Inflammation‐dependent and independent airway remodelling in asthma

Elliot, John; Noble, Peter B.; Mauad, Thaís; Bai, Tony R.; Abramson, Michael J.; McKay, Karen; Green, Francis H. Y.; James, Alan

doi:10.1111/resp.13360

Cited by 53 publications

(35 citation statements)

References 41 publications

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“…The ASM is at the core of asthma symptoms and its thickening results from the perpetual stimulation with numerous anabolic stimuli including growth factors, spasmogens, and immune modulators (30,31). The persistent reduction of ASM thickening associated with the long-term benefits of bronchial thermoplasty indicates that punctual interventions directed against the ASM bear therapeutic potential (32)(33)(34).…”

Section: Discussionmentioning

confidence: 99%

Metabolic Adaptation of Airway Smooth Muscle Cells to an SPHK2 Substrate Precedes Cytostasis

Blais-Lecours

Laouafa

Arias‐Reyes

et al. 2020

Am J Respir Cell Mol Biol

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Section: Discussionmentioning

confidence: 99%

Metabolic Adaptation of Airway Smooth Muscle Cells to an SPHK2 Substrate Precedes Cytostasis

Blais-Lecours

Laouafa

Arias‐Reyes

et al. 2020

Am J Respir Cell Mol Biol

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“…ASMCs phenotype is linked with the activation of the deposition of extracellular matrix proteins and pro-remodeling function of recruited fibrocytes (Mattoli, 2015;Boulet, 2018), exacerbating airway remodeling. It was found that ASMCs proliferation was aggravated in asthmatic patients and there were more ASMCs from asthma subjects than from healthy subjects in post-mortem airway sections (Fujita et al, 2011;Elliot et al, 2018;James et al, 2018). In vivo, ASMCs thickening and proliferation were verified to be promoted in house dust mite-induced murine (Yang et al, 2017).…”

Section: Lncrnas Associated With Asmcs Proliferation In Asthma Pathogmentioning

confidence: 94%

Long Noncoding RNAs in the Regulation of Asthma: Current Research and Clinical Implications

2020

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Asthma is a chronic airway inflammatory disorder related to variable expiratory airflow limitation, leading to wheeze, shortness of breath, chest tightness, and cough. Its characteristic features include airway inflammation, airway remodeling and airway hyperresponsiveness. The pathogenesis of asthma remains extremely complicated and the detailed mechanisms are not clarified. Long noncoding RNAs (lncRNAs) have been reported to play a prominent role in asthma and function as modulators of various aspects in pathological progress of asthma. Here, we summarize recent advances of lncRNAs in asthma pathogenesis to guide future researches, clinical treatment and drug development, including their regulatory functions in the T helper (Th) 1/Th2 imbalance, Th17/T regulatory (Treg) imbalance, eosinophils dysfunction, macrophage polarization, airway smooth muscle cells proliferation, and glucocorticoid insensitivity.

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“…However, there is no clear hypothesis regarding by which mechanism(s) the microorganisms and non-biological factors, such as dust, lead to the same clinical symptoms that are diagnosed as asthma. Nevertheless, the hypothesis is supported by the observation that airway wall remodeling often occurs prior to the detection of any inflammation [16,23]. In children with severe asthma, airway wall remodeling correlated with eosinophilia, but not with type-2 cytokines [24].…”

Section: Asthmamentioning

confidence: 99%

Immunologic and Non-Immunologic Mechanisms Leading to Airway Remodeling in Asthma

Fang

Sun

Roth

2020

IJMS

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Asthma increases worldwide without any definite reason and patient numbers double every 10 years. Drugs used for asthma therapy relax the muscles and reduce inflammation, but none of them inhibited airway wall remodeling in clinical studies. Airway wall remodeling can either be induced through pro-inflammatory cytokines released by immune cells, or direct binding of IgE to smooth muscle cells, or non-immunological stimuli. Increasing evidence suggests that airway wall remodeling is initiated early in life by epigenetic events that lead to cell type specific pathologies, and modulate the interaction between epithelial and sub-epithelial cells. Animal models are only available for remodeling in allergic asthma, but none for non-allergic asthma. In human asthma, the mechanisms leading to airway wall remodeling are not well understood. In order to improve the understanding of this asthma pathology, the definition of “remodeling” needs to be better specified as it summarizes a wide range of tissue structural changes. Second, it needs to be assessed if specific remodeling patterns occur in specific asthma pheno- or endo-types. Third, the interaction of the immune cells with tissue forming cells needs to be assessed in both directions; e.g., do immune cells always stimulate tissue cells or are inflamed tissue cells calling immune cells to the rescue? This review aims to provide an overview on immunologic and non-immunologic mechanisms controlling airway wall remodeling in asthma.

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Inflammation‐dependent and independent airway remodelling in asthma

Cited by 53 publications

References 41 publications

Metabolic Adaptation of Airway Smooth Muscle Cells to an SPHK2 Substrate Precedes Cytostasis

Metabolic Adaptation of Airway Smooth Muscle Cells to an SPHK2 Substrate Precedes Cytostasis

Long Noncoding RNAs in the Regulation of Asthma: Current Research and Clinical Implications

Immunologic and Non-Immunologic Mechanisms Leading to Airway Remodeling in Asthma

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