Incompetence of Neutrophils to Invasive Group A streptococcus Is Attributed to Induction of Plural Virulence Factors by Dysfunction of a Regulator

• DOI: 10.1371/journal.pone.0003455
• Publication Date: 2008-10-20T17:45:15Z
• Authors: Manabu Ato; Tadayoshi Ikebe; Hiroki Kawabata; Toshitada Takemori; Haruo Watanabe
• Keywords: Toxic shock syndrome; Streptolysin; Streptococcus Pyogenes

Group A streptococcus (GAS) causes variety of diseases ranging from common pharyngitis to life-threatening severe invasive diseases, including necrotizing fasciitis and streptococcal toxic shock-like syndrome. The characteristic GAS infections has been thought attribute genetic changes in bacteria, however, no clear evidence shown due lack an intriguingly study using serotype-matched isolates clinical infections. In addition, rare outbreaks their distinctive pathology which infectious foci without neutrophil infiltration hypothesized us could evade host defense, especially functions. Herein we report that a panel GAS, were clinically isolated but not non-invaive infections, abrogate functions human polymorphnuclear neutrophils (PMN) at least two independent ways; inducing necrosis PMN by enhanced production pore-forming toxin streptolysin O (SLO) impairment migration via digesting interleukin-8, attracting chemokine, increased serine protease ScpC. Expression genes was upregulated loss repressive function with the mutation csrS gene all emm49 isolates. mutants exhibited high mortality disseminated infection paucity neutrophils, seen infection, mouse model. However, either SLO or ScpC exhibit much less than csrS-mutated parent isolate infected mice. These results suggest abilities can determine onset severity infection.