ArticlePloS one2013
Mannan-binding lectin inhibits Candida albicans-induced cellular responses in PMA-activated THP-1 cells through Toll-like receptor 2 and Toll-like receptor 4.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Immersion-Based Candida albicans Infection in Adult Zebrafish Induces Distinct Behavioral, Immune and Oxidative Responses in a Dose- and Time-Dependent Manner.Current microbiology · 2026Article
- Licochalcone A Protects Vaginal Epithelial Cells Against Candida albicans Infection Via the TLR4/NF-κB Signaling Pathway.Journal of microbiology (Seoul, Korea) · 2024Article
- Mycobiome Dysbiosis in Women with Intrauterine Adhesions.Microbiology spectrum · 2022Article
- How Gut Bacterial Dysbiosis Can PromoteMicroorganisms · 2022Review
- Mannan-Binding Lectin Regulates the Th17/Treg Axis Through JAK/STAT and TGF-β/SMAD Signaling AgainstJournal of inflammation research · 2022Article
- Antiviral lectin Q-Griffithsin suppresses fungal infection in murine models of vaginal candidiasis.Frontiers in cellular and infection microbiology · 2022Article
- Use of RNA Sequencing to Perform Comprehensive Analysis of Long Noncoding RNA Expression Profiles in Macrophages Infected with Trichosporon asahii.Mycopathologia · 2021Article
- Toll-like receptor-mediated innate immunity against herpesviridae infection: a current perspective on viral infection signaling pathways.Virology journal · 2020Review
- Review
- Collectins: Innate Immune Pattern Recognition Molecules.Advances in experimental medicine and biology · 2020Review
- Mannan-Binding Lectin Suppresses Peptidoglycan-Induced TLR2 Activation and Inflammatory Responses.Mediators of inflammation · 2019Article
- Observational
- The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors.Frontiers in immunology · 2018Review
- Candida albicans-derived mannoproteins activate NF-κB in reporter cells expressing TLR4, MD2 and CD14.PloS one · 2017Article
- C-type lectin receptors in tuberculosis: what we know.Medical microbiology and immunology · 2016Review
- Mangiferin inhibits macrophage classical activation via downregulating interferon regulatory factor 5 expression.Molecular medicine reports · 2016Article
- Role of mannose-binding lectin in intestinal homeostasis and fungal elimination.Mucosal immunology · 2016Article
- Effect of trastuzumab interchain disulfide bond cleavage on Fcγ receptor binding and antibody-dependent tumour cell phagocytosis.Journal of biochemistry · 2016Article
- Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCandida albicans (C. albicans), the most common human fungal pathogen, can cause fatal systemic infections under certain circumstances. Mannan-binding lectin (MBL),a member of the collectin family in the C-type lectin superfamily, is an important serum component associated with innate immunity. Toll-like receptors (TLRs) are expressed extensively, and have been shown to be involved in C. albicans-induced cellular responses. We first examined whether MBL modulated heat-killed (HK) C. albicans-induced cellular responses in phorbol 12-myristate 13-acetate (PMA)-activated human THP-1 macrophages. We then investigated the possible mechanisms of its inhibitory effect. METHODOLOGY/PRINCIPAL FINDING: Enzyme-linked immunosorbent assay (ELISA) and reverse transcriptasepolymerase chain reaction (RT-PCR) analysis showed that MBL at higher concentrations (10-20 µg/ml) significantly attenuated C. albicans-induced chemokine (e.g., IL-8) and proinflammatory cytokine (e.g., TNF-α) production from PMA-activated THP-1 cells at both protein and mRNA levels. Electrophoretic mobility shift assay (EMSA) and Western blot (WB) analysis showed that MBL could inhibit C. albicans-induced nuclear factor-κB (NF-κB) DNA binding and its translocation in PMA-activated THP-1 cells. MBL could directly bind to PMA-activated THP-1 cells in the presence of Ca(2+), and this binding decreased TLR2 and TLR4 expressions in C. albicans-induced THP-1 macrophages. Furthermore, the binding could be partially inhibited by both anti-TLR2 monoclonal antibody (clone TL2.1) and anti-TLR4 monoclonal antibody (clone HTA125). In addition, co-immunoprecipitation experiments and microtiter wells assay showed that MBL could directly bind to the recombinant soluble form of extracellular TLR2 domain (sTLR2) and sTLR4. CONCLUSIONS/SIGNIFICANCE: Our study demonstrates that MBL can affect proinflammatory cytokine and chemokine expressions by modifying C. albicans-/TLR-signaling pathways. This study supports an important role for MBL on the regulation of C. albicans-induced cellular responses.
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