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Staphylococcus epidermidis Biofilm-Released Cells Induce a Prompt and More Marked In vivo Inflammatory-Type Response than Planktonic or Biofilm Cells

View Article: PubMed Central - PubMed

ABSTRACT

Staphylococcus epidermidis biofilm formation on indwelling medical devices is frequently associated with the development of chronic infections. Nevertheless, it has been suggested that cells released from these biofilms may induce severe acute infections with bacteraemia as one of its major associated clinical manifestations. However, how biofilm-released cells interact with the host remains unclear. Here, using a murine model of hematogenously disseminated infection, we characterized the interaction of cells released from S. epidermidis biofilms with the immune system. Gene expression analysis of mouse splenocytes suggested that biofilm-released cells might be particularly effective at activating inflammatory and antigen presenting cells and inducing cellular apoptosis. Furthermore, biofilm-released cells induced a higher production of pro-inflammatory cytokines, in contrast to mice infected with planktonic cells, even though these had a similar bacterial load in livers and spleens. Overall, these results not only provide insights into the understanding of the role of biofilm-released cells in S. epidermidis biofilm-related infections and pathogenesis, but may also help explain the relapsing character of these infections.

No MeSH data available.


Related in: MedlinePlus

Liver and spleen bacterial load after infection with the different S. epidermidis populations. BALB/c mice were challenged intravenously with 1 × 108 planktonic (P), biofilm (B), biofilm-released (BR) cells, or sham-infected treated with PBS alone (PBS). Liver and spleen bacterial burden was assessed 2, 6, and 14 h after intravenous infection. Each symbol represents an individual mouse and horizontal bars the median of 1 (biofilms) to 3 (P and BR, 6h time point) independent experiments that, per time point, presented the following number of animals: P n = 14/16/11; BR n = 14/16/11; B n = 5/5/5. Statistical differences among groups were evaluated with Kruskal–Wallis (Overall ANOVA P < 0.05) and post hoc Dunn's multiple comparison tests. *P < 0.05, **P < 0.01.
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Figure 3: Liver and spleen bacterial load after infection with the different S. epidermidis populations. BALB/c mice were challenged intravenously with 1 × 108 planktonic (P), biofilm (B), biofilm-released (BR) cells, or sham-infected treated with PBS alone (PBS). Liver and spleen bacterial burden was assessed 2, 6, and 14 h after intravenous infection. Each symbol represents an individual mouse and horizontal bars the median of 1 (biofilms) to 3 (P and BR, 6h time point) independent experiments that, per time point, presented the following number of animals: P n = 14/16/11; BR n = 14/16/11; B n = 5/5/5. Statistical differences among groups were evaluated with Kruskal–Wallis (Overall ANOVA P < 0.05) and post hoc Dunn's multiple comparison tests. *P < 0.05, **P < 0.01.

Mentions: Biofilm-released cells had an intermediate ability, between that of planktonic and biofilm cells, to colonize the liver and spleen (Figure 3). Interestingly, while in the first 6 h of infection, biofilm-released cell burden resembled that of planktonic cells, 14 h after infection the differences between planktonic and biofilm-released cells and the similarities between biofilm-released and biofilms cells become noticeable. It is important to note that although the inoculum was adjusted by flow cytometry the quantity of bacteria injected was also confirmed by CFU counting, and the number of CFU was similar among the different populations.


Staphylococcus epidermidis Biofilm-Released Cells Induce a Prompt and More Marked In vivo Inflammatory-Type Response than Planktonic or Biofilm Cells
Liver and spleen bacterial load after infection with the different S. epidermidis populations. BALB/c mice were challenged intravenously with 1 × 108 planktonic (P), biofilm (B), biofilm-released (BR) cells, or sham-infected treated with PBS alone (PBS). Liver and spleen bacterial burden was assessed 2, 6, and 14 h after intravenous infection. Each symbol represents an individual mouse and horizontal bars the median of 1 (biofilms) to 3 (P and BR, 6h time point) independent experiments that, per time point, presented the following number of animals: P n = 14/16/11; BR n = 14/16/11; B n = 5/5/5. Statistical differences among groups were evaluated with Kruskal–Wallis (Overall ANOVA P < 0.05) and post hoc Dunn's multiple comparison tests. *P < 0.05, **P < 0.01.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5037199&req=5

Figure 3: Liver and spleen bacterial load after infection with the different S. epidermidis populations. BALB/c mice were challenged intravenously with 1 × 108 planktonic (P), biofilm (B), biofilm-released (BR) cells, or sham-infected treated with PBS alone (PBS). Liver and spleen bacterial burden was assessed 2, 6, and 14 h after intravenous infection. Each symbol represents an individual mouse and horizontal bars the median of 1 (biofilms) to 3 (P and BR, 6h time point) independent experiments that, per time point, presented the following number of animals: P n = 14/16/11; BR n = 14/16/11; B n = 5/5/5. Statistical differences among groups were evaluated with Kruskal–Wallis (Overall ANOVA P < 0.05) and post hoc Dunn's multiple comparison tests. *P < 0.05, **P < 0.01.
Mentions: Biofilm-released cells had an intermediate ability, between that of planktonic and biofilm cells, to colonize the liver and spleen (Figure 3). Interestingly, while in the first 6 h of infection, biofilm-released cell burden resembled that of planktonic cells, 14 h after infection the differences between planktonic and biofilm-released cells and the similarities between biofilm-released and biofilms cells become noticeable. It is important to note that although the inoculum was adjusted by flow cytometry the quantity of bacteria injected was also confirmed by CFU counting, and the number of CFU was similar among the different populations.

View Article: PubMed Central - PubMed

ABSTRACT

Staphylococcus epidermidis biofilm formation on indwelling medical devices is frequently associated with the development of chronic infections. Nevertheless, it has been suggested that cells released from these biofilms may induce severe acute infections with bacteraemia as one of its major associated clinical manifestations. However, how biofilm-released cells interact with the host remains unclear. Here, using a murine model of hematogenously disseminated infection, we characterized the interaction of cells released from S. epidermidis biofilms with the immune system. Gene expression analysis of mouse splenocytes suggested that biofilm-released cells might be particularly effective at activating inflammatory and antigen presenting cells and inducing cellular apoptosis. Furthermore, biofilm-released cells induced a higher production of pro-inflammatory cytokines, in contrast to mice infected with planktonic cells, even though these had a similar bacterial load in livers and spleens. Overall, these results not only provide insights into the understanding of the role of biofilm-released cells in S. epidermidis biofilm-related infections and pathogenesis, but may also help explain the relapsing character of these infections.

No MeSH data available.


Related in: MedlinePlus