生物学最新文献

{"title":"Lenacapavir's success: Revitalizing antiviral drug discovery.","authors":"Daniel Miranda, David Jesse Sanchez","doi":"10.1080/21505594.2025.2497902","DOIUrl":"https://doi.org/10.1080/21505594.2025.2497902","url":null,"abstract":"","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2497902"},"PeriodicalIF":5.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12051603/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144044705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Staphylococcus aureus nt5</i> gene mutation through CRISPR RNA-guided base editing weakens bacterial virulence and immune evasion.","authors":"Xinpeng Liu, Lan Huang, Yang Ye, Haiyi Wang, Min Tang, Fuqiang He, Zijing Xia, Shi Deng, Peng Zhang, Ruiwu Dai, Shufang Liang","doi":"10.1080/21505594.2025.2451163","DOIUrl":"10.1080/21505594.2025.2451163","url":null,"abstract":"<p><p>The resistance of commonly used clinical antibiotics, such as daptomycin (DAP), has become increasingly serious in the fight against <i>Staphylococcus aureus</i> (<i>S. aureus</i>) infection. It is essential to explore key pathogenicity-driven genes/proteins in bacterial infection and antibiotics resistance, which contributes to develop novel therapeutic strategies against <i>S. aureus</i> infections. The <i>nt5</i> gene of <i>S. aureus</i>, encoding 5'-nucleotidase (NT5), is nearly unknown for its function in drug resistance and bacterial infection. Herein, to reveal <i>nt5</i> gene role in drug resistance and infection ability of <i>S. aureus</i>, we performed <i>nt5</i>^C166T gene mutation using a clustered regulatory interspaced short palindromic repeat ribonucleic acid (RNA)-guided base editing system to investigate the lose-of-function of NT5 protein. Subsequent transcriptome sequencing of the mutant strain revealed that <i>nt5</i> inactivation caused changes in cell membrane integrity and inhibited nucleotide metabolism, suggesting the <i>nt5</i> gene may be involved in bacterial drug resistance and virulence. The mutant strain exhibited enhanced tolerance to DAP treatment by attenuating cell membrane potential dissipation and slowing deoxyribonucleic acid release. Moreover, the <i>nt5</i> mutation alleviated abscess degree of mouse kidneys caused by <i>S. aureus</i> infection byreducing the expression of IL-1β, IL-6, and IL-18. The <i>nt5</i> mutant strain was easily swallowed by host immune cells, resulting in weak bacterial toxicity of the <i>S. aureus</i> mutant in the bacterial infection process. In summary, <i>nt5</i> gene mutation confers tolerance to DAP and a lower bacterial capacity to form kidney abscesses through phagocytosis of host immune cells, which indicates the targeted inhibition of NT5 protein would offer a potential new therapeutic strategy against <i>S. aureus</i> infection.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2451163"},"PeriodicalIF":5.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759621/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143024856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pyruvate formate lyase regulates fermentation metabolism and virulence of <i>Streptococcus suis</i>.","authors":"Qingying Fan, Haikun Wang, Shuo Yuan, Yingying Quan, Rishun Li, Li Yi, Aiqing Jia, Yuxin Wang, Yang Wang","doi":"10.1080/21505594.2025.2467156","DOIUrl":"10.1080/21505594.2025.2467156","url":null,"abstract":"<p><p><i>Streptococcus suis</i>, a zoonotic pathogen, is commonly found as a commensal bacterium in the respiratory tracts of pigs. Under specific conditions, it becomes invasive and enters the blood, causing severe systemic infections. For <i>S. suis</i>, effective acquisition of carbon sources in different host niches is necessary for its survival. However, as of now, our understanding of the metabolism of <i>S. suis</i> within the host is highly restricted. Pyruvate formate lyase (PFL) plays a crucial role in bacterial survival of in glucose-limited and hypoxic host tissues. Here, we investigated the physiological and metabolic functions of PFL PflB in <i>S. suis</i> and elucidated its pivotal role in regulating virulence within the mucosal and blood niches. We demonstrate that PflB is a key enzyme for <i>S. suis</i> to support mixed-acid fermentation under glucose-limited and hypoxic conditions. Additionally, PflB is involved in regulating <i>S. suis</i> morphology and stress tolerance, and its regulation of capsular polysaccharide content depends on dynamic carbon availability. We also found that PflB is associated with the capacity of <i>S. suis</i> to cause bacteremia and persist in the upper respiratory tract to induce persistent infection. Our results provide highly persuasive evidence for the relationship between metabolic regulation and the virulence of <i>S. suis</i>.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2467156"},"PeriodicalIF":5.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11845055/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The T-type voltage-gated Ca²⁺ channel Ca_V3.1 involves in the disruption of respiratory epithelial barrier induced by <i>Pasteurella multocida</i> toxin.","authors":"Haixin Bi, Fei Wang, Lin Lin, Dajun Zhang, Menghan Chen, Yuyao Shang, Lin Hua, Huanchun Chen, Bin Wu, Zhong Peng","doi":"10.1080/21505594.2025.2466482","DOIUrl":"10.1080/21505594.2025.2466482","url":null,"abstract":"<p><p><i>Pasteurella multocida</i> toxin (PMT) is an exotoxin produced by several members of the zoonotic respiratory pathogen <i>P. multocida</i>. The role of PMT in disrupting the mammalian respiratory barrier remains to be elucidated. In this study, we showed that inoculation of recombinantly expressed PMT increased the permeability of the respiratory epithelial barrier in mouse and respiratory cell models. This was evidenced by a decreased expression of tight junctions (ZO-1, occludin) and adherens junctions (β-catenin, E-cadherin), as well as enhanced cytoskeletal rearrangement. In mechanism, we demonstrated that PMT inoculation induced cytoplasmic Ca²⁺ inflow, leading to an imbalance of cellular Ca²⁺ homoeostasis and endoplasmic reticulum stress. This process further stimulated the RhoA/ROCK signalling, promoting cytoskeletal rearrangement and reducing the expression of tight junctions and adherens junctions. Notably, the T-type voltage-gated Ca²⁺ channel Ca_V3.1 was found to participate in PMT-induced cytoplasmic Ca²⁺ inflow. Knocking out Ca_V3.1 significantly reduced the cytotoxicity induced by PMT on swine respiratory epithelial cells and mitigated cytoplasmic Ca²⁺ inflow stimulated by PMT. These findings suggest Ca_V3.1 contributes to PMT-induced respiratory epithelial barrier disruption.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":" ","pages":"2466482"},"PeriodicalIF":5.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11834503/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143415134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathogenicity and virulence of <i>Pseudomonas aeruginosa</i>: Recent advances and under-investigated topics.","authors":"Jemima Swain, Isabel Askenasy, Rahan Rudland Nazeer, Pok-Man Ho, Edoardo Labrini, Leonardo Mancini, Qingqing Xu, Franziska Hollendung, Isabella Sheldon, Camilla Dickson, Amelie Welch, Adam Agbamu, Camilla Godlee, Martin Welch","doi":"10.1080/21505594.2025.2503430","DOIUrl":"10.1080/21505594.2025.2503430","url":null,"abstract":"<p><p><i>Pseudomonas aeruginosa</i> is a model for the study of quorum sensing, protein secretion, and biofilm formation. Consequently, it has become one of the most intensely reviewed pathogens, with many excellent articles in the current literature focusing on these aspects of the organism's biology. Here, though, we aim to take a slightly different approach and consider some less well appreciated (but nonetheless important) factors that affect <i>P. aeruginosa</i> virulence. We start by reminding the reader of the global importance of <i>P. aeruginosa</i> infection and that the \"virulome\" is very niche-specific. Overlooked but obvious questions such as \"what prevents secreted protein products from being digested by co-secreted proteases?\" are discussed, and we suggest how the nutritional preference(s) of the organism might dictate its environmental reservoirs. Recent studies identifying host genes associated with genetic predisposition towards <i>P. aeruginosa</i> infection (and even infection by specific <i>P. aeruginosa</i> strains) and the role(s) of intracellular <i>P. aeruginosa</i> are introduced. We also discuss the fact that virulence is a high-risk strategy and touch on how expression of the two main classes of virulence factors is regulated. A particular focus is on recent findings highlighting how nutritional status and metabolism are as important as quorum sensing in terms of their impact on virulence, and how co-habiting microbial species at the infection site impact on <i>P. aeruginosa</i> virulence (and <i>vice versa</i>). It is our view that investigation of these issues is likely to dominate many aspects of research into this WHO-designated priority pathogen over the next decade.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":" ","pages":"2503430"},"PeriodicalIF":5.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12087490/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144029782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mannan is a context-dependent shield that modifies virulence in <i>Nakaseomyces glabratus</i>.","authors":"Gabriela Fior Ribeiro, Emily L Priest, Helen Heaney, Jonathan P Richardson, Delma S Childers","doi":"10.1080/21505594.2025.2491650","DOIUrl":"https://doi.org/10.1080/21505594.2025.2491650","url":null,"abstract":"<p><p>Fungal-host interaction outcomes are influenced by how the host recognizes fungal cell wall components. Mannan is a major cell wall carbohydrate and can be a glycoshield that blocks the inner cell wall β-1,3-glucan from activating pro-inflammatory immune responses. Disturbing this glycoshield in <i>Candida albicans</i> results in enhanced antifungal host responses and reduced fungal virulence. However, deletions affecting mannan synthesis can lead to systemic hypervirulence for <i>Nakaseomyces glabratus</i> (formerly <i>Candida glabrata</i>) suggesting that proper mannan architecture dampens virulence for this organism. <i>N. glabratus</i> is the second leading cause of invasive and superficial candidiasis, but little is known about how the cell wall affects <i>N. glabratus</i> pathogenesis. In order to better understand the importance of these species-specific cell wall adaptations in infection, we set out to investigate how the mannan polymerase II complex gene, <i>MNN10</i>, contributes to <i>N. glabratus</i> cell wall architecture, immune recognition, and virulence in reference strains BG2 and CBS138. <i>mnn10</i>Δ cells had thinner inner and outer cell wall layers and elevated mannan, chitin, and β-1,3-glucan exposure compared to wild-type cells. Consistent with these observations, <i>mnn10</i>Δ cells activated the β-1,3-glucan receptor in oral epithelial cells (OECs), EphA2, and caused less OEC damage than wild-type. <i>mnn10</i>Δ replication was also restricted in macrophages compared to wild-type controls. Yet, during systemic infection in <i>Galleria mellonella</i> larvae, <i>mnn10</i>Δ cells induced rapid larval melanization and BG2 <i>mnn10</i>Δ cells killed larvae significantly faster than wild-type. Thus, our data suggest that mannan plays context-dependent roles in <i>N. glabratus</i> pathogenesis, acting as a glycoshield in superficial disease models and modulating virulence during systemic infection.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2491650"},"PeriodicalIF":5.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12001547/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144001362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zinc nanoparticles mitigate azoxystrobin and its nanoencapsulation-induced hepatic and renal toxicity in rats.","authors":"Nashwa Elshaer, Ahmed M Eldeeb, Ahmed A A Aioub, Ahmed S Hashem, Soumya Ghosh, Lamya Ahmed Alkeridis, Mohammed Ali Alshehri, Mustafa Shukry, Daklallah A Almalki, Hind A Alkhatabi, Mohamed Afifi, Ammar Al-Farga, Mohamed A Hendawy, Ahmed E A El-Sobki","doi":"10.1080/13510002.2025.2491318","DOIUrl":"https://doi.org/10.1080/13510002.2025.2491318","url":null,"abstract":"<p><p>This study sought to ascertain if zinc nanoparticles (ZnNPs) could lessen the toxicity of azoxystrobin (AZ). This naturally occurring methoxyacrylate is one of the most often used fungicides in agriculture in male albino rats. Six sets of 60 mature male albino rats were randomly assigned: control (distilled water), Azoxystrobin formulation (AZOF), Azoxystrobin nano-formula (AZON), ZnNPs, AZOF + ZnNPs, and AZON + ZnNPs. Blood and tissues were obtained for further immunohistochemical, pathological, and biochemical examination. The results showed that exposure to AZOF and AZON significantly increased the levels of the oxidative stress indicators glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA). Additionally, AZOF significantly impacts liver function bioindicators, including aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. AZOF and AZON induced damage to the liver and kidney by disrupting vascular dilatation and causing hemorrhages, apoptosis, inflammatory lymphocytes, and necrosis. Furthermore, co-administration of ZnNPs with fungicides (AZOF and AZON) can gently enhance the alterations of oxidative stress and liver function bioindicators levels. These findings showed that ZnNPs could help male rats receiving AZ treat their histologically abnormal liver and kidney.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2491318"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12010655/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143996445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Statement of Retraction: Graphene based scaffolds on bone tissue engineering.","authors":"","doi":"10.1080/21655979.2025.2491936","DOIUrl":"https://doi.org/10.1080/21655979.2025.2491936","url":null,"abstract":"","PeriodicalId":8919,"journal":{"name":"Bioengineered","volume":"16 1","pages":"2491936"},"PeriodicalIF":4.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143973738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Statement of Retraction: miR-647 inhibits hepatocellular carcinoma cell progression by targeting protein tyrosine phosphatase receptor type F.","authors":"","doi":"10.1080/21655979.2025.2491949","DOIUrl":"https://doi.org/10.1080/21655979.2025.2491949","url":null,"abstract":"","PeriodicalId":8919,"journal":{"name":"Bioengineered","volume":"16 1","pages":"2491949"},"PeriodicalIF":4.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12026219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143962772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An overview of potential of natural compounds to regulate epigenetic modifications in colorectal cancer: a recent update.","authors":"Susmita Roy, Dikshita Deka, Suresh Babu Kondaveeti, Pavithra Ayyadurai, Sravani Siripragada, Neha Philip, Surajit Pathak, Asim K Duttaroy, Antara Banerjee","doi":"10.1080/15592294.2025.2491316","DOIUrl":"https://doi.org/10.1080/15592294.2025.2491316","url":null,"abstract":"<p><p>Colorectal cancer (CRC) remains an alarming global health concern despite advancements in treatment modalities over recent decades. Among the various factors contributing to CRC, this review emphasizes the critical role of epigenetic mechanisms in its pathogenesis and progression. This review also describes the potential role of natural compounds in altering the epigenetic landscape, focused mainly on DNA methylation, histone modification, and non-coding RNAs. Publications from the previous five years were searched and retrieved using well-known search engines and databases like PubMed, Google Scholar, and ScienceDirect. Keywords like CRC/colorectal cancer, CAC/Colitis associated CRC, inflammasomes, epigenetic modulation, genistein, curcumin, quercetin, resveratrol, anthocyanins, sulforaphane, and epigallocatechin-3-gallate were used in various combinations during the search. These natural compounds predominantly affect pathways such as Wnt/β-catenin, NF-κB, and PI3K/AKT to suppress CRC cell proliferation and oxidative stress and enhance anti-inflammation and apoptosis. However, their clinical use is restricted due to their low bioavailability. However, multiple methods exist to overcome challenges like this, including but not limited to structural modifications, nanoparticle encapsulations, bio-enhancers, and novel advanced delivery systems. These methods improve their potential as supportive therapies that target CRC progression epigenetically with fewer side effects. Current research focuses on enhancing epigenetic targeting to control CRC progression while minimizing side effects, emphasizing improved specificity, bioavailability, and efficacy as standalone or synergistic therapies.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2491316"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005453/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143986001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}