Hyaluronan Breakdown Contributes to Immune Defense against Group A Streptococcus

Schommer, Nina N.; Muto, Jun; Nizet, Victor; Gallo, Richard L.

doi:10.1074/jbc.m114.575621

Cited by 30 publications

(19 citation statements)

References 35 publications

(44 reference statements)

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“…Large-molecular weight HA is highly abundant and is the major component of the ECM (Tammi et al, 1994). HA digestion into small fragments after injury has been shown to have important implications for inflammatory responses in vivo (Jiang et al, 2005;Muto et al, 2014;Noble et al, 1996;Taylor et al, 2004) and can modify infection by GAS through digestion of the HA-rich bacterial capsule of this organism (Schommer et al, 2014). However, a clear understanding of the mechanism responsible for HA catabolism or its connection to host antimicrobial defense has not been previously defined.…”

Section: Discussionmentioning

confidence: 99%

Hyaluronan Degradation by Cemip Regulates Host Defense against Staphylococcus aureus Skin Infection

Dokoshi

Zhang

et al. 2020

Cell Reports

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Section: Discussionmentioning

confidence: 99%

Hyaluronan Degradation by Cemip Regulates Host Defense against Staphylococcus aureus Skin Infection

Dokoshi

Zhang

et al. 2020

Cell Reports

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“…Previous study showed that inactivation in hyaluronate lyase (HylA) restored full encapsulation in partially encapsulated M-4 GAS strains, thus demonstrating the mutually exclusive interaction between the hyaluronan capsule and active hyaluronidase (32). In addition, Schommer et al demonstrated in a mouse model that the difference in capsule size was regulated by bacterial hyaluronidase and that the high molecular mass of the hyaluronan capsule influences GAS virulence by facilitating deep tissue infections (34). Based on our findings, we hypothesize that inactivation of HylP.2 could determine a different encapsulation (i.e., capsule sizing) of M-18 GAS strains, thus resulting in a more virulent clone.…”

Section: Discussionmentioning

confidence: 99%

Matrix-Assisted Laser Desorption Ionization–Time of Flight and Comparative Genomic Analysis of M-18 Group A Streptococcus Strains Associated with an Acute Rheumatic Fever Outbreak in Northeast Italy in 2012 and 2013

et al. 2015

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f Acute rheumatic fever (ARF) is a postsuppurative sequela caused by Streptococcus pyogenes infections affecting school-age children. We describe here the occurrence of an ARF outbreak that occurred in Bologna province, northeastern Italy, between November 2012 and May 2013. Molecular analysis revealed that ARF-related group A Streptococcus (GAS) strains belonged to the M-18 serotype, including subtypes emm18.29 and emm18.32. All M-18 GAS strains shared the same antigenic profile, including SpeA, SpeB, SpeC, SpeL, SpeM, and SmeZ. Matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) analysis revealed that M-18 GAS strains grouped separately from other serotypes, suggesting a different S. pyogenes lineage. Single nucleotide polymorphisms and phylogenetic analysis based on whole-genome sequencing showed that emm18.29 and emm18.32 GAS strains clustered in two distinct groups, highlighting genetic variations between these subtypes. Comparative analysis revealed a similar genome architecture between emm18.29 and emm18.32 strains that differed from noninvasive emm18.0 strains. The major sources of differences between M-18 genomes were attributable to the prophage elements. Prophage regions contained several virulence factors that could have contributed to the pathogenic potential of emm18.29 and emm18.32 strains. Notably, phage ⌽SPBO.1 carried erythrogenic toxin A gene (speA1) in six ARF-related M-18 GAS strains but not in emm18.0 strains. In addition, a phage-encoded hyaluronidase gene (hylP.2) presented different variants among M-18 GAS strains by showing internal deletions located in the ␣-helical and TS␤H regions. In conclusion, our study yielded insights into the genome structure of M-18 GAS strains responsible for the ARF outbreak in Italy, thus expanding our knowledge of this serotype. Streptococcus pyogenes, group A streptococcus (GAS), is a Gram-positive bacterium responsible for a wide spectrum of diseases ranging from moderate or mild infections to severe invasive diseases such as necrotizing fasciitis and toxic shock-like syndrome (TSLS). Several GAS infections can cause severe postinfectious sequelae, including acute poststreptococcal glomerulonephritis, acute rheumatic fever (ARF), and rheumatic heart disease (1).ARF is a systemic disorder resulting from an autoimmune disease following a GAS infection that usually occurs in children between 5 and 15 years of age (2). During the last several decades, the incidence of ARF cases has significantly declined in the United States and Western Europe, whereas it remains high in Eastern Europe, Asia, and Australia (3). However, the resurgence of ARF in several geographical areas, including United States, is a matter of concern (4).S. pyogenes possesses different virulence factors such as the M protein and superantigens (SAgs) that contribute to the pathogenesis of GAS infection (1). On the basis of the high variability of the M protein among GAS strains, the 5=-terminal sequence of the emm gene (emm typing) is considered a reliable molecular marke...

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“…GAGs are widely distributed and function in cellular and extracellular signalling in all biological processes. Bacteria express GAGs and are used to inhibit phagocytosis by increasing molecular weight; for example, Streptococcus has a cellular coating of high-molecular weight hyaluronan [68]. Manipulation of GAGs, by removal of heparin sulfate or reducing its synthesis, inhibits attachment of S. aureus and S. pneumonia in lung epithelial cells and fibroblasts [69].…”

Section: The Basement Membrane Matrix In Copdmentioning

confidence: 99%

The consequence of matrix dysfunction on lung immunity and the microbiome in COPD

et al. 2018

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The pulmonary extracellular matrix (ECM) is a complex network of proteins which primarily defines tissue architecture and regulates various biochemical and biophysical processes. It is a dynamic system comprising two main structures (the interstitial matrix and the basement membrane) which undergo continuous, yet highly regulated, remodelling. This remodelling process is essential for tissue homeostasis and uncontrolled regulation can lead to pathological states including chronic obstructive pulmonary disease (COPD). Altered expression of ECM proteins, as observed in COPD, can contribute to the degradation of alveolar walls and thickening of the small airways which can cause limitations in airflow. Modifications in ECM composition can also impact immune cell migration and retention in the lung with migrating cells becoming entrapped in the diseased airspaces. Furthermore, ECM changes affect the lung microbiome, aggravating and advancing disease progression. A dysbiosis in bacterial diversity can lead to infection, inducing epithelial injury and pro-inflammatory reactions. Here we review the changes noted in the different ECM components in COPD and discuss how an imbalance in microbial commensalism can impact disease development.

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Hyaluronan Breakdown Contributes to Immune Defense against Group A Streptococcus

Cited by 30 publications

References 35 publications

Hyaluronan Degradation by Cemip Regulates Host Defense against Staphylococcus aureus Skin Infection

Hyaluronan Degradation by Cemip Regulates Host Defense against Staphylococcus aureus Skin Infection

Matrix-Assisted Laser Desorption Ionization–Time of Flight and Comparative Genomic Analysis of M-18 Group A Streptococcus Strains Associated with an Acute Rheumatic Fever Outbreak in Northeast Italy in 2012 and 2013

The consequence of matrix dysfunction on lung immunity and the microbiome in COPD

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