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Updated: Aug 1, 2026
Deciphering the Molecular Mechanism and Function of Pore-Forming Toxins Using Leishmania major
Published on: October 28, 2022
Identification of molecular mechanisms causing skin lesions of cutaneous leishmaniasis using weighted gene
Kavoos Momeni1, Saeid Ghorbian2, Ehsan Ahmadpour3
1Department of Molecular Genetics, Ahar Branch, Islamic Azad University, Ahar, Iran.
Abstract:
Leishmaniasis is an infectious disease, caused by a protozoan parasite. Its most common form is cutaneous leishmaniasis, which leaves scars on exposed body parts from bites by infected female phlebotomine sandflies. Approximately 50% of cases of cutaneous leishmaniasis fail to respond to standard treatments, creating slow-healing wounds which cause permanent scars on the skin. We performed a joint bioinformatics analysis to identify differentially expressed genes (DEGs) in healthy skin biopsies and Leishmania cutaneous wounds. DEGs and WGCNA modules were analyzed based on the Gene Ontology function, and the Cytoscape software. Among almost 16,600 genes that had significant expression changes on the skin surrounding Leishmania wounds, WGCNA determined that one of the modules, with 456 genes, has the strongest correlation with the size of the wounds. Functional enrichment analysis indicated that this module includes three gene groups with significant expression changes. These produce tissue-damaging cytokines or disrupt the production and activation of collagen, fibrin proteins, and the extracellular matrix, causing skin wounds or preventing them from healing. The hub genes of these groups are OAS1, SERPINH1, and FBLN1 respectively. This information can provide new ways to deal with unwanted and harmful effects of cutaneous leishmaniasis.
Insights
Cutaneous leishmaniasis causes non-healing skin wounds and scars. Bioinformatics identified key genes disrupting tissue repair, offering potential new therapeutic targets for this neglected tropical disease.
Area of Science:
- Genomics
- Bioinformatics
- Dermatology
Background:
- Leishmaniasis is an infectious disease caused by protozoan parasites.
- Cutaneous leishmaniasis, the most common form, results in non-healing skin wounds and permanent scarring.
- Standard treatments for cutaneous leishmaniasis have a high failure rate, necessitating novel therapeutic strategies.
Purpose of the Study:
- To identify differentially expressed genes (DEGs) in healthy skin versus Leishmania-infected cutaneous wounds using a joint bioinformatics analysis.
- To analyze WGCNA modules and Gene Ontology functions to understand molecular mechanisms underlying wound healing impairment.
- To pinpoint key genes and pathways involved in the pathogenesis of cutaneous leishmaniasis-induced skin damage.
Main Methods:
- Joint bioinformatics analysis of healthy skin and Leishmania cutaneous wound biopsies.
- Weighted Gene Co-expression Network Analysis (WGCNA) to identify gene modules correlated with wound size.
- Functional enrichment analysis using Gene Ontology and Cytoscape for pathway identification.
Main Results:
- Identified nearly 16,600 DEGs in skin surrounding Leishmania wounds.
- A specific WGCNA module of 456 genes showed the strongest correlation with wound size.
- This module contains genes involved in producing tissue-damaging cytokines and disrupting collagen/extracellular matrix production, hindering wound healing. Hub genes include OAS1, SERPINH1, and FBLN1.
Conclusions:
- The identified gene module and hub genes offer insights into the molecular mechanisms of impaired wound healing in cutaneous leishmaniasis.
- Targeting these specific genes or pathways may lead to novel therapeutic interventions for non-healing cutaneous leishmaniasis wounds.
- This research provides a foundation for developing treatments to mitigate the harmful effects of cutaneous leishmaniasis and improve patient outcomes.
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