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Published on: May 2, 2018
CD14 major role during lipopolysaccharide-induced inflammation in chick embryo cardiomyocytes
Maria Antonietta Panaro1, Antonia Cianciulli, Nicoletta Gagliardi
1Department of Human Anatomy and Histology, University of Bari, Bari, Italy. ma.panaro@anatomia.uniba.it
Insights
CD14, a receptor for bacterial lipopolysaccharide, is present on cardiomyocytes. This receptor mediates the internalization of lipopolysaccharide, influencing inflammatory responses in sepsis-related heart dysfunction.
Area of Science:
- Cardiovascular Biology
- Immunology
- Cell Biology
Background:
- Sepsis-induced myocardial dysfunction is linked to inflammatory mediators.
- Bacterial lipopolysaccharide (LPS) triggers inflammatory responses via cell surface receptors.
- CD14 acts as a receptor for LPS, playing a crucial role in innate immunity.
Purpose of the Study:
- To investigate the role of CD14 in chick embryo cardiomyocytes stimulated with LPS.
- To determine if CD14 mediates LPS internalization and subsequent inflammatory responses in cardiomyocytes.
Main Methods:
- Detection of CD14 expression using confocal laser microscopy and immunoblotting.
- Stimulation of cardiomyocytes with LPS and assessment of TNF-alpha and NO production.
- Treatment with anti-CD14 antibodies and cytochalasin D to evaluate CD14's function and LPS internalization.
Main Results:
- CD14 is expressed on the surface membrane of cardiomyocytes.
- LPS internalization by cardiomyocytes is CD14-dependent and involves the cytoskeleton.
- Anti-CD14 treatment attenuated LPS-induced TNF-alpha and NO production, indicating CD14's role in LPS-mediated responses.
Conclusions:
- CD14 is expressed on cardiomyocytes and mediates LPS internalization.
- CD14 plays a significant role in LPS-induced inflammatory mediator production by cardiomyocytes.
- Targeting CD14 may offer a therapeutic strategy for sepsis-related myocardial dysfunction.
Abstract:
CD14 is a surface differentiation antigen that functions as a receptor for bacterial lipopolysaccharide. The cellular signaling events that lead to lipopolysaccharide-induced production of inflammatory mediators are the primary cause of myocardial dysfunction observed in sepsis. Here, we evaluated the role of CD14 in chick embryo cardiomyocytes stimulated with lipopolysaccharide. CD14 expression was detected by confocal laser microscopy observation and by immunoblotting analysis. Moreover, we provided evidence for CD14-dependent functional responses of lipopolysaccharide-stimulated cardiomyocytes in terms of tumor necrosis factor (TNF)-alpha and nitric oxide (NO) production. Attenuated TNF-alpha and NO secretion, following anti-CD14 treatment of cardiomyocytes, suggested a role for this receptor in lipopolysaccharide-mediated cell responses. We also evidenced that labeled lipopolysaccharide was internalized and localized next to the Golgi complex, at the level of lysosomes, and in the perinuclear zone. The intracytoplasmatic transport seems to depend on the contractile apparatus, because cell pretreatment with cytochalasin D prevented lipopolysaccharide internalization and reduced both TNF-alpha and NO release. Lipopolysaccharide internalization was dependent on CD14 receptor, since anti-CD14 pre-treatment prevented endotoxin uptake by cardiomyocytes. Results demonstrated: (1) CD14 is expressed on the surface membrane of cardiomyocytes; (2) CD14 is involved in cytoskeletal dependent lipopolysaccharide internalization at specific cytoplasmatic locations; (3) CD14 plays a role in lipopolysaccharide-mediated responses by cardiomyocytes after lipopolysaccharide internalization.
