Evidence map›Paper›PMID 24886588›Full record

ArticleJournal of translational medicine2014

Sulfur compounds block MCP-1 production by Mycoplasma fermentans-infected macrophages through NF-κB inhibition.

Francesca Benedetti, Sergio Davinelli, Selvi Krishnan, Robert C Gallo, Giovanni Scapagnini, Davide Zella, Sabrina Curreli

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 19% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
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  5. The Role of Copper Homeostasis in Brain Disease.International journal of molecular sciences · 2022
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  6. Utility of NO and HNitric oxide : biology and chemistry · 2022
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  11. Hydrogen Sulfide and Carbon Monoxide Tolerance in Bacteria.Antioxidants (Basel, Switzerland) · 2021
    Review
  12. Article
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  15. Article
  16. Review
  17. Review
  18. Article
  19. The Role of Host-Generated HFrontiers in cellular and infection microbiology · 2020
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Francesca Benedetti
Sergio Davinelli
Selvi Krishnan
Robert C Gallo
Giovanni Scapagnini
Davide Zella
Sabrina CurreliInstitute of Human Virology, University of Maryland School of Medicine, Baltimore, MD 21201, USA. SCurreli@ihv.umaryland.edu.
University of Maryland, Baltimore · USUniversity of Molise · ITOspedale di Parma · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsHydrogen sulfide (H2S), together with nitric oxide (NO) and carbon monoxide (CO), belongs to a family of endogenous signaling mediators termed "gasotransmitters". Recent studies suggest that H2S modulates many cellular processes and it has been recognized to play a central role in inflammation, in the cardiovascular and nervous systems. By infecting monocytes/macrophages with Mycoplasma fermentans (M.F.), a well-known pro-inflammatory agent, we evaluated the effects of H2S.

methodsM.F.-infected cells were analyzed by ELISA and real time RT-PCR to detect the M.F. effects on MCP-1 and on MMP-12 expression. The role of two different H2S donors (NaHS and GYY4137) on MF-infected cells was determined by treating infected cells with H2S and then testing the culture supernatants for MCP-1 and on MMP-12 production by ELISA assay. In order to identify the pathway/s mediating H2S- anti-inflammatory activity, cells were also treated with specific pharmaceutical inhibitors. Cytoplasmic and nuclear accumulation of NF-κB heterodimers was analyzed.

resultsWe show that H2S was able to reduce the production of pro-inflammatory cytokine MCP-1, that was induced in monocytes/macrophages during M.F. infection. Moreover, MCP-1 was induced by M.F. through Toll-like receptor (TLR)-mediated nuclear factor-κB (NF-κB) activation, as demonstrated by the fact that TLR inhibitors TIRAP and MyD88 and NF-κB inhibitor IKK were able to block the cytokine production. In contrast H2S treatment of M.F. infected macrophages reduced nuclear accumulation of NF-κB heterodimer p65/p52.

conclusionsOur data demonstrate that under the present conditions H2S is effective in reducing Mycoplasma-induced inflammation by targeting the NF-κB pathway. This supports further studies for possible clinical applications.

Indexed as

Base SequenceChemokine CCL2DNA PrimersEnzyme InductionEnzyme-Linked Immunosorbent AssayHumansHydrogen SulfideMacrophagesMatrix Metalloproteinase 12Mycoplasma fermentansNF-kappa BReal-Time Polymerase Chain ReactionU937 CellsChemokine CCL2DNA PrimersHydrogen SulfideMatrix Metalloproteinase 12NF-kappa B

Identifiers

PMID24886588
PMCPMC4046042
OpenAlexW2045490526

What OpenQuestion holds

Textmetadata
LicenceCC BY
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Registered trials

None linked

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.