Staphylococcus epidermidis polysaccharide intercellular adhesin activates complement.
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Staphylococcus epidermidis polysaccharide intercellular adhesin activates complement. / Fredheim, Elizabeth G Aarag; Granslo, Hildegunn Norbakken; Flægstad, Trond; Figenschau, Yngve; Rohde, Holger; Sadovskaya, Irina; Mollnes, Tom Eirik; Klingenberg, Claus.
in: FEMS IMMUNOL MED MIC, Jahrgang 63, Nr. 2, 2, 2011, S. 269-280.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Staphylococcus epidermidis polysaccharide intercellular adhesin activates complement.
AU - Fredheim, Elizabeth G Aarag
AU - Granslo, Hildegunn Norbakken
AU - Flægstad, Trond
AU - Figenschau, Yngve
AU - Rohde, Holger
AU - Sadovskaya, Irina
AU - Mollnes, Tom Eirik
AU - Klingenberg, Claus
PY - 2011
Y1 - 2011
N2 - Staphylococcus epidermidis is a frequent cause of nosocomial infections. The central virulence factor of S. epidermidis is biofilm formation. Polysaccharide intercellular adhesin (PIA) constitutes the major biofilm matrix-component. PIA and biofilm have been implicated in S. epidermidis evasion of host immune defence. We examined the effects of S. epidermidis PIA on the inflammatory response with focus on complement activation. We used a human whole-blood ex vivo model of infection and compared the effects of a PIA-positive S. epidermidis strain (SE1457) and its PIA-negative isogenic mutant (M10). The independent effect of purified PIA on complement activation was investigated. In glucose-rich media, the mutant formed a proteinacious DNA-rich biofilm, whereas SE1457 formed a thick PIA-biofilm. In biofilm growth, SE1457 induced a stronger activation of the complement system compared with M10. We verified that purified PIA was independently responsible for a strong activation of the complement system. In contrast, M10 induced higher granulocyte activation by expression of CD11b and higher secretion of cytokines. We conclude that PIA has potent pro-inflammatory properties by activating the complement system. However, in a complex balance of the immune response, the decreased activation of granulocytes and cytokines by a PIA biofilm may limit host eradication of S. epidermidis.
AB - Staphylococcus epidermidis is a frequent cause of nosocomial infections. The central virulence factor of S. epidermidis is biofilm formation. Polysaccharide intercellular adhesin (PIA) constitutes the major biofilm matrix-component. PIA and biofilm have been implicated in S. epidermidis evasion of host immune defence. We examined the effects of S. epidermidis PIA on the inflammatory response with focus on complement activation. We used a human whole-blood ex vivo model of infection and compared the effects of a PIA-positive S. epidermidis strain (SE1457) and its PIA-negative isogenic mutant (M10). The independent effect of purified PIA on complement activation was investigated. In glucose-rich media, the mutant formed a proteinacious DNA-rich biofilm, whereas SE1457 formed a thick PIA-biofilm. In biofilm growth, SE1457 induced a stronger activation of the complement system compared with M10. We verified that purified PIA was independently responsible for a strong activation of the complement system. In contrast, M10 induced higher granulocyte activation by expression of CD11b and higher secretion of cytokines. We conclude that PIA has potent pro-inflammatory properties by activating the complement system. However, in a complex balance of the immune response, the decreased activation of granulocytes and cytokines by a PIA biofilm may limit host eradication of S. epidermidis.
KW - Humans
KW - Gene Deletion
KW - Biofilms/growth & development
KW - Blood/immunology/microbiology
KW - Complement Activation
KW - Complement System Proteins/immunology
KW - Cytokines/secretion
KW - Granulocytes/immunology
KW - Human Experimentation
KW - Polysaccharides, Bacterial/genetics/immunology
KW - Staphylococcus epidermidis/genetics/immunology/physiology
KW - Humans
KW - Gene Deletion
KW - Biofilms/growth & development
KW - Blood/immunology/microbiology
KW - Complement Activation
KW - Complement System Proteins/immunology
KW - Cytokines/secretion
KW - Granulocytes/immunology
KW - Human Experimentation
KW - Polysaccharides, Bacterial/genetics/immunology
KW - Staphylococcus epidermidis/genetics/immunology/physiology
M3 - SCORING: Journal article
VL - 63
SP - 269
EP - 280
IS - 2
M1 - 2
ER -
