Gene Expression Profiling of Nerve Biopsies from Pure Neural Leprosy Patients
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1215390 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32114724_1.fastq.gz | Fastqsanger.gz | |||
| SRR32114724_2.fastq.gz | Fastqsanger.gz | |||
| SRR32114725_1.fastq.gz | Fastqsanger.gz | |||
| SRR32114725_2.fastq.gz | Fastqsanger.gz | |||
| SRR32114726_1.fastq.gz | Fastqsanger.gz |
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Project description:Leprosy may affect skin and nerves, leading to disability. Pure neural leprosy (PNL) lacks skin lesions, complicating diagnosis. Transcriptomic profiling reveals unique gene expression changes in PNL nerves, shedding light on immune response and pathogenesis. These findings may guide early diagnosis and improve patient outcomes. In the present study, gene profiling of nerve biopsies from patients with PNL revealed significant transcriptomic alterations compared to non-leprosy controls. Principal Component Analysis (PCA) of the 500 most differentially expressed genes separated the groups, with 1,199 genes showing differential expression (|log2FC| ≥ 1, FDR ≤ 0.1). Downregulated genes included GAS2L2, TRIM67, IL1RAPL1, MAP1LC3B2, and NTNG1, implicated in neuronal development and autophagy, while upregulated genes were linked to immune responses. Functional analyses highlighted inflammasome activation and autophagy impairment in PNL, correlating with nerve inflammation and architecture loss. We hope that our data will aid in identifying new markers, fostering strategies for early diagnosis, preventing disabilities, and improving the management of PNL patients.
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Project description:Leprosy is a chronic disease of the skin and peripheral nerves caused by Mycobacterium leprae. A major public health and clinical problem are leprosy reactions, which are inflammatory episodes that often contribute to nerve damage and disability. Type I reversal reactions (T1R) can occur after microbiological cure of leprosy and affect up to 50% of leprosy patients. Early intervention to prevent T1R and, hence, nerve damage, is a major focus of current leprosy control efforts. In this study, we compared transcript (i.e. isoform) expression and usage profiles from leprosy patients free of T1R at enrollment (who eventually developed T1R) against T1R-free leprosy patients. Our results showed that, at baseline, cells from T1R-destined and T1R-free subjects had no main difference in their transcripts expression and usage. However, the cells of T1R patients displayed a transcriptomic immune response to M. leprae antigens that was significantly different from the one of cells from leprosy patients who remained T1R-free. Transcripts with significantly higher upregulation in the T1R-destined group, compared to the cells from T1R-free patients, were enriched for pathways and GO terms involved in response to intracellular pathogens, apoptosis regulation and inflammatory processes. Similarly, transcript usage analysis pinpointed different transcript proportions in response to the in-vitro challenge of cells from T1R-destined patients. Hence, transcript usage in concert with transcript expression suggested a dysregulated inflammatory response including increased apoptosis regulation in the peripheral blood cells of T1R-destined patients before the onset of T1R symptoms. Combined, these results provided detailed insight into the pathogenesis of T1R.
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Project description:Leprosy is classified from paucibacillary leprosy (TT and BT) to multibacillary leprosy (BB, BL, and LL). In our study, we focus on selecting or classfying the significant genes to discriminate between paucibacillary and multibacillary group and the important genes to distinguish between blood and the corresponding tissue in patients.
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Project description:Leprosy is classified from paucibacillary leprosy (TT and BT) to multibacillary leprosy (BB, BL, and LL). In our study, we focus on selecting or classfying the significant genes to discriminate between paucibacillary and multibacillary group and the important genes to distinguish between blood and the corresponding tissue in patients. · Human Adult Normal Skin Sample (Commercial;Cat#1234218); 6 patients of leprosy (Blood and Tissue sample (Pathologic classification: BT); 6 patients of leprosy (Blood and Tissue sample (Pathologic classification: MB)) · In blood sample, BT sample vs MB sample · In tissue sample, Normal Skin sample vs tissue BT sample or tissue MB sample · Single Color Microarray · All experiments are performed one replicate
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Project description:In this study, a comprehensive assessment of human miRNA was performed on leprosy skin lesions using DNA chip microarrays, which included the entire spectrum of the disease along with its reactional states. Sixty-eight samples from leprotic lesions (10TT, 10BT, 10BB, 10BL, 4LL, 14R1, and 10R2) and nine skin biopsies from healthy individuals were used as controls (CC) (ages ranged from 06 to 83 years, 48 were male and 29 female). The evaluation identified differentially expressed miRNAs [Fold Change (FC)≥2.0, p<0.05] in disease lesions versus healthy controls or between them. Some of these miRNAs were validated by RT-PCR.
2017-10-31 | GSE102314 | GEO
Project description:Skin biopsy specimens of skin lesions were profiled for miRNA expression. In this study, we indentified miRNA species that were differentially expressed in the skin lesions of either the lepromatous or tuberculoid forms of leprosy. One miRNA species, hsa-mir-21, found in the lepromatous lesions was capable of downregulating the vitamin D-dependent antimicrobial pathway. Scalpel or punch skin biopsy specimens were obtained after informed consent from patients with tuberculoid leprosy and patients with lepromatous leprosy at the time of diagnosis. Specimens were embedded in OCT medium, snap-frozen in liquid nitrogen and stored at 80°C until sectioning.
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Project description:Spiral ganglion neurons (SGNs) and the associated components of the auditory nerve are primary carriers of auditory information from hair cells to the brain. Loss of SGNs occurs with many pathological conditions, resulting in permanent sensorineural hearing loss. Neural stem/progenitors (NSPs) have been well-characterized in several locations of adult brain and retina. However, it is unclear whether NSPs are present in the adult auditory nerve. Here we examined the self-renewal potential of the adult auditory nerve using ouabain application as a well-established mouse model of acute SGN injury. The observed increase in cell proliferation, alteration in enchromatin/heterochromatin ratio and down-regulation of histone deacetylase expression in glial cells suggest that the quiescent glial cells convert to an activated state after SGN degeneration. This was further confirmed by global gene expression analysis of injured auditory nerves, which showed up-regulation of numerous neurogenesis- and/or development-associated genes shortly after ouabain exposure. These genes include molecular markers commonly used for the identification of NSPs. Under a strict culture regimen, auditory nerve-derived cells of adult mouse ears gave rise to neurospheres, suggesting that multipotent NSPs are present in adult cochlear nerve. Neurosphere assays on Sox2 transgenic mice revealed that Sox2+ glial cells are the source for NSPs. Our data also showed that acute injury or hypoxia enhances neurosphere formation. Taken together, our study revealed that glial cells of adult cochlea exhibit several NSP characteristics, and hence these mature non-neuronal cells may be important targets for promoting self-repair of degenerative auditory nerves. Auditory nerves were removed from the temporal bones of adult CBA/CaJ mice, aged 8 to 12 weeks. Tissues were either collected and used directly as the tissue samples or dissociated and used for the cell culture samples. Dissociated auditory nerve cells were propagated and grown to full confluency (5-7 days), constituting the cultured cell samples. For neurosphere samples, growth medium was changed to neurosphere formation medium and the cells were cultured for an additional 12 days. All samples were prepared in triplicate (n=3).
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