Surface protein Esp enhances pro-inflammatory cytokine expression through NF-κB activation during enterococcal infection
Enterococcal surface protein (Esp) is encoded on a pathogenicity island in Enterococcus faecalis and E. faecium and is involved in biofilm formation and binding to epithelial cells. In this study, using Esp-expressing E. faecalis MMH594 and its isogenic Esp-deficient strain, as well as purified Esp,...
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| Veröffentlicht in: | Innate immunity (London, England) England), 2016-01, Vol.22 (1), p.31-39 |
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| creator | Zou, Jun Shankar, Nathan |
| description | Enterococcal surface protein (Esp) is encoded on a pathogenicity island in Enterococcus faecalis and E. faecium and is involved in biofilm formation and binding to epithelial cells. In this study, using Esp-expressing E. faecalis MMH594 and its isogenic Esp-deficient strain, as well as purified Esp, we show that Esp is sufficient for activation of NF-κB and the subsequent production of pro-inflammatory cytokines IL-1β and TNF-α in macrophages in vitro. In a mouse peritonitis model, we also show that mice infected with Esp-expressing E. faecalis showed comparatively higher levels of cytokines TNF-α, IL-1β and IL-6 in peritoneal fluid, and IL-6 in serum. Moreover, neutrophil infiltration and tissue damage in the liver was higher in the mice infected with the Esp-expressing strain compared with mice infected with the Esp-deficient mutant. These results add Esp to the growing list of enterococcal virulence factors that can modulate inflammation during infection and has implications for enterococcal pathogenesis. |
| doi_str_mv | 10.1177/1753425915611237 |
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In this study, using Esp-expressing E. faecalis MMH594 and its isogenic Esp-deficient strain, as well as purified Esp, we show that Esp is sufficient for activation of NF-κB and the subsequent production of pro-inflammatory cytokines IL-1β and TNF-α in macrophages in vitro. In a mouse peritonitis model, we also show that mice infected with Esp-expressing E. faecalis showed comparatively higher levels of cytokines TNF-α, IL-1β and IL-6 in peritoneal fluid, and IL-6 in serum. Moreover, neutrophil infiltration and tissue damage in the liver was higher in the mice infected with the Esp-expressing strain compared with mice infected with the Esp-deficient mutant. 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| subjects | Animals Bacterial Proteins - genetics Bacterial Proteins - metabolism Cell Line Cytokines - metabolism Disease Models, Animal Enterococcus faecalis Enterococcus faecalis - immunology Gram-Positive Bacterial Infections - immunology Humans Inflammation Mediators - metabolism Macrophages - immunology Membrane Proteins - genetics Membrane Proteins - metabolism Mice NF-kappa B - metabolism Peritonitis - immunology RNA, Small Interfering - genetics Sequence Deletion - genetics Virulence Factors |
| title | Surface protein Esp enhances pro-inflammatory cytokine expression through NF-κB activation during enterococcal infection |
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