ArticleInfection and immunity2013
Exacerbated type II interferon response drives hypervirulence and toxic shock by an emergent epidemic strain of Streptococcus suis.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed.
- The IL-17A/Neutrophil axis plays a critical role in lethal infection induced by an emerging ultra-virulentVirulence · 2026Article
- Lessons from a case report of thrombocytopenia-associated multiple organ failure secondary to Streptococcus suis infection: Diagnosis and treatment strategies.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Article
- The cholesterol-dependent cytolysin promotesInfection and immunity · 2026Article
- Article
- Article
- Lipoteichoic acids influence cell shape and bacterial division of Streptococcus suis serotype 2, but play a limited role in the pathogenesis of the infection.Veterinary research · 2024Article
- Study of the Role of Lipoprotein Maturation Enzymes in the Pathogenesis of the Infection Caused by thePathogens (Basel, Switzerland) · 2023Article
- Canagliflozin Inhibited the Activity of Hemolysin and Reduced the Inflammatory Response Caused byInternational journal of molecular sciences · 2023Article
- IL-18 Signaling Is Essential for Causing Streptococcal Toxic Shock-like Syndrome (STSLS).Life (Basel, Switzerland) · 2022Article
- Piglet innate immune response to Streptococcus suis colonization is modulated by the virulence of the strain.Veterinary research · 2021Article
- Acquiring high expression of suilysin enable non-epidemicEmerging microbes & infections · 2021Article
- Genomic and pathogenic investigations ofEmerging microbes & infections · 2021Article
- Role of Maturation of Lipoproteins in the Pathogenesis of the Infection Caused byMicroorganisms · 2021Article
- Investigation of the Genomic and Pathogenic Features of the Potentially ZoonoticPathogens (Basel, Switzerland) · 2021Article
- Apigenin and Ampicillin as Combined Strategy to Treat SevereMolecules (Basel, Switzerland) · 2021Article
- Review of the speculative role of co-infections in Streptococcus suis-associated diseases in pigs.Veterinary research · 2021Review
- Annexin A1 Attenuates Neutrophil Migration and IL-6 Expression through Fpr2 in a Mouse Model of Streptococcus suis-Induced Meningitis.Infection and immunity · 2021Article
- Auranofin Has Advantages over First-Line Drugs in the Treatment of SevereAntibiotics (Basel, Switzerland) · 2020Article
- Article
- TRIM32 Drives Pathogenesis in Streptococcal Toxic Shock-Like Syndrome and Streptococcus suis Meningitis by Regulating Innate Immune Responses.Infection and immunity · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Streptococcus suis, a major porcine pathogen, can be transmitted to humans and cause severe symptoms. A large human outbreak associated with an unusual streptococcal toxic shock-like syndrome (STSLS) was described in China. Albeit an early burst of proinflammatory cytokines following Chinese S. suis infection was suggested to be responsible for STSLS case severity, the mechanisms involved are still poorly understood. Using a mouse model, the host response to S. suis infection with a North American intermediately pathogenic strain, a European highly pathogenic strain, and the Chinese epidemic strain was investigated by a whole-genome microarray approach. Proinflammatory genes were expressed at higher levels in mice infected with the Chinese strain than those infected with the European strain. The Chinese strain induced a fast and strong gamma interferon (IFN-γ) response by natural killer (NK) cells. In fact, IFN-γ-knockout mice infected with the Chinese strain showed significantly better survival than wild-type mice. Conversely, infection with the less virulent North American strain resulted in an IFN-β-subjugated, low inflammatory response that might be beneficial for the host to clear the infection. Overall, our data suggest that a highly virulent epidemic strain has evolved to massively activate IFN-γ production, mainly by NK cells, leading to a rapid and lethal STSLS.
Indexed as
Identifiers
What OpenQuestion holds
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.