International journal of inflammation · 2025
Joint Microbiota Suggests Articular Dysbiosis in Experimental Murine Spondyloarthritis and Histological Detection of Bacteria in Human SpA Joints.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
González-Chávez Susana Aideé, Alvarado-Jáquez María Fernanda, Salas-Leiva Joan Sebastian, Mohl Jonathon E, Chaparro-Barrera Eduardo, Prieto-Carrasco Rodrigo, Loya-Rivera Mario, Pacheco-Silva César, Pacheco-Tena César
Аннотация
BACKGROUND: Recent studies have provided evidence supporting the presence of a commensal joint microbiome; however, its role in the pathogenesis of spondyloarthritis (SpA) remains unclear. This study aimed to characterize the joint microbiome and assess its role in bacterial dissemination and systemic involvement.
METHODS: DBA/1 mice with spontaneous arthritis (SpAD) and healthy BALB/c mice, as well as biopsies from SpA patients, were analyzed by histology (Gram staining and IHC), short-read next-generation sequencing of the 16S rRNA gene amplicons, and transcriptomics. Shared bacterial species were evaluated across tissues, including the liver and heart, and the colocalization of bacterial and inflammatory markers was assessed using double indirect immunofluorescence (IIF).
RESULTS: Bacteria were detected in the joints of healthy and SpAD mice, with significantly greater abundance in the latter. Microbiome analysis revealed distinct bacterial communities, with genera, such as Pelomonas and Aerococcus uniquely identified in the joints of SpAD mice, indicating a state of dysbiosis. Several bacterial species, including Prevotella sp., Ruminococcus gnavus, Lactobacillus johnsonii, and Limosilactobacillus reuteri, were detected in both the gut and joints of SpAD mice. Additionally, bacterial DNA from these taxa was also amplified from liver and heart tissues, indicating systemic dissemination. Transcriptomic analysis revealed dysregulated bacterial response pathways in SpAD joints, with an inflammatory profile distinct from that observed in gut tissues. Double IIF confirmed the colocalization of bacterial components with proinflammatory cytokines in joint cells. In human SpA biopsies, Gram staining and IHC also identified bacteria in sacroiliac and tarsal tissues.
CONCLUSIONS: These findings confirm the presence of bacteria in the joints of healthy and SpAD mice, as well as SpA patients. The joint microbiome differs between healthy and diseased mice, contributing to inflammation through dysregulated bacterial responses. Additionally, the identification of shared bacterial species between the gut and joints, as well as their detection in the liver and heart, supports the hypothesis of bacterial dissemination consistent with translocation and systemic involvement.
METHODS: DBA/1 mice with spontaneous arthritis (SpAD) and healthy BALB/c mice, as well as biopsies from SpA patients, were analyzed by histology (Gram staining and IHC), short-read next-generation sequencing of the 16S rRNA gene amplicons, and transcriptomics. Shared bacterial species were evaluated across tissues, including the liver and heart, and the colocalization of bacterial and inflammatory markers was assessed using double indirect immunofluorescence (IIF).
RESULTS: Bacteria were detected in the joints of healthy and SpAD mice, with significantly greater abundance in the latter. Microbiome analysis revealed distinct bacterial communities, with genera, such as Pelomonas and Aerococcus uniquely identified in the joints of SpAD mice, indicating a state of dysbiosis. Several bacterial species, including Prevotella sp., Ruminococcus gnavus, Lactobacillus johnsonii, and Limosilactobacillus reuteri, were detected in both the gut and joints of SpAD mice. Additionally, bacterial DNA from these taxa was also amplified from liver and heart tissues, indicating systemic dissemination. Transcriptomic analysis revealed dysregulated bacterial response pathways in SpAD joints, with an inflammatory profile distinct from that observed in gut tissues. Double IIF confirmed the colocalization of bacterial components with proinflammatory cytokines in joint cells. In human SpA biopsies, Gram staining and IHC also identified bacteria in sacroiliac and tarsal tissues.
CONCLUSIONS: These findings confirm the presence of bacteria in the joints of healthy and SpAD mice, as well as SpA patients. The joint microbiome differs between healthy and diseased mice, contributing to inflammation through dysregulated bacterial responses. Additionally, the identification of shared bacterial species between the gut and joints, as well as their detection in the liver and heart, supports the hypothesis of bacterial dissemination consistent with translocation and systemic involvement.