THP-1 cells increase TNF-α production upon LPS + soluble human IgG co-stimulation supporting evidence for TLR4 and Fcγ receptors crosstalk
| Autor: | María Laura Ventura-Ayala, Martha Torres, Sigifredo Pedraza-Sánchez, Omar Vargas-Hernández, Alejandro Zentella, José Luis Ventura-Gallegos |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Lipopolysaccharides Lipopolysaccharide THP-1 Cells medicine.medical_treatment Immunology Lymphocyte Antigen 96 Syk Stimulation Biology Monocytes Proinflammatory cytokine 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Humans Cells Cultured Kinase Tumor Necrosis Factor-alpha Macrophages Receptors IgG NF-kappa B Receptor Cross-Talk Molecular biology Toll-Like Receptor 4 030104 developmental biology Cytokine Interleukin-1 Receptor-Associated Kinases chemistry Immunoglobulin G TLR4 Leukocytes Mononuclear Cytokines Interleukin-2 lipids (amino acids peptides and proteins) Tumor necrosis factor alpha 030215 immunology Signal Transduction |
| Zdroj: | Cellular immunology. 355 |
| ISSN: | 1090-2163 |
| Popis: | The lipopolysaccharide (LPS) of Gram-negative bacteria is recognized on human monocytes and macrophages by TLR4 and MD2 and induces the production of inflammatory cytokines; the LPS + IgG complexes co-stimulation increases the cytokine production, mediated by the Fc-γRIIa (CD32a). We stimulated human CD14 + monocytes or THP-1 cells with LPS or LPS + soluble human IgG (sIgG) and TNF-α transcription and production, assessed RT-qPCR, ELISA, or flow cytometry, was enhanced by 30% upon LPS + sIgG compared to LPS stimulation. LPS + sIgG co-stimulation affected the NF-κB pathway (p65 phosphorylation and nucleus translocation, and IkB- α degradation). The biochemical inhibition of IRAK 1/4 and Syk kinases suppressed the enhancer effect of LPS + sIgG on TNF- α production, suggesting the involvement of both MyD88 dependent and independent pathways. Our results suggest that during LPS activation, sIgG may participate in a TLR4 - Fc-γR crosstalk. |
| Databáze: | OpenAIRE |
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