Effect of controlled human exposure to diesel exhaust and allergen on airway surfactant protein D, myeloperoxidase and club (Clara) cell secretory protein 16

Biagioni, Bradly J.; Tam, Sheena; Chen, Yu‐Wei Roy; Sin, Don D.; Carlsten, Christopher

doi:10.1111/cea.12732

Cited by 20 publications

(12 citation statements)

References 58 publications

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“…A major hub that was suppressed following DEA co-exposure was the MAPK1-ERK1/2 axis, a critical pathway that both positively and negatively regulates inflammation [20]. This is consistent with our previous studies using targeted approaches, demonstrating increase in the expression of specific inflammatory markers both in circulation and in the airways following inhaled DE+allergen co-exposure [14,21]. We have also shown that expression of miRNAs, such as miR-132-3p, associated with inflammatory gene regulation are altered following DEA co-exposure in the controlled human exposure model [12], as used in this study.…”

Section: Discussionsupporting

confidence: 88%

Inhaled diesel exhaust alters the allergen-induced bronchial secretome in humans

et al. 2018

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Diesel exhaust (DE) is a paradigm for traffic-related air pollution. Human adaptation to DE is poorly understood and currently based on oversimplified models. DE promotes allergic responses, but protein expression changes mediated by this interaction have not been systematically investigated. The aim of this study was to define the effect of inhaled DE on allergen-induced proteins in the lung.We performed a randomised and blinded controlled human crossover exposure study. Participants inhaled filtered air or DE; thereafter, contralateral lung segments were challenged with allergen or saline. Using label-free quantitative proteomics, we comprehensively defined DE-mediated alteration of allergen-driven secreted proteins (secretome) in bronchoalveolar lavage. We further examined expression of proteins selected from the secretome data in independent validation experiments using Western blots, ELISA and immunohistochemistry.We identified protein changes unique to co-exposure (DE+allergen), undetected with mono-exposures (DE or allergen alone). Validation studies confirmed that specific proteins ( the antimicrobial peptide cystatin-SA) were significantly enhanced with DE+allergen compared to either mono-exposure.This study demonstrates that common environmental co-exposures can uniquely alter protein responses in the lungs, illuminating biology that mono-exposures cannot. This study highlights the value of complex human models in detailing airway responses to inhaled pollution.

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Section: Discussionsupporting

confidence: 88%

Inhaled diesel exhaust alters the allergen-induced bronchial secretome in humans

et al. 2018

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“…Current research has associated prolonged exposure to tobacco smoke (25), household heating with fossil fuels (wood in particular) (26), and chronic exposure to urban air pollutants (27) with decreases in CC16 levels in both serum and nasal secretions. Biagioni et al (28) reported lower CC16 in nasal secretions and bronchoalveolar lavage in atopic individuals exposed to diesel exhaust. Although unknown, the mechanism leading to lower CC16 production could be similar to the one in cigarette smoking, which over time affects airway tissue repair.…”

Section: Cc16 and Prolonged Exposure To Air Pollutantsmentioning

confidence: 98%

Clara cell protein 16 release from the nasal mucosa in allergic rhinitis, chronic rhinosinusitis, and exposure to air pollutants

Perić

Mirković

Vojvodić

2018

Archives of Industrial Hygiene and Toxicology

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Clara cell protein 16 (CC16) is a small protein mainly produced by non-ciliated Clara cells in the respiratory epithelium. It has an anti-inflammatory role in chronic upper and lower airway eosinophilic inflammations. Decreased levels of CC16 are found in the nasal secretions and plasma of patients with chronic eosinophilic inflammatory disorders, such as asthma, allergic rhinitis, and chronic rhinosinusitis with or without nasal polyps, as well as in people exposed to high levels of air pollutants. Intranasal corticosteroid administration suppresses chronic inflammation of the nasal mucosa driven by eosinophils and stimulates local CC16 production. CC16 can be a reliable biomarker of the beneficial effects of perennial allergic rhinitis and chronic rhinosinusitis therapy and of the functional recovery of the nasal mucosa after treatment with topical glucocorticoids.

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“…In addition to the well-established epidemiologic relationship, experimental data have emerged on the effect of air pollutants and allergens. [87][88][89][90][91] Various studies showed that O 3 , NO 2 , and diesel exhaust particles are able to increase the permeability of the bronchial epithelium and to reduce the clearance of inhalable allergens and irritants, facilitating their access to the submucosa, where they interact with both resident and recruited cells. 88 Carlsten's research team contributed to our knowledge with a series of experiments on the effects of coexposure to diesel exhaust and allergen on the airways.…”

Section: Considering Interactions To Implement the Exposomic Approachmentioning

confidence: 99%

“…88 Carlsten's research team contributed to our knowledge with a series of experiments on the effects of coexposure to diesel exhaust and allergen on the airways. 89,90 In atopic patients they found that coexposure has differential effects on Clara cell secretory protein 16, surfactant protein D, and myeloperoxidase and that surfactant protein D and myeloperoxidase levels in bronchoalveolar lavage fluid are responsive to allergen, whereas Clara cell secretory protein 16 is more responsive to diesel exhaust particle exposure. 89 In a case-crossover study on bronchial epithelial cells (the first cells exposed to inhalants) of atopic subjects, allergens were able to modulate gene and microRNA expression, even 48 hours after a transient exposure, whereas no effects were detected when diesel exhaust was added.…”

Section: Considering Interactions To Implement the Exposomic Approachmentioning

confidence: 99%

External exposome and allergic respiratory and skin diseases

Cecchi

D’Amato²,

Annesi‐Maesano

2018

Journal of Allergy and Clinical Immunology

165

141

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Allergies are complex diseases that result from interactions between multiple genetic and environmental factors. However, the increase in allergies observed in the past decades is explained exclusively by environmental changes occurring in the same period. Presently, the exposome, the totality of specific and nonspecific external environmental exposures (external exposome) to which a subject is exposed from preconception onward and their consequences at the organ and cell levels (internal exposome), is being considered to explain the inception, development, and exacerbations of allergic diseases. Among the best-studied environmental factors of the specific external exposome, indoor and outdoor aeroallergens and air pollutants play a key role in the etiopathogenesis of the inflammatory response to allergens and in clinical manifestations of allergic disease. Climate change, urbanization, and loss of biodiversity affect sources, emissions, and concentrations of main aeroallergens and air pollutants and are among the most critical challenges facing the health and quality of life of the still increasing number of allergic patients today and in the coming decades. Thunderstorm-related asthma is a dramatic example of the effects of combined environmental factors and an in vivo model for understanding the mechanisms at work in respiratory allergy. Environment- or lifestyle-driven aberrancies in the gut and skin microbiome composition represent key mediators of allergic diseases. A better knowledge of the effect of the external exposome on allergy development is crucial for urging patients, health professionals, and policymakers to take actions to mitigate the effect of environmental changes and to adapt to them.

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Effect of controlled human exposure to diesel exhaust and allergen on airway surfactant protein D, myeloperoxidase and club (Clara) cell secretory protein 16

Cited by 20 publications

References 58 publications

Inhaled diesel exhaust alters the allergen-induced bronchial secretome in humans

Inhaled diesel exhaust alters the allergen-induced bronchial secretome in humans

Clara cell protein 16 release from the nasal mucosa in allergic rhinitis, chronic rhinosinusitis, and exposure to air pollutants

External exposome and allergic respiratory and skin diseases

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