ArticleJournal of innate immunity2013
Prognostic value and therapeutic potential of TREM-1 in Streptococcus pyogenes- induced sepsis.
Article in Journal of innate immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- sTREM-1 as a biomarker for sepsis diagnosis and prognosis following abdominal surgery.Laboratory medicine · 2026Article
- TREM-1 Interacts with Rotavirus Proteins and Drives Inflammatory Responses: A Combined Experimental and Computational Approach.Pathogens (Basel, Switzerland) · 2025Article
- Triggering receptor expressed on myeloid cells-1 in sepsis, and current insights into clinical studies.Critical care (London, England) · 2024Review
- An appraisal of studies using mouse models to assist the biomarker discovery for sepsis prognosis.Heliyon · 2023Review
- TREM-1 Modulation Strategies for Sepsis.Frontiers in immunology · 2022Review
- Rapid proliferation due to better metabolic adaptation results in full virulence of a filament-deficient Candida albicans strain.Nature communications · 2021Article
- Soluble Triggering Receptors Expressed on Myeloid Cells-1 as a Neonatal Ventilator-Associated Pneumonia Biomarker.International journal of general medicine · 2021Article
- Review
- Infection-induced innate antimicrobial response disorders: from signaling pathways and their modulation to selected biomarkers.Central-European journal of immunology · 2020Review
- TREM-1 deficiency attenuates the inflammatory responses in LPS-induced murine endometritis.Microbial biotechnology · 2019Article
- TREM-1 modulation produces positive outcome on the histopathology and cytokines release profile ofJournal of parasitic diseases : official organ of the Indian Society for Parasitology · 2019Article
- Neonatal corticosterone mitigates autoimmune neuropsychiatric disorders associated with streptococcus in mice.Scientific reports · 2018Article
- Triggering Receptor Expressed on Myeloid Cells-1 Signaling: Protective and Pathogenic Roles on Streptococcal Toxic-Shock-Like Syndrome Caused byFrontiers in immunology · 2018Review
- Soluble triggering receptor expressed on myeloid cell-1 (sTREM-1): a potential biomarker for the diagnosis of infectious diseases.Frontiers of medicine · 2017Review
- Inhibition of triggering receptor expressed on myeloid cells-1 ameliorates experimental autoimmune neuritis.Molecular medicine reports · 2017Article
- TREM-1 signaling promotes host defense during the early stage of infection with highly pathogenic Streptococcus suis.Infection and immunity · 2015Article
- The triggering receptor expressed on myeloid cells (TREM) in inflammatory bowel disease pathogenesis.Journal of translational medicine · 2014Review
- Host responses to group a streptococcus: cell death and inflammation.PLoS pathogens · 2014Review
- A novel ligand-independent peptide inhibitor of TREM-1 suppresses tumor growth in human lung cancer xenografts and prolongs survival of mice with lipopolysaccharide-induced septic shock.International immunopharmacology · 2014Article
- A farewell to arms: streptococcal strategies to cope with innate immunity.Journal of innate immunity · 2014Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TREM-1 (triggering receptor expressed on myeloid cells) is a surface molecule expressed on neutrophils and macrophages which has been implicated in the amplification of inflammatory responses triggered during infection. In the present study, we have investigated the clinical significance of TREM-1 in Streptococcus pyogenes-induced severe sepsis in both experimentally infected mice as well as in patients with streptococcal toxic shock. We found that S. pyogenes induced a dose-dependent upregulation of TREM-1 in in vitro cultured phagocytic cells and in the organs of S. pyogenes-infected mice. Furthermore, we reported a positive correlation between serum levels of soluble TREM-1 (sTREM-1) and disease severity in infected patients as well as in experimentally infected mice. Hence, sTREM-1 may represent a useful surrogate marker for streptococcal sepsis. We found that modulation of TREM-1 by administration of the TREM-1 decoy receptor rTREM-1/Fc substantially attenuated the synthesis of inflammatory cytokines. More importantly, treatment of S. pyogenes-infected septic mice with rTREM-1/Fc or the synthetically produced conserved extracellular domain LP17 significantly improved disease outcome. In summary, our data suggest that TREM-1 may not only represent a valuable marker for S. pyogenes infection severity but it may also be an attractive target for the treatment of streptococcal sepsis.
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