ArticleJournal of immunology (Baltimore, Md. : 1950)2012
NO is a macrophage autonomous modifier of the cytokine response to streptococcal single-stranded RNA.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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.
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Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Potential Immunoregulatory and Antiviral/SARS-CoV-2 Activities of Nitric Oxide.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Intrinsic Maturational Neonatal Immune Deficiencies and Susceptibility to Group B Streptococcus Infection.Clinical microbiology reviews · 2017Review
- Interaction of Streptococcus agalactiae and Cellular Innate Immunity in Colonization and Disease.Frontiers in immunology · 2014Review
- Neonatal immune adaptation of the gut and its role during infections.Clinical & developmental immunology · 2013Review
- The pore-forming toxin β hemolysin/cytolysin triggers p38 MAPK-dependent IL-10 production in macrophages and inhibits innate immunity.PLoS pathogens · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
Group B streptococci, a major cause of sepsis, induce inflammatory cytokines in strict dependence on bacterial ssRNA and the host molecules MyD88 and UNC-93B. In this study, we show that NO plays an important role in Group B streptococci-induced transcriptional activation of cytokine genes. Phagocytosis induced NO in a MyD88-dependent fashion. In turn, NO propagated the acidification of phagosomes and the processing of phagosomal bacterial nucleic acids and was required for potent transcriptional activation of cytokine genes by streptococci. This NO-dependent amplification loop has important mechanistic implications for the anti-streptococcal macrophage response and sepsis pathogenesis.
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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.