Staphylococci planktonic and biofilm environments differentially affect osteoclast formation

Introduction The pathophysiology of chronic implant-related bone infections is characterized by an increase in osteoclast numbers and enhanced bone resorption. Biofilms are a major reason for chronicity of such infections as the biofilm matrix protects bacteria against antibiotics and impairs the fu...

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Published in:Inflammation research 2023-07, Vol.72 (7), p.1465-1484
Main Authors: Seebach, Elisabeth, Kraus, Franziska V., Elschner, Tabea, Kubatzky, Katharina F.
Format: Article
Language:English
Subjects:
Allergology
Antibiotics
Bacteria
Biofilms
Biomedical and Life Sciences
Biomedicine
Bone Resorption
Cell differentiation
Dermatology
Destruction
Giant cells
Humans
Immune response
Immune system
Immunology
Inflammation
Macrophages
Neurology
Original Research Paper
Osteoclastogenesis
Osteoclasts
Pharmacology/Toxicology
Plankton - physiology
Priming
Proteins
RANK Ligand - pharmacology
Rheumatology
Staphylococcus
Staphylococcus aureus
Stimulation
Toll-like receptors
TRANCE protein
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Summary:Introduction The pathophysiology of chronic implant-related bone infections is characterized by an increase in osteoclast numbers and enhanced bone resorption. Biofilms are a major reason for chronicity of such infections as the biofilm matrix protects bacteria against antibiotics and impairs the function of immune cells. Macrophages are osteoclast precursor cells and therefore linked to inflammation and bone destruction. Objective and method Investigations on the impact of biofilms on the ability of macrophages to form osteoclasts are yet missing and we, therefore, analyzed the effect of Staphylococcus aureus (SA) and Staphylococcus epidermidis (SE) planktonic and biofilm environments on osteoclastogenesis using RAW 264.7 cells and conditioned media (CM). Results Priming with the osteoclastogenic cytokine RANKL before CM addition enabled the cells to differentiate into osteoclasts. This effect was highest in SE planktonic or SA biofilm CM. Simultaneous stimulation with CM and RANKL, however, suppressed osteoclast formation and resulted in formation of inflammation-associated multinucleated giant cells (MGCs) which was most pronounced in SE planktonic CM. Conclusion Our data indicate that the biofilm environment and its high lactate levels are not actively promoting osteoclastogenesis. Hence, the inflammatory immune response against planktonic bacterial factors through Toll-like receptors seems to be the central cause for the pathological osteoclast formation. Therefore, immune stimulation or approaches that aim at biofilm disruption need to consider that this might result in enhanced inflammation-mediated bone destruction.
ISSN:1023-3830
1420-908X
DOI:10.1007/s00011-023-01745-9