Phenotypic and genetic analysis of biofilm formation by Staphylococcus epidermidis.

OBJECTIVE: The most important virulence factor of Staphylococcus epidermidis is their capability to form a biofilm on the surfaces of implanted medical devices. The accumulative phase of biofilm formation is linked to the production of intercellular adhesin encoded by the icaADBC operon and accumulation-associated protein by the aap gene. The aim of the study was to investigate biofilm formation phenotypically and genetically in clinical strains of S. epidermidis in comparison with commensal strains. MATERIAL AND METHODS: The study was carried out in 4 hospitals in Riga, Latvia. In total, 105 clinical strains of Staphylococcus epidermidis isolated from patients' blood (n=67) and intravenous catheters (n=38) in a case of laboratory-confirmed bacteremia were studied. Moreover, 60 Staphylococcus epidermidis commensal strains isolated from nose epithelium of healthy people were included as a control group. Appearance of the icaA and aap genes was tested by polymerase chain reaction. The microtiter plate method was used. RESULTS: Biofilm formation was detected in 50 (47%) of Staphylococcus epidermidis isolates in the clinical group and 15 (25%) of isolates in the control group (P=0.0049). Among 50 biofilm-forming clinical isolates, 46 (92%) were positive for the icaA and/or aap genes. The icaA and aap genes were not found only in 4 strains. CONCLUSIONS: The clinical isolates of Staphylococcus epidermidis were more likely to form biofilms than the commensal strains. The carriage of the icaA or aap gene alone, or their absence, is not applicable as a molecular marker for the discrimination invasive Staphylococcus epidermidis strains from contaminants.

TpF1 from Treponema pallidum activates inflammasome and promotes the development of regulatory T cells.

Human syphilis is a multistage disease, with diverse and wide-ranging manifestations caused by Treponema pallidum. Despite the fact that a cell-mediated immune response takes part in the course of syphilis, T. pallidum often manages to evade host immunity and, in untreated individuals, may trigger chronic infection. With this study, we demonstrate for the first time, to our knowledge, that Treponema pallidum induces a regulatory T (Treg) response in patients with secondary syphilis and we found that the miniferritin TpF1, produced by the bacterium, is able to expand this response and promote the production of TGF-ß. Accordingly, TpF1 stimulates monocytes to release IL-10 and TGF-ß, the key cytokines in driving Treg cell differentiation. Interestingly, we also found that TpF1 stimulates monocytes to synthesize and release several proinflammatory cytokines, such as TNF-α, IL-6, and IL-1ß, the latter following the activation of the multiprotein complex inflammasome. Collectively, these data strongly support a central role for TpF1 both in the inflammation process, which occurs in particular during the early stage of syphilis, and in the long-term persistence of the spirochete within the host by promoting Treg response and TGF-ß production.