Evidence map›Paper›PMID 18974840›Full record

ArticlePloS one2008

Identification of novel single nucleotide polymorphisms in inflammatory genes as risk factors associated with trachomatous trichiasis.

Berna Atik, Troy A Skwor, Ram Prasad Kandel, Bassant Sharma, Him Kant Adhikari, Lori Steiner, Henry Erlich, Deborah Dean

Open access · goldAbstract readComparative StudyMulticenter Study
In one paragraph

Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

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  2. Association of polymorphisms ofJournal of genetics · 2024
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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

8 authors at 2 institutions in 2 countries.

Berna AtikCenter for Immunobiology and Vaccine Development, Children's Hospital Oakland Research Institute, Oakland, California, USA.
Troy A Skwor
Ram Prasad Kandel
Bassant Sharma
Him Kant Adhikari
Lori Steiner
Henry Erlich
Deborah Dean
Lumbini Eye Institute · NPUniversity of California, San Francisco · US

Funding

C. trachomatis genomics, strain typing, and evolutionR01AI059647 · NIAID · CHILDREN'S HOSPITAL &RES CTR AT OAKLAND · PI DEAN, DEBORAH ANNE · 2004 to 2008
$2.8M
NIAID NIH HHS R01 AI059647NIAID NIH HHS R01 AI059647-1S1NIAID NIH HHS R01 EY/AI012219
6 · The paper itself

Abstract

backgroundTrachoma is the leading preventable cause of global blindness. A balanced Th1/Th2/Th3 immune response is critical for resolving Chlamydia trachomatis infection, the primary cause of trachoma. Despite control programs that include mass antibiotic treatment, reinfection and recurrence of trachoma are common after treatment cessation. Furthermore, a subset of infected individuals develop inflammation and are at greater risk for developing the severe sequela of trachoma known as trachomatous trichiasis (TT). While there are a number of environmental and behavioral risk factors for trachoma, genetic factors that influence inflammation and TT risk remain ill defined. METHODOLOGY/

findingsWe identified single nucleotide polymorphisms (SNP) in 36 candidate inflammatory genes and interactions among these SNPs that likely play a role in the overall risk for TT. We conducted a case control study of 538 individuals of Tharu ethnicity residing in an endemic region of Nepal. Trachoma was graded according to World Health Organization guidelines. A linear array was used to genotype 51 biallelic SNPs in the 36 genes. Analyses were performed using logic regression modeling, which controls for multiple comparisons. We present, to our knowledge, the first significant association of TNFA (-308GA), LTA (252A), VCAM1 (-1594TC), and IL9 (T113M) polymorphisms, synergistic SNPs and risk of TT. TT risk decreased 5 times [odds ratio = 0.2 (95% confidence interval 0.11.-0.33), p = 0.001] with the combination of TNFA (-308A), LTA (252A), VCAM1 (-1594C), SCYA 11 (23T) minor allele, and the combination of TNFA (-308A), IL9 (113M), IL1B (5'UTR-T), and VCAM1 (-1594C). However, TT risk increased 13.5 times [odds ratio = 13.5 (95% confidence interval 3.3-22), p = 0.001] with the combination of TNFA (-308G), VDR (intron G), IL4R (50V), and ICAM1 (56M) minor allele.

conclusionsEvaluating genetic risk factors for trachoma will advance our understanding of disease pathogenesis, and should be considered in the context of designing global control programs.

Indexed as

Inflammation MediatorsPolymorphism, Single NucleotideAdolescentAdultAgedCase-Control StudiesChlamydia InfectionsChlamydia trachomatisCytokinesFemaleGenetic Predisposition to DiseaseHumansInflammationMaleMiddle AgedNepalCytokinesInflammation Mediators

Identifiers

PMID18974840
PMCPMC2572999
OpenAlexW1994637378

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.