{"title":"低丰度口腔细菌生物膜诱导细胞因子释放和NLRP3炎性体活化。","authors":"Maribasappa Karched, Radhika Guleri Bhardwaj, Manal Abu Al-Melh, Muawia Abdalla Qudeimat","doi":"10.1080/20002297.2025.2552167","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Low-abundance bacterial (LAB) species, despite their low prevalence, may contribute to oral inflammatory diseases by triggering host immune responses. The NLRP3 inflammasome plays a key role in inflammation, but its activation by LAB species remains unclear.</p><p><strong>Aim: </strong>This study examined whether selected LAB species and their biofilm-secreted components induce cytokine production and inflammasome activation in human peripheral blood mononuclear cells (PBMCs).</p><p><strong>Methods: </strong>Biofilms of selected LAB species were established, and supernatants were collected. PBMCs were stimulated with biofilms or supernatants, and cytokine levels were quantified using ELISA. The expression of NLRP3 and Caspase-1 genes was analyzed through real-time PCR.</p><p><strong>Results: </strong>Biofilms induced significantly higher levels of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, and IL-18) compared to supernatants, with C. hominis, N. flavescens, and D. pneumosintes being the most potent inducers. Biofilms also led to a marked increase in NLRP3 expression, while supernatants primarily activated Caspase-1 expression, indicating distinct inflammasome activation pathways.</p><p><strong>Conclusions: </strong>These findings highlight the immunostimulatory potential of LAB species, particularly their ability to activate NLRP3 and drive inflammation. The differential activation of NLRP3/Caspase-1 by biofilms and supernatants suggests distinct pathogenic mechanisms. Targeting such mechanisms/pathways could offer new therapeutic strategies to mitigate inflammation linked to oral infections.</p>","PeriodicalId":16598,"journal":{"name":"Journal of Oral Microbiology","volume":"17 1","pages":"2552167"},"PeriodicalIF":5.5000,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12395623/pdf/","citationCount":"0","resultStr":"{\"title\":\"Cytokine release and NLRP3 inflammasome activation induced by low-abundance oral bacterial biofilms.\",\"authors\":\"Maribasappa Karched, Radhika Guleri Bhardwaj, Manal Abu Al-Melh, Muawia Abdalla Qudeimat\",\"doi\":\"10.1080/20002297.2025.2552167\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Low-abundance bacterial (LAB) species, despite their low prevalence, may contribute to oral inflammatory diseases by triggering host immune responses. The NLRP3 inflammasome plays a key role in inflammation, but its activation by LAB species remains unclear.</p><p><strong>Aim: </strong>This study examined whether selected LAB species and their biofilm-secreted components induce cytokine production and inflammasome activation in human peripheral blood mononuclear cells (PBMCs).</p><p><strong>Methods: </strong>Biofilms of selected LAB species were established, and supernatants were collected. PBMCs were stimulated with biofilms or supernatants, and cytokine levels were quantified using ELISA. The expression of NLRP3 and Caspase-1 genes was analyzed through real-time PCR.</p><p><strong>Results: </strong>Biofilms induced significantly higher levels of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, and IL-18) compared to supernatants, with C. hominis, N. flavescens, and D. pneumosintes being the most potent inducers. Biofilms also led to a marked increase in NLRP3 expression, while supernatants primarily activated Caspase-1 expression, indicating distinct inflammasome activation pathways.</p><p><strong>Conclusions: </strong>These findings highlight the immunostimulatory potential of LAB species, particularly their ability to activate NLRP3 and drive inflammation. The differential activation of NLRP3/Caspase-1 by biofilms and supernatants suggests distinct pathogenic mechanisms. Targeting such mechanisms/pathways could offer new therapeutic strategies to mitigate inflammation linked to oral infections.</p>\",\"PeriodicalId\":16598,\"journal\":{\"name\":\"Journal of Oral Microbiology\",\"volume\":\"17 1\",\"pages\":\"2552167\"},\"PeriodicalIF\":5.5000,\"publicationDate\":\"2025-08-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12395623/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Oral Microbiology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/20002297.2025.2552167\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q2\",\"JCRName\":\"MICROBIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Oral Microbiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/20002297.2025.2552167","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"MICROBIOLOGY","Score":null,"Total":0}
Cytokine release and NLRP3 inflammasome activation induced by low-abundance oral bacterial biofilms.
Background: Low-abundance bacterial (LAB) species, despite their low prevalence, may contribute to oral inflammatory diseases by triggering host immune responses. The NLRP3 inflammasome plays a key role in inflammation, but its activation by LAB species remains unclear.
Aim: This study examined whether selected LAB species and their biofilm-secreted components induce cytokine production and inflammasome activation in human peripheral blood mononuclear cells (PBMCs).
Methods: Biofilms of selected LAB species were established, and supernatants were collected. PBMCs were stimulated with biofilms or supernatants, and cytokine levels were quantified using ELISA. The expression of NLRP3 and Caspase-1 genes was analyzed through real-time PCR.
Results: Biofilms induced significantly higher levels of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, and IL-18) compared to supernatants, with C. hominis, N. flavescens, and D. pneumosintes being the most potent inducers. Biofilms also led to a marked increase in NLRP3 expression, while supernatants primarily activated Caspase-1 expression, indicating distinct inflammasome activation pathways.
Conclusions: These findings highlight the immunostimulatory potential of LAB species, particularly their ability to activate NLRP3 and drive inflammation. The differential activation of NLRP3/Caspase-1 by biofilms and supernatants suggests distinct pathogenic mechanisms. Targeting such mechanisms/pathways could offer new therapeutic strategies to mitigate inflammation linked to oral infections.
期刊介绍:
As the first Open Access journal in its field, the Journal of Oral Microbiology aims to be an influential source of knowledge on the aetiological agents behind oral infectious diseases. The journal is an international forum for original research on all aspects of ''oral health''. Articles which seek to understand ''oral health'' through exploration of the pathogenesis, virulence, host-parasite interactions, and immunology of oral infections are of particular interest. However, the journal also welcomes work that addresses the global agenda of oral infectious diseases and articles that present new strategies for treatment and prevention or improvements to existing strategies.
Topics: ''oral health'', microbiome, genomics, host-pathogen interactions, oral infections, aetiologic agents, pathogenesis, molecular microbiology systemic diseases, ecology/environmental microbiology, treatment, diagnostics, epidemiology, basic oral microbiology, and taxonomy/systematics.
Article types: original articles, notes, review articles, mini-reviews and commentaries