Dataset Information

S100A4/TCF complex transcription regulation drives epithelial-mesenchymal transition in chronic sinusitis through Wnt/GSK-3β/β-catenin signaling

ABSTRACT: Chronic rhinosinusitis (CRS) is closely associated with remodelling of nasal mucosal tissue during a prolonged inflammatory process, and epithelial mesenchymal transition (EMT) is thought to be involved in this process, but the underlying mechanisms driving this progression are unclear. Using a high-resolution Q Exactive Plus Orbitrap mass spectrometer, we performed a proteomic screen of CRS nasal mucosal tissue to identify differentially expressed proteins.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Nasal Mucosa

SUBMITTER: Ningyue Gong

LAB HEAD: S100A4/TCF complex transcription regulation drives epithelial-mesenchymal transition in chronic sinusitis through Wnt/GSK-3β/β-catenin signaling

PROVIDER: PXD030884 | Pride | 2022-02-21

REPOSITORIES: pride

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S100A4/TCF Complex Transcription Regulation Drives Epithelial-Mesenchymal Transition in Chronic Sinusitis Through Wnt/GSK-3β/β-Catenin Signaling.

Gong Ningyue N Shi Lei L Bing Xin X Li Hui H Hu Houyang H Zhang Pan P Yang Huiming H Guo Na N Du Hongjie H Xia Ming M Liu Chengcheng C

Frontiers in immunology 20220128

Epithelial-mesenchymal transition (EMT) is thought to be involved in the tissue remodeling and long-term inflammatory process of chronic sinusitis (CRS), but the driving mechanism is still unclear. Using high-resolution mass spectrometry, we performed a proteomic screen of CRS nasal mucosal tissue to identify differentially expressed proteins. Data are available via ProteomeXchange with identifier PXD030884. Specifically, we identified S100 calcium binding protein A4 (S100A4), an effectiv ...[more]

PMID: 35154161

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Project description:PURPOSE: Olfactory dysfunction (OD) is a debilitating symptom frequently reported by patients with chronic rhinosinusitis (CRS) and it is associated with a dysregulated sinonasal inflammation. However, little information is available about the effect of the inflammation-related nasal microbiota and related metabolites on the olfactory function in these patients. Therefore, the current study aimed to investigate the nasal microbiota-metabolites-immune interactions and their role in the pathogenesis of OD in CRS patients.METHODS: 23 and 19 CRS patients with and without OD (NOD), respectively, were enrolled in the present study. The 'Sniffin' Sticks' was used to measure the olfactory function, while the metagenomic shotgun sequencing and the untargeted metabolomic profiling were performed to assess the differences in terms of the nasal microbiome and metabolome between the two groups. The levels of nasal mucus inflammatory mediators were investigated by a multiplex flow Cytometric Bead Array (CBA).RESULTS: A decreased diversity in the nasal microbiome from the OD group compared to the NOD group was evidenced. The metagenomic analysis revealed a significant enrichment of Acinetobacter johnsonii in the OD group, while Mycoplasma arginini, Aeromonas dhakensis and Salmonella enterica were significantly less represented (LDA value > 3, p < 0.05). The nasal metabolome profiles were significantly different between the OD and NOD groups (P < 0.05). The purine metabolism was the most significantly enriched metabolic subpathway in OD patients compared with NOD patients (P < 0.001). The expressions of IL-5, IL-8, MIP-1alpha, MCP-1 and TNF were statistically and significantly increased in the OD group (P < 0.05). All these data, including the dysregulation of the nasal microbiota, differential metabolites and elevated inflammatory mediators in OD patients demonstrated a clear interaction relationship.CONCLUSIONS: The disturbed nasal microbiota-metabolite-immune interaction networks may be implicated in the pathogenesis of OD in CRS patients and the underlying pathophysiological mechanisms need to be further investigated in future studies.

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