ArticleBiochemical and biophysical research communications2017
Pseudomonas aeruginosa increases MUC1 expression in macrophages through the TLR4-p38 pathway.
Article in Biochemical and biophysical research communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- MUC1 in the upper-lower airway inflammatory continuum: an endotype-centered perspective.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Modeling Host-Pathogen Interactions inInternational journal of molecular sciences · 2024Review
- MicroRNA-23a-5p regulates cell proliferation, migration and inflammation of TNF-α-stimulated human fibroblast-like MH7A synoviocytes by targeting TLR4 in rheumatoid arthritis.Experimental and therapeutic medicine · 2021Article
- The role of mucin 1 in respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2021Review
- Pathogen Challenge and Dietary Shift Alter Microbiota Composition and Activity in a Mucin-AssociatedFrontiers in microbiology · 2021Article
- The role of the innate immune system on pulmonary infections.Biological chemistry · 2019Review
- MUC1: The First Respiratory Mucin with an Anti-Inflammatory Function.Journal of clinical medicine · 2017Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Alveolar macrophages (AMs) play a critical role in the clearance of Pseudomonas aeruginosa (Pa) from the airways. However, hyper-activation of macrophages can impair bacterial clearance and contribute to morbidity and mortality. MUC1 mucin is a membrane-tethered, high molecular mass glycoprotein expressed on the apical surface of mucosal epithelial cells and some hematopoietic cells, including macrophages, where it counter-regulates inflammation. We recently reported that Pa up-regulates the expression of MUC1 in primary human AMs and THP-1 macrophages, and that increased MUC1 expression in these cells prevents hyper-activation of macrophages that appears to be important for host defense against severe pathology of Pa lung infection. The aims of this study were to elucidate the mechanism by which Pa increases MUC1 expression in macrophages. The results showed that: (a) Pa stimulation of THP-1 macrophages increased MUC1 expression both at transcriptional and protein levels in a dose-dependent manner; (b) Both Pa- and LPS-induced MUC1 expression in THP-1 cells were significantly diminished by an inhibitory peptide of TLR4; and (c) LPS-stimulated MUC1 expression was diminished at both the mRNA and protein levels by an inhibitor of the p38 mitogen-activated protein kinase, but not by inhibitors of ERK1/2, JNK, or IKK. We conclude that Pa-stimulated MUC1 expression in THP-1 macrophages is regulated mainly through the TLR4-p38 signaling pathway.
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Registered trials
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