
Prothrombotic and Proinflammatory Activities of the β-Hemolytic Group B Streptococcal Pigment
Author(s) -
Siemens Nikolai,
Oehmcke-Hecht Sonja,
Hoßmann Jörn,
Skorka Sebastian B.,
Nijhuis Roel H.T.,
Ruppen Corinne,
Skrede Steinar,
Rohde Manfred,
Schultz Daniel,
Lalk Michael,
Itzek Andreas,
Pieper Dietmar H.,
van den Bout Christiaan J.,
Claas Eric C.J.,
Kuijper Ed J.,
Mauritz Robert,
Sendi Parham,
Wunderink Herman F.,
Norrby-Teglund Anna
Publication year - 2019
Publication title -
journal of innate immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.078
H-Index - 64
eISSN - 1662-8128
pISSN - 1662-811X
DOI - 10.1159/000504002
Subject(s) - research article
A prominent feature of severe streptococcal infections is the profound inflammatory response that contributes to systemic toxicity. In sepsis the dysregulated host response involves both immunological and nonimmunological pathways. Here, we report a fatal case of an immunocompetent healthy female presenting with toxic shock and purpura fulminans caused by group B streptococcus (GBS; serotype III, CC19). The strain (LUMC16) was pigmented and hyperhemolytic. Stimulation of human primary cells with hyperhemolytic LUMC16 and STSS/NF-HH strains and pigment toxin resulted in a release of proinflammatory mediators, including tumor necrosis factor, interleukin (IL)-1β, and IL-6. In addition, LUMC16 induced blood clotting and showed factor XII activity on its surface, which was linked to the presence of the pigment. The expression of pigment was not linked to a mutation within the CovR/S region. In conclusion, our study shows that the hemolytic lipid toxin contributes to the ability of GBS to cause systemic hyperinflammation and interferes with the coagulation system.