scholarly journals Hyaluronic acid capsule modulates M protein-mediated adherence and acts as a ligand for attachment of group A Streptococcus to CD44 on human keratinocytes.

1998 ◽  
Vol 101 (8) ◽  
pp. 1708-1716 ◽  
Author(s):  
H M Schrager ◽  
S Albertí ◽  
C Cywes ◽  
G J Dougherty ◽  
M R Wessels
Keyword(s):  
Hyaluronic Acid ◽  
Group A Streptococcus ◽  
Human Keratinocytes ◽  
M Protein ◽  
Group A ◽  
Hyaluronic Acid Capsule

scholarly journals Relative contributions of hyaluronic acid capsule and M protein to virulence in a mucoid strain of the group A Streptococcus.

1997 ◽  
Vol 65 (1) ◽  
pp. 64-71 ◽  
Author(s):  
A E Moses ◽  
M R Wessels ◽  
K Zalcman ◽  
S Albertí ◽  
S Natanson-Yaron ◽  
...  
Keyword(s):  
Hyaluronic Acid ◽  
Group A Streptococcus ◽  
M Protein ◽  
Group A ◽  
Hyaluronic Acid Capsule

scholarly journals STUDIES ON THE PATHOGENICITY OF GROUP A STREPTOCOCCI

1959 ◽  
Vol 110 (4) ◽  
pp. 617-628 ◽  
Author(s):  
Marie Judith Foley ◽  
W. Barry Wood
Keyword(s):  
Hyaluronic Acid ◽  
Virulent Strain ◽  
Critical Role ◽  
M Protein ◽  
Group A Streptococci ◽  
Streptococcal Infections ◽  
Full Complement ◽  
Group A ◽  
Hyaluronic Acid Capsule

A quantitative study of the combined antiphagocytic effects of the M protein and the hyaluronic acid capsules of four strains of Group A streptococci revealed the following facts relating to their intraperitoneal virulence in mice and rats: 1. The most virulent strain, S23M (matt), produced both a large hyaluronic acid capsule and a full complement of M protein, the combined effects of which rendered the organism highly resistant to surface phagocytosis. 2. The slightly less virulent strain, T14/46 (matt virulent) was somewhat more susceptible to surface phagocytosis owing to the fact that its smaller capsule was less antiphagocytic than that of the S23M organism. 3. The glossy variant of the S23 strain (S23G), which ranked third in virulence, was still more susceptible to surface phagocytosis because of its lack of detectable M substance. Its large hyaluronic acid capsule, however, was capable of protecting it against phagocytosis on glass. 4. The least virulent strain, T14 (matt avirulent), was the most susceptible of all to phagocytosis. Though it possessed both M substance and capsule, which together prevented its phagocytosis on glass, each of them was shown to be quantitatively and functionally deficient as compared to Strain S23M. The differences in phagocytability, which appear to be directly related to the pathogenicity of the organisms, could be adequately demonstrated in vitro only by phagocytic tests designed to measure surface phagocytosis in the absence of opsonins. This fact is in keeping with the observation, previously reported, that surface phagocytosis plays a critical role in the defense of the host, particularly during the earliest stages of experimental streptococcal infections. Its possible relation to suppuration during the later stages of infection is also discussed.

scholarly journals Human Disease Isolates of Serotype M4 and M22 Group A Streptococcus Lack Genes Required for Hyaluronic Acid Capsule Biosynthesis

mBio ◽  
2012 ◽  
Vol 3 (6) ◽  
Author(s):  
Anthony R. Flores ◽  
Brittany E. Jewell ◽  
Nahuel Fittipaldi ◽  
Stephen B. Beres ◽  
James M. Musser
Keyword(s):  
Hyaluronic Acid ◽  
Virulence Factor ◽  
Group A Streptococcus ◽  
Ex Vivo ◽  
Upper Respiratory Tract ◽  
Major Virulence Factor ◽  
Invasive Infections ◽  
Group A ◽  
Human Infections ◽  
Hyaluronic Acid Capsule

ABSTRACTGroup A streptococcus (GAS) causes human pharyngitis and invasive infections and frequently colonizes individuals asymptomatically. Many lines of evidence generated over decades have shown that the hyaluronic acid capsule is a major virulence factor contributing to these infections. While conducting a whole-genome analysis of thein vivomolecular genetic changes that occur in GAS during longitudinal human pharyngeal interaction, we discovered that serotypes M4 and M22 GAS strains lack thehasABCgenes necessary for hyaluronic acid capsule biosynthesis. Using targeted PCR, we found that all 491 temporally and geographically diverse disease isolates of these two serotypes studied lack thehasABCgenes. Consistent with the lack of capsule synthesis genes, none of the strains produced detectable hyaluronic acid. Despite the lack of a hyaluronic acid capsule, all strains tested multiplied extensivelyex vivoin human blood. Thus, counter to the prevailing concept in GAS pathogenesis research, strains of these two serotypes do not require hyaluronic acid to colonize the upper respiratory tract or cause abundant mucosal or invasive human infections. We speculate that serotype M4 and M22 GAS have alternative, compensatory mechanisms that promote virulence.IMPORTANCEA century of study of the antiphagocytic hyaluronic acid capsule made by group A streptococcus has led to the concept that it is a major virulence factor contributing to human pharyngeal and invasive infections. However, the discovery that some strains that cause abundant human infections lack hyaluronic acid biosynthetic genes and fail to produce this capsule provides a new stimulus for research designed to understand the group A streptococcus factors contributing to pharyngeal infection and invasive disease episodes.

scholarly journals PROTECTIVE EFFECT OF HYALURONIDASE AND TYPE-SPECIFIC ANTI-M SERUM ON EXPERIMENTAL GROUP A STREPTOCOCCUS INFECTIONS IN MICE

1948 ◽  
Vol 88 (3) ◽  
pp. 325-342 ◽  
Author(s):  
Sidney Rothbard
Keyword(s):  
Hyaluronic Acid ◽  
Group A Streptococcus ◽  
Single Injection ◽  
Group A Streptococci ◽  
Enzyme Therapy ◽  
Fundamental Factor ◽  
Combined Use ◽  
Group A ◽  
Hyaluronic Acid Capsule ◽  
Experimental Group

Five strains of encapsulated group A streptococci of different serological types, each with a glossy and a matt variant, were studied to compare the rôles of the M substance and the hyaluronic acid capsule in virulence of these microorganisms. The results indicated that both contribute to the virulence of group A streptococci but that the M antigen is the more fundamental factor. Encapsulated variants, both glossy and matt, were slightly less susceptible to phagocytosis than those from which the capsule had been removed with hyaluronidase. Glossy variants, containing no M substance, were readily phagocyted; matt, M-containing variants were resistant to phagocytosis except in the presence of anti-M serum when they became fully susceptible. Only the M-containing, matt strains were mouse-virulent. Mice were protected against infections with these strains: (a) By removal of the capsule with hyaluronidase, which resulted in slight protection, but only against 10 M.L.D. Early and intensive treatment was required to produce this effect; i.e., simultaneous injection of enzyme and streptococci followed by prolonged enzyme therapy. (b) By a single injection of anti-M serum administered the day before inoculation of the streptococci, which resulted in protection against 100,000 M.L.D. (c) By combined use of enzyme and anti-M serum, an additive effect of the two protective agents occurred, which resulted in protection against 1,000,000 M.L.D.

scholarly journals Role of CsrR, Hyaluronic Acid, and SpeB in the Internalization of Streptococcus pyogenes M Type 3 Strain by Epithelial Cells

2002 ◽  
Vol 70 (2) ◽  
pp. 462-469 ◽  
Author(s):  
Jeries Jadoun ◽  
Osnat Eyal ◽  
Shlomo Sela
Keyword(s):  
Hyaluronic Acid ◽  
Epithelial Cells ◽  
Group A Streptococcus ◽  
Acid Synthesis ◽  
Complex Interactions ◽  
Bacterial Uptake ◽  
Group A ◽  
Isogenic Mutants ◽  
Hyaluronic Acid Capsule ◽  
Type 3

ABSTRACT Internalization of group A streptococcus by human epithelial cells has been extensively studied during the past 6 years. It is now clear that multiple mechanisms are involved in this process. We have previously demonstrated that the CsrR global regulator controls the internalization of an invasive M type 3 strain through regulation of the has (hyaluronic acid synthesis) operon, as well as another, unknown gene(s). Recently, it was reported that the CsrR-regulated cysteine protease (SpeB) is also involved in bacterial uptake. In this study we have examined the roles of CsrR, hyaluronic acid capsule, and SpeB in streptococcal internalization. We have constructed isogenic mutants of the M3 serotype deficient in the csrR, hasA, and speB genes and tested their ability to be internalized by HEp-2 epithelial cells. Inactivation of csrR abolished internalization, while inactivation of either hasA or speB increased the internalization efficiency. Mutation in csrR derepressed hasA transcription and lowered the activity of SpeB, while no effect on speB transcription was observed. The speB mutant expressed smaller amounts of capsule, while the hasA mutant transcribed more csrR and speB mRNAs. Thus, it seems that complex interactions between CsrR, SpeB, and capsule are involved in modulation of group A streptococcus internalization.

scholarly journals STUDIES OF PHAGOCYTOSIS OF GROUP A STREPTOCOCCI BY POLYMORPHONUCLEAR LEUCOCYTES IN VITRO

1960 ◽  
Vol 111 (3) ◽  
pp. 309-322 ◽  
Author(s):  
James G. Hirsch ◽  
Alice B. Church
Keyword(s):  
Hyaluronic Acid ◽  
M Protein ◽  
Rabbit Serum ◽  
Polymorphonuclear Leucocytes ◽  
Group A Streptococci ◽  
Test Conditions ◽  
Human Sera ◽  
Group A ◽  
Hyaluronic Acid Capsule

Studies have been made on phagocytosis and killing of Group A streptococci during mixing with suspensions of leucocytes in vitro. Under appropriate test conditions an anti-phagocytic effect can be demonstrated for the streptococcal hyaluronic acid capsule as well as for its M protein. The results obtained suggest an explanation for the suitability of human, but not rabbit, blood for opsonophagocytic tests designed to measure type-specific streptococcal antibodies. Human sera contain a factor which counteracts the anti-phagocytic effects of streptococcal hyaluronic acid capsules, and hence human blood serves well for detection of antibodies which combine with the only other phagocytosis-resisting component of this microorganism, namely M protein. In contrast, rabbit sera contain none of this factor, and addition of antibody to M protein to phagocytic test systems employing rabbit serum does not necessarily render the streptococci susceptible to engulfment by white cells, since the hyaluronic acid capsule may continue to interfere with phagocytosis. The nature of the human serum factor which opsonizes encapsulated streptococci is unknown. It does not appear to be an antibody or an enzyme capable of depolymerizing hyaluronic acid.

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