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Imbalanced Dermic Microbiome Aggravates Inflammation in Toenail Paronychia.

ABSTRACT: The commensal microbiome influences skin immunity, but its function in toenail health remains unclear. Paronychia is one of the most common inflammatory toenail diseases, but antibiotic treatment is seldom effective in clinical cases. In this study, we performed 16S rRNA sequencing to investigate the characteristics of microbes associated with paronychia in order to identify the key microorganisms involved in inflammation. Seventy dermic samples were collected from patients with paronychia and the differences in dermic microbiota were analyzed in patients with different inflammation severities. Distinct clustering of dermal microbiota was observed in the dermis with different inflammation severities. A higher relative abundance of anaerobic microorganisms such as Parvimona, Prevotella, and Peptoniphilus was observed in severe paronychia, whereas Lactobacillus disappeared with disease progression. Co-occurring network analysis suggested that the disturbance of the dermic microbiome and attenuation of antagonism by Lactobacillus against anaerobic pathogens may aggravate inflammation in paronychia. Functional analysis showed that dermic microbiome disturbance may worsen microbial metabolism and tissue repair in the skin. In conclusion, we revealed that an increased abundance of anaerobic microorganisms and loss of Lactobacillus in the dermis may promote paronychia progression and microbiological imbalance may aggravate inflammation in patients with paronychia.

SUBMITTER: Li Y

PROVIDER: S-EPMC8677670 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Retinal neurodegenerative diseases involve a scenario of inflammation and cell death that leads to morphological alterations and visual impairment. Non-ocular inflammatory processes could affect neurodegenerative retinal disorders and their progression, at least in part by activating microglial cells and releasing pro-inflammatory cytokines. Our purpose was to study the consequences of a systemic inflammatory process in the progression of retinal degeneration in P23H rats, a retinitis pigmentosa (RP) model. In order to induce a mild chronic systemic inflammation, we administered low doses of lipopolysaccharide (LPS) from age P20 to P60 to dystrophic P23H rats and healthy SD rats. Visual responsiveness was assessed by electroretinography (ERG). The morphological state of the retinas was analyzed by fluorescent immunohistochemistry (IHC), evaluating the number, morphology, and connectivity of different neuronal populations by means of cell type-specific markers. Microglia density, distribution, and degree of activation were evaluated by IHC and flow cytometry. The expression levels of inflammation- and apoptosis-related genes were analyzed by qRT-PCR arrays. Low-dose LPS administration did not induce significant functional or morphological changes in the retina of SD rats, although at the molecular level, we detected expression changes in genes related to apoptosis. Otherwise, systemic injection of LPS into P23H rats induced a further deterioration in the ERG response, with greater loss of photoreceptors and worsening of synaptic connectivity, accompanied by increasing numbers of microglial cells, which also showed a more intense activation state. Several inflammation- and apoptosis-related genes were upregulated. Our results indicate that chronic exacerbation of the inflammatory response in response to LPS accelerates neurodegeneration in dystrophic P23H rats, suggesting that in patients with ocular neurodegenerative diseases, peripheral damage, as a systemic infection or chronic inflammatory process, could accelerate disease progression, and should be taken into account in order to select an appropriate therapy to revert, block or slow-down the degenerative process.

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Imbalanced Dermic Microbiome Aggravates Inflammation in Toenail Paronychia.

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