Analyse immunoprotéomique comparative des sécrétomes de souches de Staphylococcus aureus et S. epidermidis chez les patients souffrant d’infections sur prothèses articulaires

Nuyttens, Hélène; Thomas, Damien; Rogé, J; Mignon, K.

doi:10.1016/j.patbio.2010.07.018

Cited by 1 publication

(1 citation statement)

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“…In contrast, protease SepA is secreted by S. epidermidis and contributes to the evasion of S. epidermidis to neutrophils activity through the destruction of antimicrobial peptides (AMPs) produced by these immune cells 48 . Comparative serologic proteome analysis of S. aureus and S. epidermidis exoproteins in PJI identified five exoproteins in S. aureus and autolysin E and App (accumulation associated protein) in S. epidermidis 49 . The effect of secretome of both species on immune cells also differ, whereas the stimulation of monocyte-derived dendritic cells (moDC) with S. aureus secretome induces the production of IFN-ɤ and the proliferation of CD4+ T cells, the S. epidermidis secretome induce the IL-10 production in the same cells and the activation of regulatory T cells (Treg) 50 .…”

Section: Discussionmentioning

confidence: 99%

Non-biofilm-forming Staphylococcus epidermidis planktonic cell supernatant induces alterations in osteoblast biological function

Gómez-Alonso,

Betanzos-Cabrera,

Moreno-Lafont

et al. 2024

Sci Rep

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Staphylococcal biofilms significantly contribute to prosthetic joint infection (PJI). However, 40% of S. epidermidis PJI isolates do not produce biofilms, which does not explain the role of biofilms in these cases. We studied whether the supernatant from planktonic S. epidermidis alters osteoblast function. Non-biofilm-forming S. epidermidis supernatants (PJI− clinical isolate, healthy skin isolate (HS), and ATCC12228 reference strain) and biofilm-forming supernatants (PJI+ clinical isolate, ATCC35984 reference strain, and Staphylococcus aureus USA300 reference strain) were included. Osteoblasts stimulated with supernatants from non-biofilm-forming isolates for 3, 7, and 14 days showed significantly reduced cellular DNA content compared with unstimulated osteoblasts, and apoptosis was induced in these osteoblasts. Similar results were obtained for biofilm-forming isolates, but with a greater reduction in DNA content and higher apoptosis. Alkaline phosphatase activity and mineralization were significantly reduced in osteoblasts treated with supernatants from non-biofilm-forming isolates compared to the control at the same time points. However, the supernatants from biofilm-forming isolates had a greater effect than those from non-biofilm-forming isolates. A significant decrease in the expression of ATF4, RUNX2, ALP, SPARC, and BGLAP, and a significant increase in RANK-L expression were observed in osteoblasts treated with both supernatants. These results demonstrate that the supernatants of the S. epidermidis isolate from the PJI− and HS (commensal) with a non-biofilm-forming phenotype alter the function of osteoblasts (apoptosis induction, failure of cell differentiation, activation of osteoblasts, and induction of bone resorption), similar to biofilm-forming isolates (PJI+, ATCC35984, and S. aureus USA300), suggesting that biofilm status contributes to impaired osteoblast function and that the planktonic state can do so independently of biofilm production.

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Section: Discussionmentioning

confidence: 99%