Evidence map›Paper›PMID 22554650›Full record

ArticleInfection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases2012

Wound healing genes and susceptibility to cutaneous leishmaniasis in Brazil.

Léa Castellucci, Sarra E Jamieson, Lucas Almeida, Joyce Oliveira, Luiz Henrique Guimarães, Marcus Lessa, Michaela Fakiola, Amélia Ribeiro de Jesus, E Nancy Miller, Edgar M Carvalho and 1 more

Open access · greenAbstract read
In one paragraph

Article in Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

  1. Frontiers in chemistry · 2024
    Article
  2. Article
  3. Novel Insights IntoFrontiers in cellular and infection microbiology · 2022
    Article
  4. A Genome-wide Association Study Identifies SERPINB10, CRLF3, STX7, LAMP3, IFNG-AS1, and KRT80 As Risk Loci Contributing to Cutaneous Leishmaniasis in Brazil.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2021
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Cutaneous Manifestations of Human and Murine Leishmaniasis.International journal of molecular sciences · 2017
    Review
  11. Analysis of expression of FLI1 and MMP1 in American cutaneous leishmaniasis caused by Leishmania braziliensis infection.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2017
    Article
  12. Article
  13. Fine mapping under linkage peaks for symptomatic or asymptomatic outcomes of Leishmania infantum infection in Brazil.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2016
    Article
  14. Article
  15. Wound healing genes and susceptibility to cutaneous leishmaniasis in Brazil: role of COL1A1.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2015
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  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

11 authors at 5 institutions in 3 countries.

Léa CastellucciNational Institute of Science and Technology in Tropical Diseases, Brazil and Federal University of Bahia, Salvador, Brazil. leacastel@hotmail.com
Sarra E Jamieson
Lucas Almeida
Joyce Oliveira
Luiz Henrique Guimarães
Marcus Lessa
Michaela Fakiola
Amélia Ribeiro de Jesus
E Nancy Miller
Edgar M Carvalho
Jenefer M Blackwell
Universidade Federal da Bahia · BRUniversity of Cambridge · GBInstituto de Medicina Avançada · BRThe Kids Research Institute Australia · AUUniversity of Western Australia · AU

Funding

The role of Leishmania braziliensis strain polymorphism on disease outcome and ..P50AI030639 · NIAID · FEDERAL UNIVERSITY OF BAHIA · PI CARVALHO, EDGAR M · 1991 to 2023
$9.1M
Genetic Risk Factors for Visceral LeishmaniasisR01AI076233 · NIAID · UNIVERSITY OF IOWA · PI BLACKWELL, JENEFER MARY, WILSON, MARY E · 2009 to 2013
$1.6M
TROPICAL INFECTIOUS DISEASE TRAINING GRANTD43TW007127 · FIC · FEDERAL UNIVERSITY OF BAHIA · PI CARVALHO, EDGAR M · 2004 to 2009
$733k
FIC NIH HHS 1 D43 TW007127-01FIC NIH HHS D43 TW007127NIAID NIH HHS AI 30639NIAID NIH HHS P50 AI030639NIAID NIH HHS R01 AI076233Wellcome Trust
6 · The paper itself

Abstract

Leishmania braziliensis causes cutaneous (CL) and mucosal (ML) leishmaniasis. In the mouse, Fli1 was identified as a gene influencing enhanced wound healing and resistance to CL caused by Leishmania major. Polymorphism at FLI1 is associated with CL caused by L. braziliensis in humans, with an inverse association observed for ML disease. Here we extend the analysis to look at other wound healing genes, including CTGF, TGFB1, TGFBR1/2, SMADS 2/3/4/7 and FLII, all functionally linked along with FLI1 in the TGF beta pathway. Haplotype tagging single nucleotide polymorphisms (tag-SNPs) were genotyped using Taqman technology in 325 nuclear families (652 CL cases; 126 ML cases) from Brazil. Robust case-pseudocontrol (CPC) conditional logistic regression analysis showed associations between CL and SNPs at CTGF (SNP rs6918698; CC genotype; OR 1.67; 95%CI 1.10-2.54; P=0.016), TGFBR2 (rs1962859; OR 1.50; 95%CI 1.12-1.99; P=0.005), SMAD2 (rs1792658; OR 1.57; 95%CI 1.04-2.38; P=0.03), SMAD7 (rs4464148; AA genotype; OR 2.80; 95%CI 1.00-7.87; P=0.05) and FLII (rs2071242; OR 1.60; 95%CI 1.14-2.24; P=0.005), and between ML and SNPs at SMAD3 (rs1465841; OR 2.15; 95%CI 1.13-4.07; P=0.018) and SMAD7 (rs2337107; TT genotype; OR 3.70; 95%CI 1.27-10.7; P=0.016). Stepwise logistic regression analysis showed that all SNPs associated with CL at FLI1, CTGF, TGFBR2, and FLII showed independent effects from each other, but SNPs at SMAD2 and SMAD7 did not add independent effects to SNPs from other genes. These results suggest that TGFβ signalling via SMAD2 is important in directing events that contribute to CL, whereas signalling via SMAD3 is important in ML. Both are modulated by the inhibitory SMAD7 that acts upstream of SMAD2 and SMAD3 in this signalling pathway. Along with the published FLI1 association, these data further contribute to the hypothesis that wound healing processes are important determinants of pathology associated with cutaneous forms of leishmaniasis.

Indexed as

AdultBrazilCohort StudiesFamilyFemaleGenetic Predisposition to DiseaseHaplotypesHumansLeishmaniasis, CutaneousLinkage DisequilibriumLogistic ModelsMaleMicrofilament ProteinsPolymorphism, Single NucleotideReceptors, Cytoplasmic and NuclearSignal TransductionFLII protein, humanMicrofilament ProteinsReceptors, Cytoplasmic and NuclearTrans-ActivatorsTransforming Growth Factor beta

Identifiers

PMID22554650
PMCPMC3372530
OpenAlexW2081350230

What OpenQuestion holds

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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.