ArticleNature communications2023
Interplay between human STING genotype and bacterial NADase activity regulates inter-individual disease variability.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Purine and pyrimidine-based bacterial cyclic dinucleotides egress the phagosome and activate the innate immune sensor STING.Immunity · 2026Article
- Group A Streptococcal Virulence Factors and Vaccine Development-An Update.Microorganisms · 2026Review
- A validated model for early prediction of group A streptococcal aetiology in necrotising soft tissue infections using minimal patient data.BMC medicine · 2026Article
- IFI204-STING drives protective innate immunity against gangrenousFrontiers in immunology · 2026Article
- Revisiting the streptococcal M protein: modern perspectives on antibody function, host interactions, and therapeutic targeting.Frontiers in immunology · 2026Review
- The commoneLife · 2024Article
- The commonbioRxiv : the preprint server for biology · 2024Article
- The germ theory revisited: A noncentric view on infection outcome.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024Review
- Reduced interleukin-18 secretion by human monocytic cells in response to infections with hyper-virulent Streptococcus pyogenes.Journal of biomedical science · 2024Article
- Immunomodulating Enzymes fromMicroorganisms · 2024Review
- ADP-heptose attenuatesGut microbesArticle
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Variability in disease severity caused by a microbial pathogen is impacted by each infection representing a unique combination of host and pathogen genomes. Here, we show that the outcome of invasive Streptococcus pyogenes infection is regulated by an interplay between human STING genotype and bacterial NADase activity. S. pyogenes-derived c-di-AMP diffuses via streptolysin O pores into macrophages where it activates STING and the ensuing type I IFN response. However, the enzymatic activity of the NADase variants expressed by invasive strains suppresses STING-mediated type I IFN production. Analysis of patients with necrotizing S. pyogenes soft tissue infection indicates that a STING genotype associated with reduced c-di-AMP-binding capacity combined with high bacterial NADase activity promotes a 'perfect storm' manifested in poor outcome, whereas proficient and uninhibited STING-mediated type I IFN production correlates with protection against host-detrimental inflammation. These results reveal an immune-regulating function for bacterial NADase and provide insight regarding the host-pathogen genotype interplay underlying invasive infection and interindividual disease variability.
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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.