Evidence map›Paper›PMID 22461696›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Heme oxygenase-1 promotes the persistence of Leishmania chagasi infection.

Nívea F Luz, Bruno B Andrade, Daniel F Feijó, Théo Araújo-Santos, Graziele Q Carvalho, Daniela Andrade, Daniel R Abánades, Enaldo V Melo, Angela M Silva, Cláudia I Brodskyn and 6 more

Open access · bronzeAbstract read
In one paragraph

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 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

58 citing papers in PubMed, 87 citations in OpenAlex.

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  19. Insights intoVeterinary sciences · 2021
    Review
  20. Review
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

16 authors at 6 institutions in 2 countries.

Nívea F LuzCentro de Pesquisas Gonçalo Moniz/Fundação Oswaldo Cruz, Salvador 40295-001, Brazil.
Bruno B Andrade
Daniel F Feijó
Théo Araújo-Santos
Graziele Q Carvalho
Daniela Andrade
Daniel R Abánades
Enaldo V Melo
Angela M Silva
Cláudia I Brodskyn
Manoel Barral-Netto
Aldina Barral
Rodrigo P Soares
Roque P Almeida
Marcelo T Bozza
Valéria M Borges
Fundação Oswaldo Cruz · BRUniversidade Federal da Bahia · BRInstituto Federal da Bahia · BRUniversidade Federal de Sergipe · BRUniversidade Federal do Rio de Janeiro · BRNational Institute of Allergy and Infectious Diseases · US

Funding

Intramural NIH HHS Z99 AI999999NIAID NIH HHS Y99 AI999999
6 · The paper itself

Abstract

Visceral leishmaniasis (VL) remains a major public health problem worldwide. This disease is highly associated with chronic inflammation and a lack of the cellular immune responses against Leishmania. It is important to identify major factors driving the successful establishment of the Leishmania infection to develop better tools for the disease control. Heme oxygenase-1 (HO-1) is a key enzyme triggered by cellular stress, and its role in VL has not been investigated. In this study, we evaluated the role of HO-1 in the infection by Leishmania infantum chagasi, the causative agent of VL cases in Brazil. We found that L. chagasi infection or lipophosphoglycan isolated from promastigotes triggered HO-1 production by murine macrophages. Interestingly, cobalt protoporphyrin IX, an HO-1 inductor, increased the parasite burden in both mouse and human-derived macrophages. Upon L. chagasi infection, macrophages from Hmox1 knockout mice presented significantly lower parasite loads when compared with those from wild-type mice. Furthermore, upregulation of HO-1 by cobalt protoporphyrin IX diminished the production of TNF-α and reactive oxygen species by infected murine macrophages and increased Cu/Zn superoxide dismutase expression in human monocytes. Finally, patients with VL presented higher systemic concentrations of HO-1 than healthy individuals, and this increase of HO-1 was reduced after antileishmanial treatment, suggesting that HO-1 is associated with disease susceptibility. Our data argue that HO-1 has a critical role in the L. chagasi infection and is strongly associated with the inflammatory imbalance during VL. Manipulation of HO-1 pathways during VL could serve as an adjunctive therapeutic approach.

Indexed as

AnimalsBrazilGene Expression Regulation, EnzymologicGlycosphingolipidsHeme Oxygenase-1HumansLeishmaniaLeishmaniasis, VisceralMacrophages, PeritonealMembrane ProteinsMiceMice, Inbred BALB CMice, KnockoutMice, SCIDPhotosensitizing AgentsProtoporphyrinsGlycosphingolipidsHeme Oxygenase-1HMOX1 protein, humanHmox1 protein, mouselipophosphonoglycanMembrane ProteinsPhotosensitizing Agentsprotoporphyrin IXProtoporphyrins

Identifiers

PMID22461696
PMCPMC3331931
OpenAlexW1925193485

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.