ArticleInfection and immunity2000
Salmonella enterica serovar typhimurium-dependent regulation of inducible nitric oxide synthase expression in macrophages by invasins SipB, SipC, and SipD and effector SopE2.
Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 40 citations in OpenAlex.
- Reactive oxygen species and reactive nitrogen species are double-edged swords in Salmonella infection.Archives of microbiology · 2025Review
- The rpoS gene confers resistance to low osmolarity conditions in Salmonella enterica serovar Typhi.PloS one · 2022Article
- Intracellular Pathogens: Host Immunity and Microbial Persistence Strategies.Journal of immunology research · 2019Review
- Analysis of Shigella flexneri Resistance, Biofilm Formation, and Transcriptional Profile in Response to Bile Salts.Infection and immunity · 2017Article
- SecretEPDB: a comprehensive web-based resource for secreted effector proteins of the bacterial types III, IV and VI secretion systems.Scientific reports · 2017Article
- Evolution ofFrontiers in cellular and infection microbiology · 2017Review
- Human Milk Oligosaccharides and Synthetic Galactosyloligosaccharides Contain 3'-, 4-, and 6'-Galactosyllactose and Attenuate Inflammation in Human T84, NCM-460, and H4 Cells and Intestinal Tissue Ex Vivo.The Journal of nutrition · 2016Article
- Role of Nitric Oxide in Salmonella Infection.Indian journal of clinical biochemistry : IJCB · 2012Article
- Salmonella pathogenesis and processing of secreted effectors by caspase-3.Science (New York, N.Y.) · 2010Article
- Bacterial manipulation of innate immunity to promote infection.Nature reviews. Microbiology · 2010Review
- Article
- Transcriptome of Salmonella enterica serovar Typhi within macrophages revealed through the selective capture of transcribed sequences.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Cooperative interactions between flagellin and SopE2 in the epithelial interleukin-8 response to Salmonella enterica serovar typhimurium infection.Infection and immunity · 2004Article
- Developmentally regulated IkappaB expression in intestinal epithelium and susceptibility to flagellin-induced inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Role of Toll-like receptor 4 in macrophage activation and tolerance during Salmonella enterica serovar Typhimurium infection.Infection and immunity · 2003Article
- Salmonella pathogenicity island 2 mediates protection of intracellular Salmonella from reactive nitrogen intermediates.The Journal of experimental medicine · 2002Article
- Activation of epigenetic regulator KDM6B byGut microbesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
When Salmonella enterica invades mammalian cells, it activates signals leading to increased expression of inflammatory mediators. One such mediator is nitric oxide (NO), which is produced under control of the enzyme inducible NO synthase (iNOS). Induction of iNOS in response to Salmonella infection has been demonstrated, but the bacterial effector molecules that regulate expression of the enzyme have not been identified. In the study reported here, an analysis of Salmonella-dependent iNOS expression in macrophages was carried out. Wild-type Salmonella strains increased the levels of both iNOS protein and mRNA in murine macrophage cell lines in an invasion-independent fashion. Mutant strains lacking a functional pathogenicity island 1-encoded type III secretion system, as well as strains lacking the invasins SipB, SipC, and SipD, were impaired in iNOS induction. Complementation experiments indicated that all three of the invasins were required for induction of iNOS expression. These results suggested that an effector protein, translocated into macrophages via the type III secretion system in a SipB-, SipC-, and SipD-dependent manner, might be the ultimate mediator of iNOS induction. In keeping with this idea, a mutant strain deficient in SopE2, a recently described homolog of SopE, was found to be impaired in the induction of iNOS expression. These observations suggest that iNOS expression is regulated by signals activated by SopE2 (and possibly SopE) and that the role of SipB, SipC, and SipD in this process is to facilitate translocation of the relevant effector.
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.