticosteroids. Compared with postinfectious cough (PIC) and NAEB, CVA had significantly higher median eosinophil count in induced sputum (0.5% vs 7.5% vs 20.0%, P < 0.01). MMEF in CVA was significantly lower than PIC and NAEB (P < 0.05). The common causes of subacute cough following acute upper respiratory tract infection (AURTI) were PIC (37.8%), NAEB (18.5%), CVA (14.3%) and upper airway cough syndrome (UACS) (10.1%). Atopic cough (AC) (5.2%) and gastroesophageal refluxrelated cough (GERC) (3.4%) were less common in subacute cough following AURTI, while 9 (7.8%) patients had unexplained cough. Conclusion: Subacute cough following AURTI can be attributed to different entities, eosinophilic airway inflammation is common. Induced sputum should be considered when evaluating patients with subacute cough following acute upper respiratory tract infection.

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Section: Discussionmentioning

confidence: 98%

Eosinophilic airway inflammation is common in subacute cough following acute upper respiratory tract infection

et al. 2016

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“…Eosinophilia in the lower airway is common in patients with allergic rhinitis who only presented with nasal symptoms, as evaluated by bronchoalveolar lavage fluids, bronchial mucosa biopsies, and induced sputum [25,26]. Furthermore, sinusitis is usually characterized by chronic upper and lower airway inflammation [27].…”

Section: Discussionmentioning

confidence: 99%

“…As demonstrated by Bardin et al [9], aspiration of nasolaryngeal secretions into the lung could not explain the occurrence of cough in the patients with UACS, even though the possibility could not completely excluded in our study. We believe the lower airway inflammation in the patients with UACS may represent the airway manifestation of systematic allergic reaction in the case of allergic rhinitis [26,33] or the extension of upper airway inflammation by unknown mechanisms as observed in sinusitis [34]. …”

Section: Discussionmentioning

confidence: 99%

Capsaicin-sensitive cough receptors in lower airway are responsible for cough hypersensitivity in patients with upper airway cough syndrome

Wang

et al. 2013

Med Sci Monit

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BackgroundCough hypersensitivity may be related to the pathogenesis of upper airway cough syndrome (UACS). The purpose of the study was to investigate the role of capsaicin-sensitive cough receptors on the laryngopharynx and lower airway in the cough hypersensitivity of patients with UACS.Material/Methods59 patients with UACS, 33 patients with rhinitis/sinusitis without cough, and 39 healthy volunteers were recruited for the study. Cough threshold C5, defined as the lowest concentration of capsaicin required for the induction of ≥5 coughs upon esposure to capsaicin, were determined at baseline and after laryngopharngeal anesthesia with lidocaine in all the subjects. After induced sputum cytology, the concentrations of histamine, prostaglandin E2 (PGE2), and calcitonin-gene-related peptide (CGPR) in the induced sputum were measured by ELISA. In 15 patients with UACS, sputum cytology and measurement of the above mediators were repeated after successful therapy.ResultsC5 response to capsaicin was significantly lower in the UACS group than in the rhinitis/sinusitis group and healthy control groups [3.9 (0.98, 7.8) μmol/L vs. 7.8 (3.9, 93.75) μmol/L vs. 31.2 (15.6, 62.5) μmol/L, H=40.12, P=0.000]. Laryngopharngeal anesthesia with lidocaine dramatically increased C5 to capsaicin in the subjects of all 3 groups by a similar degree, but the increase in the UACS group was still the lowest, with an increased level of histamine, PGE2, and CGRP in the induced sputum. When cough resolved with the treatment of cetirizine alone or in combination with erythromycin, the levels of CGRP and histamine in the induced sputum decreased significantly in 15 patients with UACS, with no obvious change in cell differential or concentration of PGE2 in the induced sputum.ConclusionsLaryngeal TRPV1 plays an important role in cough sensitivity, but sensitization of capsaicin-sensitive cough receptors in the lower airway may be more responsible for the cough hypersensitivity in patients with UACS.

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“…A possible explanation could be that, whereas nasal lavage fluid levels represent the local inflammatory ‘burden’, serum levels reflect the systemic nature of inflammation, including the presence of subclinical inflammation in bronchial mucosa. Several studies have demonstrated an increased bronchial hyper‐responsiveness in non‐asthmatic patients with allergic rhinitis as well as a correlation between the level of hyper‐responsiveness and sputum eosinophils (13–15). Activated eosinophils in bronchial tissue have been observed in patients with clinical asthma as well as in atopic non‐asthmatics, demonstrating the presence of subclinical mucosal inflammation (16), and it would seem natural to expect this in future patients with symptomatic asthma.…”

Section: Discussionmentioning

confidence: 99%

Serum eosinophil granule proteins predict asthma risk in allergic rhinitis

Nielsen

Peterson

Dahl³

2009

Allergy

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Background: Allergic rhinitis is a common disease, in which some patients will deteriorate or develop asthma. It is important to characterize these patients, thereby offering the possibility for prevention. This study evaluated eosinophil parameters as potential indicators of deteriorating allergic airway disease. Methods: The subjects of the study included all patients who suffered seasonal allergic rhinitis and had participated in a study 6 years earlier, in which blood eosinophils, serum eosinophil cationic protein (ECP) serum eosinophil peroxidase (EPO), nasal lavage ECP and nasal lavage EPO levels were measured. Patients in the present study were interviewed on occurrence of rhinitis symptoms during the last season, rhinitis outside season, asthma‐like symptoms and asthma diagnosis, and were skin‐prick tested for common aeroallergens. Eosinophil parameters from the study 6 years earlier were then tested for the ability to predict occurrence of new allergies, worsening of rhinitis and occurrence of asthma. Results: Forty‐four patients participated in the study. In four patients seasonal rhinitis symptoms had deteriorated, 10 had experienced perennial rhinitis symptoms, 14 reported asthma‐like symptoms and seven had been diagnosed with asthma. Thirteen had developed additional sensitization. Patients developing asthma‐like symptoms compared with patients with no such symptoms had significantly higher serum ECP (16.7 μg/l vs 8.2 μg/l; P ≤ 0.01) and serum EPO (17.9 μg/l vs 8.8 μg/l; P ≤ 0.05). Results were similar, considering patients diagnosed with asthma. Blood eosinophils and nasal lavage parameters were not related to development of asthma and asthma‐like symptoms. No eosinophil parameter was related to deterioration of rhinitis or additional sensitization. Conclusion: Serum ECP and EPO in patients with seasonal rhinitis demonstrated a high predictive ability for later development of asthma.

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Eosinophilic Inflammation, Remodeling of Lower Airway, Bronchial Responsiveness and Cough Reflex Sensitivity in Non-Asthmatic Subjects with Nasal Allergy

Cited by 11 publications

References 42 publications

Eosinophilic airway inflammation is common in subacute cough following acute upper respiratory tract infection

Eosinophilic airway inflammation is common in subacute cough following acute upper respiratory tract infection

Capsaicin-sensitive cough receptors in lower airway are responsible for cough hypersensitivity in patients with upper airway cough syndrome

Serum eosinophil granule proteins predict asthma risk in allergic rhinitis

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