Damage of the Airway Epithelium and Bronchial Reactivity in Patients with Asthma

Laitinen, Lauri A.; Heino, Matti T. J.; Laitinen, Annika; Kava, T; Haahtela, Tari

doi:10.1164/arrd.1985.131.4.599

Cited by 1,186 publications

(291 citation statements)

References 11 publications

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“…Although several studies have assessed FeNO levels in school-children with asthma or AR,3031 limited data are available about FeNO levels in preschool-aged children. The FeNO level is low at younger age32 and a study that suggested FeNO level of recurrent wheezers in preschool children was approximately 10-15 ppb, which is lower than school-aged children's levels 33. Our study focused on the presentation of FeNO levels in preschool children with AR who were 3-7 years old and controlled for the confounding factor of asthma, which is one of the most powerful determinants of increased FeNO levels.…”

Section: Discussionmentioning

confidence: 99%

Allergic Rhinitis in Preschool Children and the Clinical Utility of FeNO

Yoon

Choi

Lee

et al. 2017

Allergy Asthma Immunol Res

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PurposeThe nature of allergic rhinitis (AR) in preschool aged children remains incompletely characterized. This study aimed to investigate the prevalence of AR and its associated risk factors in preschool-aged children and to assess the clinical utility of fractional exhaled nitric oxide (FeNO).MethodsThis general population-based, cross-sectional survey included 933 preschool-aged (3- to 7-year-old) children from Korea. Current AR was defined as having nasal symptoms within the last 12 months and physician-diagnosed AR.ResultsThe prevalence of current AR in preschool children was 17.0% (156/919). Mold exposure (adjusted odds ratio [aOR], 1.67; 95% confidence interval [CI], 1.15-2.43) and the use of antibiotics (aOR, 1.97; 95% CI, 1.33-2.90) during infancy were associated with an increased risk of current AR, whereas having an older sibling (aOR, 0.52; 95% CI, 0.35-0.75) reduced the risk. Children with current atopic AR had significantly higher geometric mean levels of FeNO compared to those with non-atopic rhinitis (12.43; range of 1standard deviation [SD], 7.31-21.14 vs 8.25; range of 1SD, 5.62-12.10, P=0.001) or non-atopic healthy children (8.58; range of 1SD, 5.51-13.38, P<0.001). The FeNO levels were higher in children with current atopic AR compared with atopic healthy children (9.78; range of 1SD, 5.97-16.02, P=0.083).ConclusionsMold exposure and use of antibiotics during infancy increases the risk of current AR, whereas having an older sibling reduces it. Children with current atopic AR exhibit higher levels of FeNO compared with non-atopic rhinitis cases, suggesting that FeNO levels may be a useful discriminatory marker for subtypes of AR in preschool children.

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Section: Discussionmentioning

confidence: 99%

Allergic Rhinitis in Preschool Children and the Clinical Utility of FeNO

Yoon

Choi

Lee

et al. 2017

Allergy Asthma Immunol Res

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“…Epithelial fragility 100 and epithelial shedding 101 in asthmatic patients have been recognized for many years, but this remains a controversial area 102 . Nonetheless, through use of specific markers of response to injury, such as increased expression of EGFR, epithelial damage has been confirmed in bronchial biopsy specimens from asthmatic adults 103 and children 104 .…”

Section: Dysregulation Of the Epithelial Barrier In Asthmatic Patientsmentioning

confidence: 99%

Phenotypic and genetic aspects of epithelial barrier function in asthmatic patients

Loxham

Davies

2017

Journal of Allergy and Clinical Immunology

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The bronchial epithelium is continuously exposed to a multitude of noxious challenges in inhaled air. Cellular contact with most damaging agents is reduced by the action of the mucociliary apparatus and by formation of a physical barrier that controls passage of ions and macromolecules. In conjunction with these defensive barrier functions, immunomodulatory cross-talk between the bronchial epithelium and tissue-resident immune cells controls the tissue microenvironment and barrier homeostasis. This is achieved by expression of an array of sensors that detect a wide variety of viral, bacterial, and nonmicrobial (toxins and irritants) agents, resulting in production of many different soluble and cell-surface molecules that signal to cells of the immune system. The ability of the bronchial epithelium to control the balance of inhibitory and activating signals is essential for orchestrating appropriate inflammatory and immune responses and for temporally modulating these responses to limit tissue injury and control the resolution of inflammation during tissue repair. In asthmatic patients abnormalities in many aspects of epithelial barrier function have been identified. We postulate that such abnormalities play a causal role in immune dysregulation in the airways by translating gene-environment interactions that underpin disease pathogenesis and exacerbation.

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“…In the early to mid 20th century, asthma was seen as a disease of intermittent bronchospasm and treated with various bronchodilators. But from the 1920s, inflammation was recognized as pathogenetic to asthma (for a review see [121]), and, more recently, the concept of “remodeling”, a description of a chronically inflamed, narrowed asthmatic airway with smooth muscle hypertrophy, a thickened basement membrane, and—importantly for this discussion—chronic, persistent, focal to widespread epithelial damage along with goblet cell hyperplasia [98]—as an end result of inflammation, has defined the disease process [122, 123]. …”

Section: Apoptosis In Airway Epithelium In Diseasementioning

confidence: 99%

“…Epithelial injury is common even when the clinical state of asthma is mild [123, 124] and is persistent over time [1]. Epithelial damage correlates with airway hyperreactivity and may be seen in newly diagnosed asthma [125, 126].…”

Section: Apoptosis In Airway Epithelium In Diseasementioning

confidence: 99%

Apoptosis and the Airway Epithelium

White

2011

Journal of Allergy

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The airway epithelium functions as a barrier and front line of host defense in the lung. Apoptosis or programmed cell death can be elicited in the epithelium as a response to viral infection, exposure to allergen or to environmental toxins, or to drugs. While apoptosis can be induced via activation of death receptors on the cell surface or by disruption of mitochondrial polarity, epithelial cells compared to inflammatory cells are more resistant to apoptotic stimuli. This paper focuses on the response of airway epithelium to apoptosis in the normal state, apoptosis as a potential regulator of the number and types of epithelial cells in the airway, and the contribution of epithelial cell apoptosis in important airways diseases.

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Damage of the Airway Epithelium and Bronchial Reactivity in Patients with Asthma

Cited by 1,186 publications

References 11 publications

Allergic Rhinitis in Preschool Children and the Clinical Utility of FeNO

Allergic Rhinitis in Preschool Children and the Clinical Utility of FeNO

Phenotypic and genetic aspects of epithelial barrier function in asthmatic patients

Apoptosis and the Airway Epithelium

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