Prothrombotic and Proinflammatory Activities of the β-Hemolytic Group B Streptococcal Pigment

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 pr...

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Bibliographic Details
Published in:	Journal of innate immunity 2020-07, Vol.12 (4), p.291-303
Main Authors:	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
Format:	Article
Language:	eng
Subjects:	coagulation group b streptococcus hemolysis inflammation Medicin och hälsovetenskap pigment Research Article streptococcus agalactiae
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Summary:	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.
ISSN:	1662-811X 1662-8128 1662-8128