title: Synergistic effects of streptolysin S and streptococcal pyrogenic exotoxin B on the mouse model of group A streptococcal infection.
abstract: Streptococcus pyogenes is a group A streptococcus (GAS) and an important human pathogen that causes a variety of diseases. Streptococcal pyrogenic exotoxin B (SPE B) and streptolysin S (SLS) are important virulence factors involved in GAS infection, but it is not clear which one is more virulent. Using an air pouch infection model, the wild-type strain NZ131, its isogenic mutants, and complementary mutants were used to examine the effects of SPE B and SLS on GAS infection. The results of the skin lesion and mouse mortality assays showed that although SPE B and SLS had a synergistic effect on GAS infection, SPE B played a more important role in local tissue damage while SLS had a more prominent effect on mouse mortality. Surveys of the exudates from the air pouch revealed that the expression of inflammatory cytokines was significantly inhibited in the sagB/speB-double-mutant JM4-infected mice. Furthermore, in vivo and in vitro studies showed that the isogenic mutant strains were more susceptible to the immune cell killing than the wild-type strain and that the sagB/speB-double-mutant JM4 was the most sensitive among these strains. Moreover, infection with the sagB/speB-double-mutant JM4 strain caused the least amount of macrophage apoptosis compared to infection with the wild-type NZ131 and the other complementary strains, which express only SPE B or SLS or both. Taken together, these results indicate that both SPE B and SLS contributed to GAS evasion from immune cell killing, local tissue damage, and mouse mortality.
authors.affiliation: Institute of Biotechnology and Chemical Engineering, I-Shou University, Kaohsiung City, Taiwan.
authors.forename: Chih-Hsin
authors.initials: CH
authors.lastname: Hung
authors.forename: Nina
authors.initials: N
authors.lastname: Tsao
authors.forename: Yi-Fang
authors.initials: YF
authors.lastname: Zeng
authors.forename: Shiou-Ling
authors.initials: SL
authors.lastname: Lu
authors.forename: Chiang-Ni
authors.initials: CN
authors.lastname: Chuan
authors.forename: Yee-Shin
authors.initials: YS
authors.lastname: Lin
authors.forename: Jiunn-Jong
authors.initials: JJ
authors.lastname: Wu
authors.forename: Chih-Feng
authors.initials: CF
authors.lastname: Kuo
mesh_terms: D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D004357:Drug Synergism; D005098:Exotoxins / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D057131:Immune Evasion; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D013290:Streptococcal Infections / Q000276:immunology / Q000382:microbiology / Q000401:mortality* / Q000473:pathology*; D013297:Streptococcus pyogenes / Q000235:genetics / Q000472:pathogenicity*; D013301:Streptolysins / Q000235:genetics / Q000378:metabolism*; D014774:Virulence; D037521:Virulence Factors / Q000235:genetics / Q000378:metabolism*
chemical_list: D001426:Bacterial Proteins; D005098:Exotoxins; D013301:Streptolysins; D037521:Virulence Factors; C027951:erythrogenic toxin; C026050:streptolysin S