YKL-40 mediates airway remodeling in asthma via activating FAK and MAPK signaling pathway

Sun, Yinghao; Shi, Zhenxiang; Liu, Bing; Li, Xian'Gui; Li, Ge; Yang, Feng; Tang, Hao

doi:10.1080/15384101.2020.1750811

Cited by 17 publications

(16 citation statements)

References 35 publications

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“…The “antigen processing and presentation” and “two-component system” pathways associated with allergies were also upregulated at this stage. MAPK signaling was shown to be involved in airway inflammation and hyper-responsiveness in asthma ( Bao et al, 2017 ; Sun X. et al, 2020 ; Sun Y. et al, 2020 ). The members of the NOD-like receptor family promote inflammatory cell recruitment and regulate immune responses in different tissues, such as lung tissues ( Donovan et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Respiratory Microbiota Profiles Associated With the Progression From Airway Inflammation to Remodeling in Mice With OVA-Induced Asthma

Zheng

et al. 2021

Front. Microbiol.

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BackgroundThe dysbiosis of respiratory microbiota plays an important role in asthma development. However, there is limited information on the changes in the respiratory microbiota and how these affect the host during the progression from acute allergic inflammation to airway remodeling in asthma.ObjectiveAn ovalbumin (OVA)-induced mouse model of chronic asthma was established to explore the dynamic changes in the respiratory microbiota in the different stages of asthma and their association with chronic asthma progression.MethodsHematoxylin and eosin (H&E), periodic acid-schiff (PAS), and Masson staining were performed to observe the pathological changes in the lung tissues of asthmatic mice. The respiratory microbiota was analyzed using 16S rRNA gene sequencing followed by taxonomical analysis. The cytokine levels in bronchoalveolar lavage fluid (BALF) specimens were measured. The matrix metallopeptidase 9 (MMP-9) and vascular endothelial growth factor (VEGF-A) expression levels in lung tissues were measured to detect airway remodeling in OVA-challenged mice.ResultsAcute allergic inflammation was the major manifestation at weeks 1 and 2 after OVA atomization stimulation, whereas at week 6 after the stimulation, airway remodeling was the most prominent observation. In the acute inflammatory stage, Pseudomonas was more abundant, whereas Staphylococcus and Cupriavidus were more abundant at the airway remodeling stage. The microbial compositions of the upper and lower respiratory tracts were similar. However, the dominant respiratory microbiota in the acute inflammatory and airway remodeling phases were different. Metagenomic functional prediction showed that the pathways significantly upregulated in the acute inflammatory phase and airway remodeling phase were different. The cytokine levels in BALF and the expression patterns of proteins associated with airway remodeling in the lung tissue were consistent with the metagenomic function results.ConclusionThe dynamic changes in respiratory microbiota are closely associated with the progression of chronic asthma. Metagenomic functional prediction indicated the changes associated with acute allergic inflammation and airway remodeling.

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Section: Discussionmentioning

confidence: 99%

Respiratory Microbiota Profiles Associated With the Progression From Airway Inflammation to Remodeling in Mice With OVA-Induced Asthma

Zheng

et al. 2021

Front. Microbiol.

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“…Furthermore, chitinase 3-like 1 (CHI3L1), also known as breast regression protein 39 in mice and YKL-40 in humans, is known to bind IL-13Ra2. 29,133 The elevated levels of CHI3L1/YKL-40 are shown in the sera and skin lesions in AD patients. 133 CHI3L1/YKL-40 promotes fibrotic process 133 and further accelerates Th2 deviation.…”

Section: Il-13ra2 and Scratch Injurymentioning

confidence: 99%

“…29,133 The elevated levels of CHI3L1/YKL-40 are shown in the sera and skin lesions in AD patients. 133 CHI3L1/YKL-40 promotes fibrotic process 133 and further accelerates Th2 deviation. 134 These results suggest a possibility that the scratch-induced IL-13Ra2 upregulation may convert the keratinocyte response from IL-13-dominant to CHI3L1/YKL-40-dominant pattern.…”

Section: Il-13ra2 and Scratch Injurymentioning

confidence: 99%

Pathogenic implication of epidermal scratch injury in psoriasis and atopic dermatitis

Furue

Ulzii

Tanaka

et al. 2020

The Journal of Dermatology

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Mechanical scratching, a common external stress affecting the skin, is induced by various causes, such as pruritus. Scratch injury to epidermal keratinocytes upregulates the production and release of chemokine (C‐C motif) ligand 20 (CCL20) in vitro, which selectively chemoattracts interleukin (IL)‐17A‐producing immune cells that express chemokine (C‐C motif) receptor 6 (CCR6). In IL‐17A‐dominant psoriasis, scratch‐induced CCL20 upregulation and subsequent accumulation of IL‐17A‐producing immune cells and CCR6+ mature dendritic cells may trigger the development of psoriatic lesions, a process known as the Koebner phenomenon. In IL‐4/IL‐13‐dominant atopic dermatitis, pruritus and subsequent scratching are the primary symptoms. Scratch‐induced CCL20 production from keratinocytes may explain why IL‐17A levels are also elevated in atopic dermatitis. In contrast, mechanical scratching is likely to negatively regulate IL‐13 signaling by upregulating the expression of IL‐13 receptor α2, which serves as a decoy receptor for IL‐13 in keratinocytes. In this review, we summarize current reports on topics related to the pathogenic role of epidermal scratch injury in psoriasis and atopic dermatitis.

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“…YKL40 may promote the airway remodeling of asthma by activating FAK and MAPK signalling pathways, inducing epithelial mesenchymal transition (EMT) and subepithelial fibrosis. 93 Tang and colleagues 94 showed that serum YKL40 levels of Chinese patients with asthma were increased and correlated with the number of exacerbations. Serum YKL40 levels were correlated with total IgE, blood eosinophils and inversely with lung function and could predict the T A B L E 1 (Continued)…”

Section: Emerging Biomarkersmentioning

confidence: 99%

Mechanisms and biomarkers of airway epithelial cell damage in asthma: A review

Yang

Jia

et al. 2021

Clinical Respiratory J

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Bronchial asthma, or asthma for short, is a chronic disease of the airway characterised by symptoms such as respiratory distress, chest tightness, wheezing, coughing, sputum formation and exercise intolerance. The asthmatic airway is chronically inflamed due to the activation and/or recruitment of a variety of tissue resident and infiltrating cells including eosinophils, mast cells, T lymphocytes, macrophages, airway epithelial cells (AECs), fibroblasts and airway smooth muscle (ASM) cells. The AEC, which sits at the interface between the host and the external environment, is not only an efficient physical barrier but also represents the first line of defence against microorganisms, airborne irritants and allergens. 1 The airway epithelium maintains the health of the respiratory tract mucosa through its physical barrier function, cilia removal function and natural immune defence function. It plays a central role in the pathogenesis of asthma. On the one hand, changes in its structure and function directly affect the inflammatory response and promote disease formation. On the other hand, the airway epithelium is also significantly damaged by inflammation. At present, the epithelial barrier has been placed in the forefront of the pathophysiology of airway inflammation. Epigenetic studies have confirmed that

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YKL-40 mediates airway remodeling in asthma via activating FAK and MAPK signaling pathway

Cited by 17 publications

References 35 publications

Respiratory Microbiota Profiles Associated With the Progression From Airway Inflammation to Remodeling in Mice With OVA-Induced Asthma

Respiratory Microbiota Profiles Associated With the Progression From Airway Inflammation to Remodeling in Mice With OVA-Induced Asthma

Pathogenic implication of epidermal scratch injury in psoriasis and atopic dermatitis

Mechanisms and biomarkers of airway epithelial cell damage in asthma: A review

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