ArticlePLoS neglected tropical diseases2016
Genetic Variation in Autophagy-Related Genes Influences the Risk and Phenotype of Buruli Ulcer.
Article in PLoS neglected tropical diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.
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Who cites it
25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Individual and clinical variables associated with the risk of Buruli ulcer acquisition: A systematic review and meta-analysis.PLoS neglected tropical diseases · 2020Pooled it
- Targeting Autophagy as a Strategy for Developing New Host-Directed Therapeutics Against Nontuberculous Mycobacteria.Pathogens (Basel, Switzerland) · 2025Review
- Micronutrient-deficient diets and possible environmental enteric dysfunction in Buruli ulcer endemic communities in Ghana: Lower dietary diversity and reduced serum zinc and vitamin C implicate micronutrient status a possible susceptibility factor.PLoS neglected tropical diseases · 2025Article
- Autophagy Gene BECN1 Intronic Variant rs9890617 Predisposes Individuals to Hepatitis B Virus Infection.Biochemical genetics · 2024Article
- PARK2 as a susceptibility factor for nontuberculous mycobacterial pulmonary disease.Respiratory research · 2024Article
- Type-I interferons promote innate immune tolerance in macrophages exposed to Mycobacterium ulcerans vesicles.PLoS pathogens · 2023Article
- A nod to the bond between NOD2 and mycobacteria.PLoS pathogens · 2023Review
- Autophagopathies: from autophagy gene polymorphisms to precision medicine for human diseases.Autophagy · 2022Article
- Article
- Mice Dually Disrupted forFrontiers in immunology · 2022Article
- Offense and Defense in Granulomatous Inflammation Disease.Frontiers in cellular and infection microbiology · 2022Review
- Genetic variants in humanEmerging microbes & infections · 2021Article
- Understanding the transmission of Mycobacterium ulcerans: A step towards controlling Buruli ulcer.PLoS neglected tropical diseases · 2021Review
- Autophagy and Host Defense in Nontuberculous Mycobacterial Infection.Frontiers in immunology · 2021Review
- The One That Got Away: How Macrophage-Derived IL-1β Escapes the Mycolactone-Dependent Sec61 Blockade in Buruli Ulcer.Frontiers in immunology · 2021Article
- Human genetics of Buruli ulcer.Human genetics · 2020Review
- The immunology of other mycobacteria: M. ulcerans, M. leprae.Seminars in immunopathology · 2020Review
- Genome-wide association study of Buruli ulcer in rural Benin highlights role of two LncRNAs and the autophagy pathway.Communications biology · 2020Article
- Buruli ulcer: The Efficacy of Innate Immune Defense May Be a Key Determinant for the Outcome of Infection WithFrontiers in microbiology · 2020Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionBuruli ulcer (BU) is a severe necrotizing human skin disease caused by Mycobacterium ulcerans. Clinically, presentation is a sum of these diverse pathogenic hits subjected to critical immune-regulatory mechanisms. Among them, autophagy has been demonstrated as a cellular process of critical importance. Since microtubules and dynein are affected by mycolactone, the critical pathogenic exotoxin produced by M. ulcerans, cytoskeleton-related changes might potentially impair the autophagic process and impact the risk and progression of infection.
objectiveGenetic variants in the autophagy-related genes NOD2, PARK2 and ATG16L1 has been associated with susceptibility to mycobacterial diseases. Here, we investigated their association with BU risk, its severe phenotypes and its progression to an ulcerative form.
methodsGenetic variants were genotyped using KASPar chemistry in 208 BU patients (70.2% with an ulcerative form and 28% in severe WHO category 3 phenotype) and 300 healthy endemic controls.
resultsThe rs1333955 SNP in PARK2 was significantly associated with increased susceptibility to BU [odds ratio (OR), 1.43; P = 0.05]. In addition, both the rs9302752 and rs2066842 SNPs in NOD2 gee significantly increased the predisposition of patients to develop category 3 (OR, 2.23; P = 0.02; and OR 12.7; P = 0.03, respectively, whereas the rs2241880 SNP in ATG16L1 was found to significantly protect patients from presenting the ulcer phenotype (OR, 0.35; P = 0.02).
conclusionOur findings indicate that specific genetic variants in autophagy-related genes influence susceptibility to the development of BU and its progression to severe phenotypes.
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