title: Differential interactions of Streptococcus gordonii and Staphylococcus aureus with cultured osteoblasts.
abstract: The impedance of normal osteoblast function by microorganisms is at least in part responsible for the failure of dental or orthopedic implants. Staphylococcus aureus is a major pathogen of bone, and exhibits high levels of adhesion and invasion of osteoblasts. In this article we show that the commensal oral bacterium Streptococcus gordonii also adheres to and is internalized by osteoblasts. Entry of S. gordonii cells had typical features of phagocytosis, similar to S. aureus, with membrane protrusions characterizing initial uptake, and closure of the osteoblast membrane leading to engulfment. The sensitivities of S. gordonii internalization to inhibitors cytochalasin D, colchicine and monensin indicated uptake through endocytosis, with requirement for actin accumulation. Internalization levels of S. gordonii were enhanced by expression of S. aureus fibronectin-binding protein A (FnBPA) on the S. gordonii cell surface. Lysosomal-associated membrane protein-1 phagosomal membrane marker accumulated with intracellular S. aureus and S. gordonii FnBPA, indicating trafficking of bacteria into the late endosomal/lysosomal compartment. Streptococcus gordonii cells did not survive intracellularly for more than 12 h, unless expressing FnBPA, whereas S. aureus showed extended survival times (>48 h). Both S. aureus and S. gordonii DL-1 elicited a rapid interleukin-8 response by osteoblasts, whereas S. gordonii FnBPA was slower. Only S. aureus elicited an interleukin-6 response. Hence, S. gordonii invades osteoblasts by a mechanism similar to that exhibited by S. aureus, and elicits a proinflammatory response that may promote bone resorption.
authors: School of Oral and Dental Sciences, University of Bristol, Bristol, UK.
authors: C E
authors: CE
authors: Jauregui
authors: J P
authors: JP
authors: Mansell
authors: M A
authors: MA
authors: Jepson
authors: H F
authors: HF
authors: Jenkinson
mesh_terms: D000199:Actins / Q000037:antagonists & inhibitors; D018829:Adhesins, Bacterial / Q000502:physiology; D001422:Bacterial Adhesion / Q000502:physiology; D001862:Bone Resorption / Q000276:immunology / Q000382:microbiology; D018929:Cell Culture Techniques; D045744:Cell Line, Tumor; D003078:Colchicine / Q000494:pharmacology; D015638:Cytochalasin D / Q000494:pharmacology; D003764:Dental Materials / Q000737:chemistry; D004705:Endocytosis / Q000187:drug effects / Q000502:physiology; D005353:Fibronectins / Q000502:physiology; D006801:Humans; D018836:Inflammation Mediators / Q000276:immunology; D015850:Interleukin-6 / Q000276:immunology; D016209:Interleukin-8 / Q000276:immunology; D052118:Lysosomal-Associated Membrane Protein 1 / Q000502:physiology; D050296:Microbial Viability; D008985:Monensin / Q000494:pharmacology; D010006:Osteoblasts / Q000276:immunology / Q000382:microbiology*; D010587:Phagocytosis / Q000502:physiology; D061209:Proton Ionophores / Q000494:pharmacology; D013211:Staphylococcus aureus / Q000187:drug effects / Q000276:immunology / Q000502:physiology*; D054773:Streptococcus gordonii / Q000187:drug effects / Q000276:immunology / Q000502:physiology*; D013997:Time Factors; D014025:Titanium / Q000737:chemistry
chemical_list: D000199:Actins; D018829:Adhesins, Bacterial; D003764:Dental Materials; D005353:Fibronectins; D018836:Inflammation Mediators; D015850:Interleukin-6; D016209:Interleukin-8; D052118:Lysosomal-Associated Membrane Protein 1; D061209:Proton Ionophores; C078635:fibronectin-binding proteins, bacterial; D015638:Cytochalasin D; D008985:Monensin; D014025:Titanium; D003078:Colchicine
keywords: adherence; cytokine; endocytosis; fibronectin; lysosome