ArticleInfection and immunity1988
Effect of Mycobacterium tuberculosis-derived sulfolipid I on human phagocytic cells.
Article in Infection and immunity, 1988. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 77 citations in OpenAlex.
- Small RNA ASpks2 promotes Mycobacterium tuberculosis survival in macrophages via targeting polyketide synthase 2.The Journal of biological chemistry · 2026Article
- The Key Roles ofFrontiers in microbiology · 2023Article
- Chemical Synthesis of Cell Wall Constituents ofChemical reviews · 2021Review
- A novel mutation alters the stability of PapA2 resulting in the complete abrogation of sulfolipids in clinical mycobacterial strains.FASEB bioAdvances · 2019Article
- Underestimated Manipulative Roles ofFrontiers in immunology · 2019Review
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- Deciphering the virulence factors of the opportunistic pathogenNew microbes and new infections · 2016Article
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- Bacterial iron-sulfur cluster sensors in mammalian pathogens.Metallomics : integrated biometal science · 2015Review
- Lipid metabolism and Type VII secretion systems dominate the genome scale virulence profile of Mycobacterium tuberculosis in human dendritic cells.BMC genomics · 2015Article
- Biosynthesis and translocation of unsulfated acyltrehaloses in Mycobacterium tuberculosis.The Journal of biological chemistry · 2014Article
- Synthesis of hydroxyphthioceranic acid using a traceless lithiation-borylation-protodeboronation strategy.Nature chemistry · 2014Article
- New targets and inhibitors of mycobacterial sulfur metabolism.Infectious disorders drug targets · 2013Review
- Virulence factors of the Mycobacterium tuberculosis complex.Virulence · 2013Review
- Sulfolipid-1 biosynthesis restricts Mycobacterium tuberculosis growth in human macrophages.ACS chemical biology · 2012Article
- Elucidation and chemical modulation of sulfolipid-1 biosynthesis in Mycobacterium tuberculosis.The Journal of biological chemistry · 2012Article
- Article
- Sulfolipid accumulation in Mycobacterium tuberculosis disrupted in the mce2 operon.Journal of microbiology (Seoul, Korea) · 2011Article
- Function and structure of a prokaryotic formylglycine-generating enzyme.The Journal of biological chemistry · 2008Article
- Synthetic studies toward Mycobacterium tuberculosis sulfolipid-I.The Journal of organic chemistry · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Experiments were performed to determine the effects of Mycobacterium tuberculosis-derived sulfolipid I on phagocytic cells. Sulfolipid I was taken up in significant amounts by human neutrophils and in lesser amounts by monocytes and lymphocytes. Superoxide (O2-) production by neutrophils was significantly increased by sulfolipid I, but the rate of production was slower than that reported previously for other stimuli. The optimal concentration of sulfolipid I for stimulation of O2- production was 27 micrograms/ml, while higher concentrations produced less. At substimulatory levels sulfolipid I caused enhancement of O2- release from neutrophils when it was subsequently stimulated by other agents. Nonadherent monocytes from most normal donors failed to produce O2- when treated with sulfolipid I; however, adherent monocytes pretreated with gamma interferon did produce O2- with sulfolipid I stimulation. Priming for an enhanced oxidative response of activated monocytes was also observed. These sulfolipid I-induced changes in phagocytic cell function may be important in altering the ability of phagocytes to respond effectively to M. tuberculosis and may also cause exaggerated inflammatory responses.
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.