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The bacterial diversity in secondary infected Buruli ulcer skin lesions

ABSTRACT: Microbiome samples derived from Buruli ulcer wounds and non-Buruli ulcer skin ulcerations

PROVIDER: PRJEB14948 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1551330_1.fastq.gz	Fastqsanger.gz
	ERR1551330_2.fastq.gz	Fastqsanger.gz
	ERR1551321_1.fastq.gz	Fastqsanger.gz
	ERR1551321_2.fastq.gz	Fastqsanger.gz
	ERR1551331_1.fastq.gz	Fastqsanger.gz

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Transcriptomics in whole-blood cells of Buruli ulcer patients identifies a signature of inflammation

Project description:Mycolactone, a lipid-like toxin, is the major virulence factor of Mycobacterium ulcerans, the etiological agent of Buruli ulcer. Its involvement in lesions development has been widely described in early stages of the disease, through its cytotoxic and immunosuppressive activities, but less is known about later stages. Here, we revisit the role of mycolactone in disease outcome and provide the first demonstration of the pro-inflammatory potential of this toxin. We found that the mycolactone-containing mycobacterial extracellular vesicles produced by M. ulcerans induced the production of IL-1β, a potent pro-inflammatory cytokine, in a TLR2-dependent manner, targeting NLRP3/1 inflammasomes. We showed our data to be relevant in a physiological context. The in vivo injection of these mycolactone-containing vesicles induced a strong local inflammatory response and tissue damages, which were prevented by corticosteroids. Finally, several soluble pro-inflammatory factors, including IL-1β, were detected in infected tissues from mice and Buruli ulcer patients. Our results revisit Buruli ulcer pathophysiology by giving a new insight, thus paving the way for development of new therapeutic strategies, taking account the pro-inflammatory potential of mycolactone.

2020-12-29 | GSE157350 | GEO

Bacterial diversity in Buruli ulcer skin lesions: Challenges in the clinical microbiome analysis of a skin disease.

Project description:BackgroundBuruli ulcer (BU) is an infectious disease caused by Mycobacterium ulcerans and considered the third most prevalent mycobacterial disease in humans. Secondary bacterial infections in open BU lesions are the main cause of pain, delayed healing and systemic illness, resulting in prolonged hospital stay. Thus, understanding the diversity of bacteria, termed the microbiome, in these open lesions is important for proper treatment. However, adequately studying the human microbiome in a clinical setting can prove difficult when investigating a neglected tropical skin disease due to its rarity and the setting.Methodology/principal findingsUsing 16S rRNA sequencing, we determined the microbial composition of 5 BU lesions, 3 non-BU lesions and 3 healthy skin samples. Although no significant differences in diversity were found between BU and non-BU lesions, the former were characterized by an increase of Bacteroidetes compared to the non-BU wounds and the BU lesions also contained significantly more obligate anaerobes. With this molecular-based study, we were also able to detect bacteria that were missed by culture-based methods in previous BU studies.Conclusions/significanceOur study suggests that BU may lead to changes in the skin bacterial community within the lesions. However, in order to determine if such changes hold true across all BU cases and are either a cause or consequence of a specific wound environment, further microbiome studies are necessary. Such skin microbiome analysis requires large sample sizes and lesions from the same body site in many patients, both of which can be difficult for a rare disease. Our study proposes a pipeline for such studies and highlights several drawbacks that must be considered if microbiome analysis is to be utilized for neglected tropical diseases.

| S-EPMC5531519 | biostudies-literature

Genetic defects affecting the development of severe Buruli Ulcer

Project description:Buruli ulcer (BU) is a tropical infectious disease caused by Mycobacterium ulcerans. BU causes profound skin ulcerations and eventually bone infections. Life-long functional sequelae are observed in more than 20% of patients, most of whom are children. Several observations, in particular the large variability in the clinical severity of the disease after infection, suggested the role of human genetic factors in the development of BU. Here, we report two children with severe BU, born of consanguineous parents. The deep genetic exploration of this family led to the identification of a small deletion on chromosome 8 in both patients. The corresponding article is in press in PloS Neglected Tropical Diseases

2018-04-23 | GSE113496 | GEO

Genetic defects affecting the development of severe Buruli Ulcer

Project description:Genetic defects affecting the development of severe Buruli Ulcer

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RNA-seq differences between patients with ulcer pressures grade II vs patients with ulcer pressures grade III-IV

Project description:we want to find those markers and pathways that differ between patients with ulcer pressures grade II (less severe) than patients with ulcer pressures grade III-IV (severe)

2025-06-02 | GSE230161 | GEO

Gastric ulcer mice gastric tissue

Project description:Indomethacin was applied to establish a mice model of gastric ulcer, 24 h later, gastric tissue were obtain

2025-05-07 | PXD058482 | Pride

Transcriptional programming of human epidermis during wound repair and in pressure ulcer at single-cell resolution

Project description:Pressure ulcer (PU) is a chronic non-healing wound caused by continuous pressure of the bodyweight to the skin, which is often seen in spinal cord injury patients and in the bedridden elderly population. In spite of high mortality, the pathophysiology of PU remains poorly understood. We performed single-cell transcriptomic analysis of epidermal cells from PU wound-edges, and compared them with epidermal cells from the intact skin and normal acute wounds (AW) of healthy donors. We identified four keratinocyte clusters, one melanocyte cluster, and one immune cell cluster, and the cellular heterogeneity and gene expression were altered in PU. Our findings provided a high-resolution map of human PU and AW, which are likely to yield new areas for exploration of the pathophysiology of chronic wounds and development of wound therapy.

2021-03-28 | GSE137897 | GEO

Secondary bacterial infections of buruli ulcer lesions before and after chemotherapy with streptomycin and rifampicin.

Project description:Buruli ulcer (BU), caused by Mycobacterium ulcerans is a chronic necrotizing skin disease. It usually starts with a subcutaneous nodule or plaque containing large clusters of extracellular acid-fast bacilli. Surrounding tissue is destroyed by the cytotoxic macrolide toxin mycolactone produced by microcolonies of M. ulcerans. Skin covering the destroyed subcutaneous fat and soft tissue may eventually break down leading to the formation of large ulcers that progress, if untreated, over months and years. Here we have analyzed the bacterial flora of BU lesions of three different groups of patients before, during and after daily treatment with streptomycin and rifampicin for eight weeks (SR8) and determined drug resistance of the bacteria isolated from the lesions. Before SR8 treatment, more than 60% of the examined BU lesions were infected with other bacteria, with Staphylococcus aureus and Pseudomonas aeruginosa being the most prominent ones. During treatment, 65% of all lesions were still infected, mainly with P. aeruginosa. After completion of SR8 treatment, still more than 75% of lesions clinically suspected to be infected were microbiologically confirmed as infected, mainly with P. aeruginosa or Proteus miriabilis. Drug susceptibility tests revealed especially for S. aureus a high frequency of resistance to the first line drugs used in Ghana. Our results show that secondary infection of BU lesions is common. This could lead to delayed healing and should therefore be further investigated.

| S-EPMC3642065 | biostudies-other

Mycobacterium ulcerans Agy99

Project description:The causal agent of Buruli ulcer

| PRJNA16230 | ENA

Transcriptomics in whole-blood cells of Buruli ulcer patients identifies a signature of inflammation

Project description:Transcriptomics in whole-blood cells of Buruli ulcer patients identifies a signature of inflammation

| PRJNA661037 | ENA