RESUMEN
PURPOSE: Mechanisms underlying systemic infections by oral species of Mitis (Streptococcus mitis, Streptococcus oralis) and Sanguinis (Streptococcus gordonii, Streptococcus sanguinis) commensal streptococci are poorly understood. This study investigates profiles of susceptibility to complement-mediated host immunity in representative strains of these four species, which were isolated from oral sites or from the bloodstream. METHODOLOGY: Deposition of complement opsonins (C3b/iC3b), and surface binding to C-reactive protein (CRP) and to IgG antibodies were quantified by flow cytometry in 34 strains treated with human serum (HS), and compared to rates of opsonophagocytosis by human PMN mediated by complement (CR1/3) and/or IgG Fc (FcγRII/III) receptors. RESULTS: S. sanguinis strains showed reduced susceptibility to complement opsonization and low binding to CRP and to IgG compared to other species. Surface levels of C3b/iC3b in S. sanguinis strains were 4.5- and 7.8-fold lower than that observed in S. gordonii and Mitis strains, respectively. Diversity in C3b/iC3b deposition was evident among Mitis species, in which C3b/iC3b deposition was significantly associated with CR/FcγR-dependent opsonophagocytosis by PMN (P<0.05). Importantly, S. gordonii and Mitis group strains isolated from systemic infections showed resistance to complement opsonization when compared to oral isolates of the respective species (P<0.05). CONCLUSIONS: This study establishes species-specific profiles of susceptibility to complement immunity in Mitis and Sanguinis streptococci, and indicates that strains associated with systemic infections have increased capacity to evade complement immunity. These findings highlight the need for studies identifying molecular functions involved in complement evasion in oral streptococci.
Asunto(s)
Complemento C3b/inmunología , Variación Genética , Boca/microbiología , Estreptococos Viridans/genética , Estreptococos Viridans/inmunología , Adhesión Bacteriana , Biopelículas , Proteína C-Reactiva/metabolismo , Humanos , Evasión Inmune , Inmunoglobulina G/inmunología , Neutrófilos/inmunología , Neutrófilos/microbiología , Fagocitosis , Infecciones Estreptocócicas/sangre , Infecciones Estreptocócicas/inmunología , Streptococcus gordonii/genética , Streptococcus gordonii/inmunología , Streptococcus mitis/genética , Streptococcus mitis/inmunología , Streptococcus sanguis/genética , Streptococcus sanguis/inmunologíaRESUMEN
Rheumatoid arthritis (RA) and periodontitis (PD) are chronic inflammatory disorders that cause bone loss. PD tends to be more prevalent and severe in RA patients. Previous experimental studies demonstrated that RA triggers alveolar bone loss similarly to PD. The aim of this study was to investigate if arthritis-induced alveolar bone loss is associated with modification in the oral microbiota. Checkerboard DNA-DNA hybridization was employed to analyze forty oral bacterial species in 3 groups of C57BL/6 mice: control (n = 12; without any challenge); Y4 (n = 8; received oral inoculation of Aggregatibacter Actinomycetemcomitans strain FDC Y4) and AIA group (n = 12; chronic antigen-induced arthritis). The results showed that AIA and Y4 group exhibited similar patterns of bone loss. The AIA group exhibited higher counts of most bacterial species analyzed with predominance of Gram-negative species similarly to infection-induced PD. Prevotella nigrescens and Treponema denticola were detected only in the Y4 group whereas Campylobacter showae, Streptococcus mitis and Streptococcus oralis were only found in the AIA group. Counts of Parvimonas micra, Selenomonas Noxia and Veillonella parvula were greater in the AIA group whereas Actinomyces viscosus and Neisseira mucosa were in large proportion in Y4 group. In conclusion, AIA is associated with changes in the composition of the oral microbiota, which might account for the alveolar bone loss observed in AIA mice.
Asunto(s)
Pérdida de Hueso Alveolar/microbiología , Proceso Alveolar/microbiología , Artritis Experimental/microbiología , Maxilar/microbiología , Microbiota/genética , Periodontitis/microbiología , Aggregatibacter actinomycetemcomitans/clasificación , Aggregatibacter actinomycetemcomitans/genética , Aggregatibacter actinomycetemcomitans/aislamiento & purificación , Pérdida de Hueso Alveolar/patología , Proceso Alveolar/patología , Animales , Artritis Experimental/patología , Campylobacter/clasificación , Campylobacter/genética , Campylobacter/aislamiento & purificación , ADN Bacteriano/genética , Humanos , Masculino , Maxilar/patología , Ratones , Ratones Endogámicos C57BL , Boca/microbiología , Boca/patología , Periodontitis/patología , Prevotella nigrescens/clasificación , Prevotella nigrescens/genética , Prevotella nigrescens/aislamiento & purificación , Streptococcus mitis/clasificación , Streptococcus mitis/genética , Streptococcus mitis/aislamiento & purificación , Streptococcus oralis/clasificación , Streptococcus oralis/genética , Streptococcus oralis/aislamiento & purificación , Treponema denticola/clasificación , Treponema denticola/genética , Treponema denticola/aislamiento & purificaciónRESUMEN
Streptococcus is a diverse bacterial lineage. Species of this genus occupy a myriad of environments inside humans and other animals. Despite the elucidation of several of these habitats, many remain to be identified. Here, we explore a methodological approach to reveal unknown bacterial environments. Specifically, we inferred the phylogeny of the Mitis group by analyzing the sequences of eight genes. In addition, information regarding habitat use of species belonging to this group was obtained from the scientific literature. The oral cavity emerged as a potential, previously unknown, environment of Streptococcus massiliensis. This phylogeny-based prediction was confirmed by species-specific polymerase chain reaction (PCR) amplification. We propose employing a similar approach, i.e., use of bibliographic data and molecular phylogenetics as predictive methods, and species-specific PCR as confirmation, in order to reveal other unknown habitats in further bacterial taxa.