ArticleThe Journal of biological chemistry2014
The fibrinogen-binding M1 protein reduces pharyngeal cell adherence and colonization phenotypes of M1T1 group A Streptococcus.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Chemically encoded pH-tunable covalent adhesion by a bacterial thioester domain.Science advances · 2026Article
- Dynamic tethering of M protein drives pathological inflammation during group A Streptococcus infections.PLoS pathogens · 2026Article
- Group A Streptococcus interacts with glycosaminoglycans via M proteins to modulate bacterial adherence in vitro.The FEBS journal · 2025Article
- Epidemiological and Clinical Features ofPathogens (Basel, Switzerland) · 2023Article
- Contribution of Streptococcus pyogenes M87 protein to innate immune resistance and virulence.Microbial pathogenesis · 2022Article
- The exploitation of human glycans by Group A Streptococcus.FEMS microbiology reviews · 2022Article
- Novel Models ofMicroorganisms · 2021Article
- Novel Tyrosine Kinase-Mediated Phosphorylation With Dual Specificity Plays a Key Role in the Modulation ofFrontiers in microbiology · 2021Article
- Playing With Fire: Proinflammatory Virulence Mechanisms of Group AFrontiers in cellular and infection microbiology · 2021Review
- Group A Streptococcus Infection of the Nasopharynx Requires Proinflammatory Signaling through the Interleukin-1 Receptor.Infection and immunity · 2020Article
- Variation, Indispensability, and Masking in the M protein.Trends in microbiology · 2018Review
- Binding host proteins to the M protein contributes to the mortality associated with influenza-Microbiology (Reading, England) · 2017Article
- Blood Group Antigen Recognition via the Group A Streptococcal M Protein Mediates Host Colonization.mBio · 2017Article
- Immunization with a streptococcal multiple-epitope recombinant protein protects mice against invasive group A streptococcal infection.PloS one · 2017Article
- Tissue tropisms in group A Streptococcus: what virulence factors distinguish pharyngitis from impetigo strains?Current opinion in infectious diseases · 2016Review
- Epidemiology Analysis of Streptococcus pyogenes in a Hospital in Southern Taiwan by Use of the Updated emm Cluster Typing System.Journal of clinical microbiology · 2016Article
- The FasX Small Regulatory RNA Negatively Regulates the Expression of Two Fibronectin-Binding Proteins in Group A Streptococcus.Journal of bacteriology · 2015Article
- Effects of penicillin and erythromycin on adherence of invasive and noninvasive isolates of Streptococcus pyogenes to laminin.Memorias do Instituto Oswaldo Cruz · 2015Article
- Mechanisms of group A Streptococcus resistance to reactive oxygen species.FEMS microbiology reviews · 2015Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Group A Streptococcus (GAS) is a leading human pathogen producing a diverse array of infections from simple pharyngitis ("strep throat") to invasive conditions, including necrotizing fasciitis and toxic shock syndrome. The surface-anchored GAS M1 protein is a classical virulence factor that promotes phagocyte resistance and exaggerated inflammation by binding host fibrinogen (Fg) to form supramolecular networks. In this study, we used a virulent WT M1T1 GAS strain and its isogenic M1-deficient mutant to examine the role of M1-Fg binding in a proximal step in GAS infection-interaction with the pharyngeal epithelium. Expression of the M1 protein reduced GAS adherence to human pharyngeal keratinocytes by 2-fold, and this difference was increased to 4-fold in the presence of Fg. In stationary phase, surface M1 protein cleavage by the GAS cysteine protease SpeB eliminated Fg binding and relieved its inhibitory effect on GAS pharyngeal cell adherence. In a mouse model of GAS colonization of nasal-associated lymphoid tissue, M1 protein expression was associated with an average 6-fold decreased GAS recovery in isogenic strain competition assays. Thus, GAS M1 protein-Fg binding reduces GAS pharyngeal cell adherence and colonization in a fashion that is counterbalanced by SpeB. Inactivation of SpeB during the shift to invasive GAS disease allows M1-Fg binding, increasing pathogen phagocyte resistance and proinflammatory activities.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.