Incompetence of Neutrophils to Invasive Group A streptococcus Is Attributed to Induction of Plural Virulence Factors by Dysfunction of a Regulator
Figure 5
Mutation of the csrS gene in the isolates of the patients with severe invasive infections is responsible for increased virulence of GAS.
(A) Expression of virulence-associated genes in non-invasive and invasive GAS isolates and mutants transduced with csrS, analyzed by RT-PCR. The expression of virulence-associated factors mRNA: IgG degrading protease of GAS, Mac-1-like protein (mac), nicotine adenine dinucleotide glycohydrolase (nga), slo, scpC, polysaccharide capsule production (hasA), C5a peptidase (scpA), and streptococcal pyrogenic endotoxin (speB), plus expression of 16S rRNA (16S) were shown. (B) The csrS mutations in GAS isolates from the patients with severe invasive streptococcal infections. The numbers at the end of the bars indicate the total amino acid residues of CsrS proteins from the start codon in non-invasive GAS (1566) and invasive Gas from the patients (NIH147, NIH200, NIH226, NIH230 and NIH 269). Solid boxes represent the newly created amino acids as a result of frameshift mutations, with length of amino acids ( “+ number” within parentheses). In the NIH200 strain, Ser replaced Gly at position 461 of the CsrS protein. Type of mutations are listed at the end of bars.