Microbes and Infection最新文献

Porphyromonas gingivalis Inhibits Ferroptosis and Promotes Malignant Phenotype in Oral Squamous Cell Carcinoma Cells via Upregulation of SIRT5. 牙龈卟啉单胞菌通过上调SIRT5抑制口腔鳞状细胞癌细胞铁下垂并促进恶性表型。

IF 2.7 4区医学

Microbes and Infection Pub Date : 2025-10-06 DOI: 10.1016/j.micinf.2025.105564

Yiqun Jia, Jing Ou, Hongxia You, Weixuan Chen, Yuyan Zheng

{"title":"Porphyromonas gingivalis Inhibits Ferroptosis and Promotes Malignant Phenotype in Oral Squamous Cell Carcinoma Cells via Upregulation of SIRT5.","authors":"Yiqun Jia, Jing Ou, Hongxia You, Weixuan Chen, Yuyan Zheng","doi":"10.1016/j.micinf.2025.105564","DOIUrl":"https://doi.org/10.1016/j.micinf.2025.105564","url":null,"abstract":"Introduction: Oral squamous cell carcinoma (OSCC) exhibits aggressive behavior and poor prognosis. Porphyromonas gingivalis (P. gingivalis) affects the tumor microenvironment, but its role in ferroptosis inhibition in OSCC remains unclear. This study explores the impact of P. gingivalis on ferroptosis through SIRT5 upregulation.Materials and methods: OSCC cell lines (Cal27, SCC9) were treated with the ferroptosis inducer RSL3, with or without P. gingivalis infection. Cell viability, ferroptosis markers (MDA, ROS, GPX4), and cell behavior (proliferation, migration, invasion) were assessed. SIRT5 and downstream targets (IDH2, GCLC) were analyzed using Western blot, qRT-PCR, and immunofluorescence. A SIRT5 knockdown model was used to evaluate its role in ferroptosis resistance.Results: P. gingivalis infection increased OSCC cell survival, reduced ROS and MDA levels, enhanced GPX4 expression, and promoted proliferation, migration, and invasion. Elevated SIRT5 and its targets IDH2 and GCLC were observed. SIRT5 knockdown reversed ferroptosis resistance.Conclusion: The findings suggest that P. gingivalis plays a critical role in promoting OSCC malignancy by inhibiting ferroptosis through the upregulation of SIRT5. This highlights the potential of targeting SIRT5 as a therapeutic strategy to counteract the effects of P. gingivalis in OSCC.","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105564"},"PeriodicalIF":2.7,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145251958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Microbiology and predictors of mortality in haematological malignancy patients with gram-negative bacterial bloodstream infections. 革兰氏阴性细菌血流感染的恶性血液病患者的微生物学和死亡率预测因素。

IF 2.7 4区医学

Microbes and Infection Pub Date : 2025-09-09 DOI: 10.1016/j.micinf.2025.105563

Jing Zheng, Jinlian Li, Xuejun Xu, Yuqing Li, Yan Yang, Ya Guo, Jing Hu, Ling Wang

{"title":"Microbiology and predictors of mortality in haematological malignancy patients with gram-negative bacterial bloodstream infections.","authors":"Jing Zheng, Jinlian Li, Xuejun Xu, Yuqing Li, Yan Yang, Ya Guo, Jing Hu, Ling Wang","doi":"10.1016/j.micinf.2025.105563","DOIUrl":"10.1016/j.micinf.2025.105563","url":null,"abstract":"Objectives: Gram-negative bacteria (GNB) bloodstream infection (BSI) pose a significant clinical challenge in patients with haematological malignancy, further complicated by rising carbapenem-resistant GNB (CRGNB) prevalence. This study aims to investigate the prevalence and risk factors for GNB BSI and associated mortality in this population.Methods: A retrospective study was conducted at a tertiary teaching hospital in southern China (2015-2023), including haematological malignancy patients with GNB BSI. Multivariate logistic analyses were performed to identify risk factors for CRGNB BSI and to establish a predictive model for 30-day mortality of GNB BSI.Results: Among 351 patients with GNB BSIs, acute myeloid leukaemia (51.3 %) was the predominant underlying disease. Escherichia coli (28.8 %) and Klebsiella pneumoniae (29.7 %) were the most common GNB BSI and CRGNB BSI pathogens, respectively. Independent risk factors for CRGNB BSI included chronic liver disease, prior carbapenems therapy (≤30 days before BSI), a platelet count <30 × 109/l and albumin concentration <30 g/l before BSI. The 30-day mortality prediction model of GNB BSI incorporated CRGNB infection, platelet count <30 × 109/l and albumin concentration <30 g/l before BSI, demonstrating good discrimination (training cohort AUC: 0.828; validation cohort: 0.791). Calibration plots and decision curve analysis confirmed robust model performance.Conclusions: Identified factors enable risk stratification for CRGNB BSI and poor prognosis in GNB BSI, facilitating timely interventions to improve outcomes.","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105563"},"PeriodicalIF":2.7,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

ESCMID workshop: Artificial intelligence and machine learning in medical microbiology diagnostics. ESCMID研讨会：医学微生物学诊断中的人工智能和机器学习。

IF 2.7 4区医学

Microbes and Infection Pub Date : 2025-09-05 DOI: 10.1016/j.micinf.2025.105562

Mariella Greutmann, Karsten Borgwardt, Sarah Brüningk, Fabian Franzeck, Christian G Giske, Anna G Green, Alejandro Guerrero-López, Margaret Ip, Catherine Jutzeler, Andre Kahles, Michael Krauthammer, Nenad Macesic, Benjamin McFadden, Eline Meijer, Nathan Moore, Jacob Moran-Gilad, Imane Lboukili, Oliver Nolte, Robin Patel, Gerold Schneider, Markus A Seeger, Tavpritesh Sethi, Robert L Skov, Chang Ho Yoon, Belén Rodríguez-Sánchez, Adrian Egli

{"title":"ESCMID workshop: Artificial intelligence and machine learning in medical microbiology diagnostics.","authors":"Mariella Greutmann, Karsten Borgwardt, Sarah Brüningk, Fabian Franzeck, Christian G Giske, Anna G Green, Alejandro Guerrero-López, Margaret Ip, Catherine Jutzeler, Andre Kahles, Michael Krauthammer, Nenad Macesic, Benjamin McFadden, Eline Meijer, Nathan Moore, Jacob Moran-Gilad, Imane Lboukili, Oliver Nolte, Robin Patel, Gerold Schneider, Markus A Seeger, Tavpritesh Sethi, Robert L Skov, Chang Ho Yoon, Belén Rodríguez-Sánchez, Adrian Egli","doi":"10.1016/j.micinf.2025.105562","DOIUrl":"10.1016/j.micinf.2025.105562","url":null,"abstract":"Rapid advancements in artificial intelligence (AI) and machine learning (ML) offer significant potential to transform medical microbiology diagnostics, improving pathogen identification, antimicrobial susceptibility prediction and outbreak detection. To address these opportunities and challenges, the ESCMID workshop, \"Artificial Intelligence and Machine Learning in Medical Microbiology Diagnostics\", was held in Zurich, Switzerland, from June 2-5, 2025. The course featured expert lectures, practical sessions and panel discussions covering foundational ML concepts and deep learning architectures, data interoperability, quality control processes, model development and validation strategies. Key applications discussed included whole-genome sequencing for antimicrobial resistance detection, AI-enhanced digital microscopy automation and MALDI-TOF mass spectrometry-based diagnostics. Participants gained hands-on experience with essential AI tools and platforms. Special emphasis was placed on standardised laboratory protocols, regulatory compliance and ethical considerations, including data governance and patient privacy. Panel sessions further highlighted critical issues of equity, global disparities in AI access, sustainability and environmental impacts related to AI infrastructure. The workshop concluded by underscoring a necessity for ongoing interdisciplinary collaboration, continued education, and substantial investment in equitable AI infrastructure to realise the full potential of AI in clinical diagnostics.","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105562"},"PeriodicalIF":2.7,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LncSSBP1/FOXO3 axis modulates autophagy: a novel insight into bronchial epithelial cells defense against Talaromyces marneffei infection. LncSSBP1/FOXO3轴调节自噬：支气管上皮细胞防御马尔尼菲塔芳菌感染的新见解

IF 2.7 4区医学

Microbes and Infection Pub Date : 2025-09-04 DOI: 10.1016/j.micinf.2025.105561

Lu Lin, Shitong Pan, Mingpeng Xu, Huan Chen, Zhiyi He, Yinghua Li

{"title":"LncSSBP1/FOXO3 axis modulates autophagy: a novel insight into bronchial epithelial cells defense against Talaromyces marneffei infection.","authors":"Lu Lin, Shitong Pan, Mingpeng Xu, Huan Chen, Zhiyi He, Yinghua Li","doi":"10.1016/j.micinf.2025.105561","DOIUrl":"10.1016/j.micinf.2025.105561","url":null,"abstract":"Background: While autophagy is pivotal in antimicrobial defense, its regulatory role in Talaromyces marneffei (TM) infected bronchial epithelium remains elusive.Objective: To elucidate the impact of TM infection on autophagy in bronchial epithelial cells and to identify the key molecular regulators involved in this process.Methods: Primary computational screening identified core autophagy modulators. Autophagy flux was monitored through LC3B-II/P62 immunoblotting and transmission electron microscopy. Mechanistic validation was performed using siRNA-mediated FOXO3 silencing, lentivirus-mediated lncSSBP1 knockdown and overexpression cell models, combined with immunofluorescence staining for nuclear localization.Results: Bioinformatics analysis identified seven autophagy modulating effectors, with FOXO3 emerging as the central regulator. Quantitative proteomics revealed biphasic autophagic responses: initial LC3B-II accumulation with P62 degradation at 4h post-infection, followed by P62 rebound at 24h, indicating time-dependent flux impairment. FOXO3 was identified as a critical mediator of TM-induced autophagy. Furthermore, we identified a strong positive correlation between lncSSBP1 and FOXO3 expression, with lncSSBP1 overexpression enhancing FOXO3 levels and promoting autophagosome maturation.Conclusion: This study uncovers a previously unrecognized lncRNA-mediated regulatory axis wherein lncSSBP1 orchestrates FOXO3-driven autophagy during TM infection. These results provide new insights into the molecular mechanisms of host-pathogen interactions.","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105561"},"PeriodicalIF":2.7,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145008388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lactococcus lactis and Bifidobacterium longum attenuate Clostridioides difficile- or Clostridium symbiosum-induced colitis and depression/anxiety-like behavior in male mice. 乳酸乳球菌和长双歧杆菌可减弱艰难梭菌或共生梭菌诱导的雄性小鼠结肠炎和抑郁/焦虑样行为。

IF 2.7 4区医学

Microbes and Infection Pub Date : 2025-08-28 DOI: 10.1016/j.micinf.2025.105560

Min-Kyung Joo, Xiaoyang Ma, Jung-Woo Shin, Yoon-Jung Shin, Dong-Hyun Kim

{"title":"Lactococcus lactis and Bifidobacterium longum attenuate Clostridioides difficile- or Clostridium symbiosum-induced colitis and depression/anxiety-like behavior in male mice.","authors":"Min-Kyung Joo, Xiaoyang Ma, Jung-Woo Shin, Yoon-Jung Shin, Dong-Hyun Kim","doi":"10.1016/j.micinf.2025.105560","DOIUrl":"https://doi.org/10.1016/j.micinf.2025.105560","url":null,"abstract":"Clostridioides difficile causes severe colitis, which induces neuroinflammation and psychiatric disorder. In a preliminary study, we isolated Clostridium symbiosum from the stools of patients with ulcerative colitis. Therefore, we first examined whether oral infection with C. difficile or C. symbiosum could induce colitis and depression in male mice. Orally gavaged C. difficile or C. symbiosum caused diarrhea, bodyweight loss, depression/anxiety-like behavior, and tumor necrosis factor (TNF)-α and interleukin (IL)-6 overexpression in the colon and hippocampus in the pseudo-germ-free (PGF) and specific germ-free (SPF) mice. However, healthy volunteer microbiota-derived Lactococcus lactis P22 and/or Bifidobacterium longum P26 suppressed C. difficile or C. symbiosum growth and TNF-α expression in macrophage cells. They alleviated C. difficile- or C. symbiosum-induced bodyweight loss, diarrhea, and neurobehavioral changes in PGF and SPF mice, while reducing pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) levels in the colon and in the hippocampus. These findings suggest that C. difficile or C. symbiosum can cause colitis and depression/anxiety. Oral administration of P22 and/or P26 may alleviate gut bacteria-induced gut inflammation and depression/anxiety through the inhibition of their growth and inflammatory response.","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105560"},"PeriodicalIF":2.7,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144959542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Conference report: The second Bacterial Genome Sequencing Pan-European Network conference. 会议报告：第二届细菌基因组测序泛欧网络会议。

IF 2.7 4区医学

Microbes and Infection Pub Date : 2025-08-08 DOI: 10.1016/j.micinf.2025.105557

Kuangyi Charles Wei, Srinithi Purushothaman, Francesca Azzato, Kate S Baker, Kira Waagner Birkeland, Sofia Brunet, Josefina Campos, Thomas R Connor, Christian G Giske, Gilbert Greub, Erika Tång Hallbäck, Dag Harmsen, Emma B Hodcroft, Matthew T G Holden, Jobin Jacob, Andre Kahles, Amaya Campillay Lagos, Samuel Lipworth, Elin Loo, Paolo Miotto, Richard A Neher, Aitana Neves, Derren Ready, Tim Roloff, Ashley Rooney, Emilie Rousseau, Jacques Schrenzel, Martin Sundqvist, Sofia Viegas, Fanny Wegner, Hege Vangstein Aamot, Stefan Niemann, Deborah A Williamson, Paula Mölling, Adrian Egli

引用次数: 0

Investigating the possible role of toxoplasmosis and Interleukin-1β variants on the immune response in Egyptian diabetic patients. 研究弓形虫病和白细胞介素-1β变异对埃及糖尿病患者免疫反应的可能作用。

IF 2.7 4区医学

Microbes and Infection Pub Date : 2025-08-07 DOI: 10.1016/j.micinf.2025.105559

Asmaa Ibrahim, Nancy O Kamel, Fatma Rageh, Rasha Elgamal, Mohamed A Sakr, Eman M Osman, Samar S Ahmed, Hend A Yassin, Yasmine N Kamel, Reham F Othman, Manar Ezzelarab Ramadan

{"title":"Investigating the possible role of toxoplasmosis and Interleukin-1β variants on the immune response in Egyptian diabetic patients.","authors":"Asmaa Ibrahim, Nancy O Kamel, Fatma Rageh, Rasha Elgamal, Mohamed A Sakr, Eman M Osman, Samar S Ahmed, Hend A Yassin, Yasmine N Kamel, Reham F Othman, Manar Ezzelarab Ramadan","doi":"10.1016/j.micinf.2025.105559","DOIUrl":"10.1016/j.micinf.2025.105559","url":null,"abstract":"The study assesses toxoplasmosis seroprevalence in Type 2 Diabetes Mellitus, identifies the potential risk factors, and examines IL-1β expression levels and polymorphisms in those infected with T. gondii. One hundred healthy controls and 200 diabetic patients participated in the study. Diagnosis was made by Immunoassay to measure antibodies of T. gondii, IgM, and IgG, and molecular by targeting the 529 RE gene. Quantitative measurement of IL-1β levels was done, and genetic polymorphisms were assessed. Among diabetic patients, 61.0 % were seropositive for T. gondii IgG, compared to 36.0 % in healthy controls. Significant associations were found with IgG and IgM (P = 0.0001, 0.022), respectively. Patients with diabetes and toxoplasmosis had significantly high levels of IL-1β (P = 0.0003). The +3954C/T variant showed a higher prevalence of CT and lower TT genotypes in T2DM patients, P = 0.017, 0.003, respectively. The CT genotype is considered a genetic risk factor for diabetic patients, and the TT genotype and T allele may increase susceptibility to infection with toxoplasmosis. The prevalence of toxoplasmosis in T2DM, levels of IL-1β, and +3954C/T polymorphism seem to be important factors for developing complications in diabetic patients infected with toxoplasmosis.","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105559"},"PeriodicalIF":2.7,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TLR3 regulation and cytokine response during BoAHV-1 and BoAHV-5 infection of neuronal-like cells. 神经元样细胞感染BoAHV-1和BoAHV-5时TLR3的调控和细胞因子反应。

IF 2.7 4区医学

Microbes and Infection Pub Date : 2025-08-07 DOI: 10.1016/j.micinf.2025.105558

María Belén Brunner, Juan José Rosales, Marla Ladera, María Victoria Nieto Farías, Andrea Verna, Sandra Pérez

{"title":"TLR3 regulation and cytokine response during BoAHV-1 and BoAHV-5 infection of neuronal-like cells.","authors":"María Belén Brunner, Juan José Rosales, Marla Ladera, María Victoria Nieto Farías, Andrea Verna, Sandra Pérez","doi":"10.1016/j.micinf.2025.105558","DOIUrl":"10.1016/j.micinf.2025.105558","url":null,"abstract":"Varicellovirus bovinealpha (BoAHV) 1 and 5 are alphaherpesviruses that differ in their neuropathogenic potential. While BoAHV-5 causes necrotizing meningoencephalitis in calves, neurological cases associated with BoAHV-1 are less frequent. In this study we used differentiated the human neuroblastoma cell line (SH-SY5Y) to evaluate the mRNA expression of Toll-like receptor 3 (TLR3), its adaptor molecule TRIF and the production of interferons and pro-inflammatory cytokines during infection with both alphaherpesviruses. TLR3 was activated with polyinosinic acid: polycytidylic acid (Poly I:C) and it was genetically silenced using TLR3-targeted siRNA. BoAHV infection induced an initial upregulation of TLR3, followed by a notable decrease, particularly in BoAHV-5-infected cells. TLR3 knockdown was effective for 72 h in uninfected cells although it was reversed shortly after BoAHV infection. In the presence of activated TLR3, virus titers remained high, indicating limited antiviral activity of TLR3 signaling. TRIF was downregulated early after infection, implying viral interference with the innate immune response. In contrast, Poly I:C upregulated TLR3 and TRIF. IFN-β was upregulated following infection and IFN-α/β, TNF-α and IL-6 were induced even in TLR3-silenced cells, implicating the involvement of alternative signaling pathways. These findings demonstrate how bovine alphaherpesviruses modulate the innate immune mechanisms, highlighting differential viral strategies to evade the immune response which may contribute to neuropathogenesis.","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105558"},"PeriodicalIF":2.7,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The impact of DeoRF on Listeria monocytogenes stress tolerance and survival. DeoRF对单核增生李斯特菌耐受性及存活的影响。

IF 2.7 4区医学

Microbes and Infection Pub Date : 2025-07-22 DOI: 10.1016/j.micinf.2025.105549

Seto C Ogunleye, Minna Hassan, Mark L Lawrence, Hossam Abdelhamed

{"title":"The impact of DeoRF on Listeria monocytogenes stress tolerance and survival.","authors":"Seto C Ogunleye, Minna Hassan, Mark L Lawrence, Hossam Abdelhamed","doi":"10.1016/j.micinf.2025.105549","DOIUrl":"10.1016/j.micinf.2025.105549","url":null,"abstract":"Listeria monocytogenes, a significant foodborne pathogen, is known for its remarkable adaptability to diverse environments through a genomic regulatory network that coordinates metabolic activities and stress responses. However, many of these genomic elements remain poorly understood. This study investigates the role of deoRF, a previously understudied member of the DeoR-family, in oxidative tolerance, intracellular infection, and virulence. Interestingly, the F2365ΔdeoRF strain showed no significant growth defects in minimal media with glucose, fructose, or sucrose, suggesting that DeoRF does not play a critical role in the uptake or metabolism of these sugars. Results showed that DeoRF plays a significant role in the ability of L. monocytogenes to adapt to oxidative stress. Additionally, DeoRF contributed significantly to cell-to-cell spread in L2 fibroblast cells, intracellular replication in macrophage cells, and virulence in mice following both intravenous and oral infection models. Transcriptomic analysis further revealed that deletion of deoRF caused downregulation of propanediol utilization, transcription regulators, phosphotransferase systems (PTS), complex networks of transcriptional regulators, and proteases genes. Conversely, sigma B regulator genes were upregulated in the ΔdeoRF strain. This study demonstrates that L. monocytogenes DeoRF contributes to pathogenicity and stress adaptation, and it is an important contributor to the complex listerial regulatory network.","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105549"},"PeriodicalIF":2.7,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Porphyromonas gingivalis-induced HuR upregulation suppresses SLC39A10-derived hsa_circ_0057552 in esophageal squamous cell carcinoma. 食管鳞状细胞癌中牙龈卟啉单胞菌诱导的HuR上调抑制slc39a10衍生的hsa_circ_0057552

IF 2.7 4区医学

Microbes and Infection Pub Date : 2025-07-21 DOI: 10.1016/j.micinf.2025.105548

Rui Yang, Bianli Gu, Qi Jiang, Linlin Shi, Shuoxuan Li, Yaowu Lang, Yongtian Li, Zhixiang Zuo, Shegan Gao

{"title":"Porphyromonas gingivalis-induced HuR upregulation suppresses SLC39A10-derived hsa_circ_0057552 in esophageal squamous cell carcinoma.","authors":"Rui Yang, Bianli Gu, Qi Jiang, Linlin Shi, Shuoxuan Li, Yaowu Lang, Yongtian Li, Zhixiang Zuo, Shegan Gao","doi":"10.1016/j.micinf.2025.105548","DOIUrl":"10.1016/j.micinf.2025.105548","url":null,"abstract":"Porphyromonas gingivalis (P. gingivalis) is one of the main risk factors of esophageal squamous cell carcinoma (ESCC). Circular RNAs (circRNAs) have been found to play a crucial role in many types of cancer. However, its functional involvement in P. gingivalis-infected ESCC remained understudied. In this study, we investigate that overexpression of hsa_circ_0057552 inhibited the proliferation and motility of ESCC cells in vitro and in vivo, whereas its silencing exerts the opposite effect. Hsa_circ_0057552 was found to be downregulated in P. gingivalis-infected ESCC tissues and cells, with the extent of downregulation correlating with both the dose and duration of P. gingivalis infection. Mechanistically, P. gingivalis infection significantly reduced the stability of hsa_circ_0057552 in ESCC cells, and Human Antigen R (HuR) was identified as a key regulator mediating this destabilization. The interaction between hsa_circ_0057552 and HuR was confirmed. Furthermore, hsa_circ_0057552 suppressed SLC39A10 mRNA expression by competitively inhibiting HuR binding to SLC39A10 transcripts. This study delineates a P. gingivalis-HuR-hsa_circ_0057552 axis that may modulate SLC39A10 availability through competitive RNA-protein interactions. This mechanistic framework suggests a dual therapeutic approach: microbial-targeted eradication of P. gingivalis combined with hsa_circ_0057552 restoration therapy to disrupt oncogenic signaling cascades.","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105548"},"PeriodicalIF":2.7,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144698989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0