Lung functional development and asthma trajectories

Decrue, Fabienne; Gorlanova, Olga; Usemann, Jakob; Frey, Urs

doi:10.1007/s00281-020-00784-2

Cited by 19 publications

(25 citation statements)

References 112 publications

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“…In the article "Lung functional development and asthma trajectories" it is illustrated that a possible mechanism for a sustained effect of impaired lung function on asthma is the influence of early life risk factors on early life lung functional growth and development, representing the most susceptible phase of lung growth and plasticity. Hereditary and environmental peri-and postnatal factors on lung functional development are summarized including air pollution, tobacco exposure, nutrition, intrauterine growth retardation, prematurity, early life infections, microbiome, and allergies and their effect on lung functional trajectories [2]. While for example prematurity impairs lung growth directly, the influence of a number of environmental factors is mediated through inflammatory processes such as infections or oxidative stress.…”

Section: Prefacementioning

confidence: 99%

“…While for example prematurity impairs lung growth directly, the influence of a number of environmental factors is mediated through inflammatory processes such as infections or oxidative stress. Timing and nature of these influences lead to degrees of impaired lung functional capacity in early adulthood [2]. Future long-term respiratory morbidity such as chronic asthma or chronic obstructive airway disease (COPD) is discussed as well as possibilities to prevent or modify early abnormal lung functional growth trajectories.…”

Section: Prefacementioning

confidence: 99%

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Preface

Schaub

2020

Semin Immunopathol

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Section: Prefacementioning

confidence: 99%

Section: Prefacementioning

confidence: 99%

Preface

Schaub

2020

Semin Immunopathol

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“…1 Children with asthma are at higher risk of developing chronic obstructive pulmonary disease (COPD). 2 In addition to acute inflammation caused by stimuli such as inhalation of allergens, other factors including microenvironments variation and viral infections can stimulate the lung structural cells and cause a strong secretion of pro-inflammatory mediators, cytokines, chemokines, and proteases. 3 Theoretically, antigen stimulation causes an increase in IL-1α and IL-1β, the typical innate immune cytokines involved in the initiation and persistence of inflammation, in peripheral blood mononuclear cells (PBMCs) during the exacerbation of asthma.…”

Section: Introductionmentioning

confidence: 99%

“…Recently, the prevalence of asthma continues to rise, especially in children 1 . Children with asthma are at higher risk of developing chronic obstructive pulmonary disease (COPD) 2 . In addition to acute inflammation caused by stimuli such as inhalation of allergens, other factors including microenvironments variation and viral infections can stimulate the lung structural cells and cause a strong secretion of pro‐inflammatory mediators, cytokines, chemokines, and proteases 3…”

Section: Introductionmentioning

confidence: 99%

IL‐1 signaling pathway molecules as key markers in childhood asthma

Wei

Huang

et al. 2020

Pediatric Allergy Immunology

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Objective The prevalence of childhood asthma has been increasing in recent years. This study aims to investigate the involvement of the key molecules of IL‐1 (interleukin‐1) signaling pathways in pediatric patients with asthma. Methods Differentially expressed genes (DEGs) associated with IL‐1 signaling pathways were identified with RNA‐seq from peripheral blood samples collected from asthmatic or healthy children and were further verified in clinical peripheral blood samples. Cellular models and asthmatic mice were subsequently developed to validate the identified asthmatic markers. Results Among the DEGs identified by RNA‐seq, eight signal transducers associated with the IL‐1 signaling network, namely IL‐1RN, IL‐1β, IL‐1RAP, IRAK3, IL‐1R1, MYD88, IRAK2, and PELI1, were found to be substantially upregulated in children with asthma. Interestingly, a significant serially increased expression of four genes (IL‐1RN, IL‐1RAP, IRAK3, and PELI1) was observed in healthy subjects, patients with chronic persistent asthma and patients with acute exacerbation asthma. In particular, these four genes were continuously overexpressed in recurrent patients. A significant induction of the above four genes was then observed in house dust mite (HDM)–stimulated peripheral blood mononuclear cells (PBMCs) and ovalbumin (OVA)–induced asthmatic mice. In addition, a time‐dependent induction of IL‐1RAP and PELI1 was also detected in HDM‐treated THP‐1 cells, an acute monocytic leukemia cell line. Conclusions These results demonstrate that IL‐1RN, IL‐1RAP, IRAK3, and PELI1, which are signal transducers of the IL‐1 signaling pathway, could serve as biomarkers for the pathogenesis of childhood asthma and for potential therapeutic targets of asthma.

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“…GR-a, the classical glucocorticoid receptor isoform (24)(25)(26)(27) has a dominant-negative inhibitor, GR-b, that does not bind corticosteroids. Overexpression of GR-b is due to abnormal activation of proinflammatory signaling pathways with emerging evidence for a contribution of oxidative stress (8,10,(28)(29)(30)(31). Oxidative stress is defined as an imbalance between reactive oxygen species and the capability of the biological system to detoxify the reactive intermediates or to repair the damage caused by oxidative free radicals (32,33).…”

mentioning

confidence: 99%

Ozone-Induced Oxidative Stress, Neutrophilic Airway Inflammation, and Glucocorticoid Resistance in Asthma

2021

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Despite recent advances in using biologicals that target Th2 pathways, glucocorticoids form the mainstay of asthma treatment. Asthma morbidity and mortality remain high due to the wide variability of treatment responsiveness and complex clinical phenotypes driven by distinct underlying mechanisms. Emerging evidence suggests that inhalation of the toxic air pollutant, ozone, worsens asthma by impairing glucocorticoid responsiveness. This review discusses the role of oxidative stress in glucocorticoid resistance in asthma. The underlying mechanisms point to a central role of oxidative stress pathways. The primary data source for this review consisted of peer-reviewed publications on the impact of ozone on airway inflammation and glucocorticoid responsiveness indexed in PubMed. Our main search strategy focused on cross-referencing “asthma and glucocorticoid resistance” against “ozone, oxidative stress, alarmins, innate lymphoid, NK and γδ T cells, dendritic cells and alveolar type II epithelial cells, glucocorticoid receptor and transcription factors”. Recent work was placed in the context from articles in the last 10 years and older seminal research papers and comprehensive reviews. We excluded papers that did not focus on respiratory injury in the setting of oxidative stress. The pathways discussed here have however wide clinical implications to pathologies associated with inflammation and oxidative stress and in which glucocorticoid treatment is essential.

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Lung functional development and asthma trajectories

Cited by 19 publications

References 112 publications

Preface

Preface

IL‐1 signaling pathway molecules as key markers in childhood asthma

Ozone-Induced Oxidative Stress, Neutrophilic Airway Inflammation, and Glucocorticoid Resistance in Asthma

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