ArticleFrontiers in cellular and infection microbiology2015
Targeting TREM-1 Signaling in the Presence of Antibiotics is Effective Against Streptococcal Toxic-Shock-Like Syndrome (STSLS) Caused by Streptococcus suis.
Article in Frontiers in cellular and infection microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Triggering receptor expressed on myeloid cells-1 in sepsis, and current insights into clinical studies.Critical care (London, England) · 2024Review
- The CDR3 region as the major driver of TREM-1 interaction with its ligands, anComputational and structural biotechnology journal · 2023Article
- IL-18 Signaling Is Essential for Causing Streptococcal Toxic Shock-like Syndrome (STSLS).Life (Basel, Switzerland) · 2022Article
- TREM-1 Modulation Strategies for Sepsis.Frontiers in immunology · 2022Review
- Acquiring high expression of suilysin enable non-epidemicEmerging microbes & infections · 2021Article
- Neutrophils inMicroorganisms · 2021Review
- Triggering Receptor Expressed on Myeloid Cells-1 (TREM-1) Contributes to Bordetella pertussis Inflammatory Pathology.Infection and immunity · 2021Article
- Interleukin-17A Contributes to Bacterial Clearance in a Mouse Model of Streptococcal Toxic Shock-Like Syndrome.Pathogens (Basel, Switzerland) · 2021Article
- Baicalein AmelioratesInternational journal of molecular sciences · 2021Article
- Effective Antibacterial and Antihemolysin Activities of Ellipticine Hydrochloride against Streptococcus suis in a Mouse Model.Applied and environmental microbiology · 2021Article
- Apigenin and Ampicillin as Combined Strategy to Treat SevereMolecules (Basel, Switzerland) · 2021Article
- TLT2 Suppresses Th1 Response by Promoting IL-6 Production in Monocyte Through JAK/STAT3 Signal Pathway in Tuberculosis.Frontiers in immunology · 2020Article
- The Impact of SsPI-1 Deletion onPathogens (Basel, Switzerland) · 2019Article
- HP1717 Contributes to Streptococcus suis Virulence by Inducing an Excessive Inflammatory Response and Influencing the Biosynthesis of the Capsule.Microorganisms · 2019Article
- An NLRP3 inflammasome-triggered cytokine storm contributes to Streptococcal toxic shock-like syndrome (STSLS).PLoS pathogens · 2019Article
- Article
- Triggering Receptor Expressed on Myeloid Cells-1 Signaling: Protective and Pathogenic Roles on Streptococcal Toxic-Shock-Like Syndrome Caused byFrontiers in immunology · 2018Review
- HP1330 Contributes toFrontiers in immunology · 2017Article
- Identification of Extracellular Actin As a Ligand for Triggering Receptor Expressed on Myeloid Cells-1 Signaling.Frontiers in immunology · 2017Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Streptococcus suis (S.suis), a major swine pathogen, is also a severe threat to human health. Infection with highly virulent strains of S. suis can cause human Streptococcal toxic-shock-like syndrome (STSLS), which is associated with high serum pro-inflammatory cytokine levels and a high mortality rate. Our previous study indicated that highly virulent S. suis infection could activate the TREM-1 signaling pathway, which promotes host clearance of S. suis during early infection. However, it remained to be elicited whether TREM-1 signaling could be a target against STSLS in the presence of antibiotic. In the present study, mice were infected with a highly virulent S. suis strain and then treated with rTREM-1 (the recombinant extracellular domain of TREM-1) to block TREM-1 signaling, antibiotics, both rTREM-1 and antibiotics, or PBS. The survival rates, clinical signs, serum IL-1β and TNF-α levels, and serum bacterial loads were evaluated. Treatment with rTREM-1 could aggravate the outcome of infection as described previously. Although the conventional treatment with antibiotics contributed to effective S. suis clearance, it did not improve survival significantly. In comparison, due to the reduction of the exaggerated pro-inflammatory response, treatment combined with rTREM-1 and antibiotics not only led to efficient bacterial clearance but also alleviated inflammation. In conclusion, TREM-1 signaling contributed to severe inflammatory response and benefited S. suis clearance. Therefore, blocking TREM-1 signaling could still be a target for the treatment of STSLS in the presence of antibiotics.
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