Cellular Microbiology最新文献

{"title":"Analysis of Effects of PTEN-Mediated TGF-β/Smad2 Pathway on Osteogenic Differentiation in Osteoporotic Tibial Fracture Rats and Bone Marrow Mesenchymal Stem Cell under Tension","authors":"Shiyong Ling,&nbsp;Chen Yan,&nbsp;Kai Huang,&nbsp;Bo Lv,&nbsp;Hua Wang,&nbsp;Xiaoyan Wang,&nbsp;Jun Chen,&nbsp;Jingchuan Sun","doi":"10.1155/2022/1004203","DOIUrl":"10.1155/2022/1004203","url":null,"abstract":"<div>\u0000 <p><i>Purpose</i>. To discuss effects of phosphatase and tensin homolog protein (PTEN)-mediated transforming growth factor-<i>β</i> (TGF-<i>β</i>)/Smad homologue 2 (Smad2) pathway on osteogenic differentiation in osteoporotic (OP) tibial fracture rats and bone marrow mesenchymal stem cell (BMSC) under tension. <i>Methods</i>. A tibial fracture model was established. The rats were divided into sham-operated group and model group, and tibia tissue was collected. Purchase well-grown cultured rat BMSC, and use the Flexercell in vitro cell mechanics loading device to apply tension. The expression of PTEN was detected by qRT-PCR. After the BMSCs were transfected with si-PTEN and oe-PTEN, the force was applied to detect cell differentiation. The expression of TGF-<i>β</i>/Smad2 protein was detected by Western blot. The formation of calcium nodules in BMSC was detected by alkaline phosphatase (ALP) staining and alizarin red (AR) staining. <i>Results</i>. The expression of PTEN was higher in the model group and tension MSC group, and the expression of TGF-<i>β</i> and Smad2 protein was lower. The expression of TGF-<i>β</i> and Smad2 protein in oe-PTEN group was lower than the oe-NC group and control group. The expression of TGF-<i>β</i> and Smad2 protein in si-PTEN group was higher than the si-NC group and control group. The results of ALP staining and AR staining also confirmed the above results. <i>Conclusion</i>. PTEN-mediated TGF-<i>β</i>/Smad2 pathway may play a key role in the osteogenic differentiation of OP tibial fracture rats. Downregulation of PTEN and upregulation of TGF-<i>β</i>/Smad2 signal can promote the osteogenic differentiation of BMSC under tension.</p>\u0000 </div>","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":"2022 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2022-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/2022/1004203","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45490596","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":"Study on the Antifatigue Effect of Compound Amino Acid Capsules","authors":"Wen Huang,&nbsp;Huaqiang Hui,&nbsp;Jiping Xu,&nbsp;Honglei Guo,&nbsp;Yunfeng Wang,&nbsp;Wei Zhu","doi":"10.1155/2022/6593811","DOIUrl":"10.1155/2022/6593811","url":null,"abstract":"<div>\u0000 <p>Supplementing amino acids was proven to relieve fatigue caused by exercise. This study explored the antifatigue effects of compound amino acid capsules (CAAC) on rats undergoing the forced swimming test (FST). CAAC augmented the endurance of FST in rats and alleviated the damage of skeletal muscle tissue and reduced the content of biochemical indicators in the serum. Furthermore, CAAC prevented skeletal muscle dysfunction in FST rats by modulating inflammation and oxidation reactions. After the treatment with CAAC, apoptosis and apoptosis-related protein and p-p65 were weakened, while the levels of SIRT1 and SIRT1/PGC-1<i>α</i>/Nrf2 pathway-related proteins were enhanced. The antifatigue properties of CAAC were associated with its antioxidant and anti-inflammatory capabilities, which were realized by activating the SIRT1/PGC-1<i>α</i>/Nrf2 pathway.</p>\u0000 </div>","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":"2022 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2022-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/2022/6593811","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47700500","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":"Bacterial Atlas of Mouse Gut Microbiota","authors":"Mengqi Chu,&nbsp;Xiaobo Zhang","doi":"10.1155/2022/5968814","DOIUrl":"10.1155/2022/5968814","url":null,"abstract":"<div>\u0000 <p><i>Background</i>. Mouse model is one of the most widely used animal models for exploring the roles of human gut microbiota, a complex system involving in human immunity and metabolism. However, the structure of mouse gut bacterial community has not been explored at a large scale. To address this concern, the diversity and composition of the gut bacteria of 600 mice were characterized in this study. <i>Results</i>. The results showed that the bacteria belonging to 8 genera were found in the gut microbiota of all mouse individuals, indicating that the 8 bacteria were the core bacteria of mouse gut microbiota. The dominant genera of the mouse gut bacteria contained 15 bacterial genera. It was found that the bacteria in the gut microbiota were mainly involved in host’s metabolisms via the collaborations between the gut bacteria. The further analysis demonstrated that the composition of mouse gut microbiota was similar to that of human gut microbiota. <i>Conclusion</i>. Our study presented a bacterial atlas of mouse gut microbiota, providing a solid basis for investing the bacterial communities of mouse gut microbiota.</p>\u0000 </div>","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":"2022 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2022-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/2022/5968814","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138518991","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":"Chlamydia pneumoniae Interferes with Macrophage Differentiation and Cell Cycle Regulation to Promote Its Replication","authors":"Eveliina Taavitsainen-Wahlroos,&nbsp;Ilkka Miettinen,&nbsp;Maarit Ylätalo,&nbsp;Inés Reigada,&nbsp;Kirsi Savijoki,&nbsp;Tuula Anneli Nyman,&nbsp;Leena Hanski","doi":"10.1155/2022/9854449","DOIUrl":"10.1155/2022/9854449","url":null,"abstract":"<div>\u0000 <p><i>Chlamydia pneumoniae</i> is a ubiquitous intracellular bacterium which infects humans via the respiratory route. The tendency of <i>C. pneumoniae</i> to persist in monocytes and macrophages is well known, but the underlying host-chlamydial interactions remain elusive. In this work, we have described changes in macrophage intracellular signaling pathways induced by <i>C. pneumoniae</i> infection. Label-free quantitative proteome analysis and pathway analysis tools were used to identify changes in human THP-1-derived macrophages upon <i>C. pneumoniae</i> CV6 infection. At 48-h postinfection, pathways associated to nuclear factor <i>κ</i>B (NF-<i>κ</i>B) regulation were stressed, while negative regulation on cell cycle control was prominent at both 48 h and 72 h. Upregulation of S100A8 and S100A9 calcium binding proteins, osteopontin, and purine nucleoside hydrolase, laccase domain containing protein 1 (LACC1) underlined the proinflammatory consequences of the infection, while elevated NF-<i>κ</i>B2 levels in infected macrophages indicates interaction with the noncanonical NF-<i>κ</i>B pathway. Infection-induced alteration of cell cycle control was obvious by the downregulation of mini chromosome maintenance (MCM) proteins MCM2-7, and the significance of host cell cycle regulation for <i>C. pneumoniae</i> replication was demonstrated by the ability of a cyclin-dependent kinase (CDK) 4/6 inhibitor Palbociclib to promote <i>C. pneumoniae</i> replication and infectious progeny production. The infection was found to suppress retinoblastoma expression in the macrophages in both protein and mRNA levels, and this change was reverted by treatment with a histone deacetylase inhibitor. The epigenetic suppression of retinoblastoma, along with upregulation of S100A8 and S100A9, indicate host cell changes associated with myeloid-derived suppressor cell (MDSC) phenotype.</p>\u0000 </div>","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":"2022 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2022-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/2022/9854449","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"93577916","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":"miR-30c Increases the Intracellular Survival of Helicobacter pylori by Inhibiting Autophagy","authors":"Qiuhua Deng,&nbsp;Yifei Xu,&nbsp;Yuanzun Zhong,&nbsp;Liyao Tang,&nbsp;Si Du,&nbsp;Jiongming Yang,&nbsp;Lingping Wu,&nbsp;Shaoju Guo,&nbsp;Bin Huang,&nbsp;Hongying Cao,&nbsp;Ping Huang","doi":"10.1155/2022/4536450","DOIUrl":"10.1155/2022/4536450","url":null,"abstract":"<div>\u0000 <p>Persistent <i>Helicobacter pylori</i> infection causes a variety of gastrointestinal diseases and even gastric cancer. <i>H. pylori</i> invades gastric epithelial cells to survive and proliferate, which is one of the key factors in persistent colonization. A Published study has confirmed that cells can eliminate intracellular <i>H. pylori</i> through xenophagy to maintain intracellular balance. However, a growing body of evidences indicate that <i>H. pylori</i> can inhibit xenophagy by miRNA through regulating the expression of key autophagy-related genes. Through western blot analysis, mRFP-GFP-LC3 transfection assay, and transmission electron microscopy, we found that <i>H. pylori</i> infection obstructed autophagy flux degradation stage in GES-1 cell lines. Gentamicin protection assay confirmed that inhibit xenophagy is benefit for intracellular <i>H. pylori</i> survive. miR-30c-1-3p and miR-30c-5p were upregulated in GES-1 cell lines after infecting with <i>H. pylori</i>, resulting in the negative regulation on xenophagy. Further studies through bioinformatics analysis and dual-luciferase reporter assays confirmed that <i>ATG14</i> and <i>ULK1</i> were the target genes of miR-30c-1-3p and that <i>ATG12</i> was the target gene of miR-30c-5p. The overexpression of miR-30c-1-3p and miR-30c-5p reduces the expression of <i>ATG14</i>, <i>ULK1</i>, and <i>ATG12</i> at mRNA level and also decreased intracellular <i>H. pylori</i> elimination in GES-1 cells. The above results suggested that the inhibition on xenophagy by miR-30c-1-3p and miR-30c-5p through <i>ATG14</i>, <i>ULK1</i>, and <i>ATG12</i> targeting benefitted intracellular <i>H. pylori</i> in the evasion of xenophagy clearance.</p>\u0000 </div>","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":"2022 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2022-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/2022/4536450","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41958616","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":"Plasmodium berghei-Mediated NRF2 Activation in Infected Hepatocytes Enhances Parasite Survival","authors":"Annina Bindschedler,&nbsp;Jacqueline Schmuckli-Maurer,&nbsp;Rahel Wacker,&nbsp;Nicolas Kramer,&nbsp;Ruth Rehmann,&nbsp;Reto Caldelari,&nbsp;Volker T. Heussler","doi":"10.1155/2022/7647976","DOIUrl":"10.1155/2022/7647976","url":null,"abstract":"<div>\u0000 <p>The protozoan parasite <i>Plasmodium</i>, causative agent of malaria, initially invades and develops in hepatocytes where it resides in a parasitophorous vacuole (PV). A single invaded parasite develops into thousands of daughter parasites. Survival of the host cell is crucial for successful completion of liver stage development. Nuclear factor erythroid-derived 2-related factor 2 (NRF2) is a transcription factor known to induce transcription of cytoprotective genes when activated. Here we show that NRF2 is activated in <i>Plasmodium berghei</i>-infected hepatocytes. We observed that this NRF2 activation depends on PV membrane resident p62 recruiting KEAP1, the negative regulator of NRF2. Disrupting the NRF2 gene results in reduced parasite survival, indicating that NRF2 signaling is an important event for parasite development in hepatocytes. Together, our observations uncovered a novel mechanism of how <i>Plasmodium</i> parasites ensure host cell survival during liver stage development.</p>\u0000 </div>","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":"2022 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2022-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/2022/7647976","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44930624","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":"Cover Image: Entry of the Varicellovirus Canid herpesvirus 1 into Madin–Darby canine kidney epithelial cells is pH-independent and occurs via a macropinocytosis-like mechanism but without increase in fluid uptake (Cellular Microbiology 12/2021)","authors":"Mohamed Eisa,&nbsp;Hamza Loucif,&nbsp;Julien van Grevenynghe,&nbsp;Angela Pearson","doi":"10.1111/cmi.13401","DOIUrl":"10.1111/cmi.13401","url":null,"abstract":"<p>Confocal micrograph showing <i>Canid herpesvirus 1</i> (red) bound to MDCK cells, and DAPI-stained nuclei (blue). Primary amines of viral glycoproteins were labelled with Alexa Fluor succinimidyl esters 568 dye. For further details, readers are referred to the article by Eisa et al. on p. e13398 of this issue.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":"23 12","pages":""},"PeriodicalIF":3.4,"publicationDate":"2021-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cmi.13401","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42370196","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":"Vam6/Vps39/TRAP1-domain proteins influence vacuolar morphology, iron acquisition and virulence in Cryptococcus neoformans","authors":"Guanggan Hu,&nbsp;Erik Bakkeren,&nbsp;Mélissa Caza,&nbsp;Linda Horianopoulos,&nbsp;Eddy Sánchez-León,&nbsp;Melanie Sorensen,&nbsp;Wonhee Jung,&nbsp;James W. Kronstad","doi":"10.1111/cmi.13400","DOIUrl":"10.1111/cmi.13400","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <p>The pathogenic fungus <i>Cryptococcus neoformans</i> must overcome iron limitation to cause disease in mammalian hosts. Previously, we reported a screen for insertion mutants with poor growth on haem as the sole iron source. In this study, we characterised one such mutant and found that the defective gene encoded a Vam6/Vps39/TRAP1 domain-containing protein required for robust growth on haem, an important iron source in host tissue. We designated this protein Vps3 based on reciprocal best matches with the corresponding protein in <i>Saccharomyces cerevisiae</i>. <i>C. neoformans</i> encodes a second Vam6/Vps39/TRAP1 domain-containing protein designated Vam6/Vlp1, and we found that this protein is also required for robust growth on haem as well as on inorganic iron sources. This protein is predicted to be a component of the homotypic fusion and vacuole protein sorting complex involved in endocytosis. Further characterisation of the <i>vam6Δ</i> and <i>vps3Δ</i> mutants revealed perturbed trafficking of iron acquisition functions (e.g., the high affinity iron permease Cft1) and impaired processing of the transcription factor Rim101, a regulator of haem and iron acquisition. The <i>vps3Δ</i> and <i>vam6Δ</i> mutants also had pleiotropic phenotypes including loss of virulence in a mouse model of cryptococcosis, reduced virulence factor elaboration and increased susceptibility to stress, indicating pleiotropic roles for Vps3 and Vam6 beyond haem use in <i>C. neoformans</i>.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Take Aways</h3>\u0000 \u0000 <div>\u0000 <ul>\u0000 \u0000 <li>Two Vam6/Vps39/TRAP1-domain proteins, Vps3 and Vam6, support the growth of <i>Cryptococcus neoformans</i> on haem.</li>\u0000 \u0000 <li>Loss of Vps3 and Vam6 influences the trafficking and expression of iron uptake proteins.</li>\u0000 \u0000 <li>Loss of Vps3 or Vam6 eliminates the ability of <i>C. neoformans</i> to cause disease in a mouse model of cryptococcosis.</li>\u0000 </ul>\u0000 </div>\u0000 </section>\u0000 </div>","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":"23 12","pages":""},"PeriodicalIF":3.4,"publicationDate":"2021-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39907834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatitis B virus envelope proteins can serve as therapeutic targets embedded in the host cell plasma membrane","authors":"Lili Zhao,&nbsp;Fuwang Chen,&nbsp;Oliver Quitt,&nbsp;Marvin Festag,&nbsp;Marc Ringelhan,&nbsp;Karin Wisskirchen,&nbsp;Julia Festag,&nbsp;Luidmila Yakovleva,&nbsp;Camille Sureau,&nbsp;Felix Bohne,&nbsp;Michaela Aichler,&nbsp;Volker Bruss,&nbsp;Maxim Shevtsov,&nbsp;Maarten van de Klundert,&nbsp;Frank Momburg,&nbsp;Britta S. Möhl,&nbsp;Ulrike Protzer","doi":"10.1111/cmi.13399","DOIUrl":"10.1111/cmi.13399","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <p>Hepatitis B virus (HBV) infection is a major health threat causing 880,000 deaths each year. Available therapies control viral replication but do not cure HBV, leaving patients at risk to develop hepatocellular carcinoma. Here, we show that HBV envelope proteins (HBs)—besides their integration into endosomal membranes—become embedded in the plasma membrane where they can be targeted by redirected T-cells. HBs was detected on the surface of HBV-infected cells, in livers of mice replicating HBV and in HBV-induced hepatocellular carcinoma. Staining with HBs-specific recombinant antibody MoMab recognising a conformational epitope indicated that membrane-associated HBs remains correctly folded in HBV-replicating cells in cell culture and in livers of HBV-transgenic mice in vivo. MoMab coated onto superparamagnetic iron oxide nanoparticles allowed to detect membrane-associated HBs after HBV infection by electron microscopy in distinct stretches of the hepatocyte plasma membrane. Last but not least, we demonstrate that HBs located on the cell surface allow therapeutic targeting of HBV-positive cells by T-cells either engrafted with a chimeric antigen receptor or redirected by bispecific, T-cell engager antibodies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Take Aways</h3>\u0000 \u0000 <div>\u0000 <ul>\u0000 \u0000 <li>HBs become translocated to the plasma membrane.</li>\u0000 \u0000 <li>Novel, recombinant antibody confirmed proper conformation of HBs on the membrane.</li>\u0000 \u0000 <li>HBs provide an interesting target by T-cell-based, potentially curative therapies.</li>\u0000 </ul>\u0000 </div>\u0000 </section>\u0000 </div>","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":"23 12","pages":""},"PeriodicalIF":3.4,"publicationDate":"2021-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cmi.13399","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39674410","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":"Chlamydia and HPV induce centrosome amplification in the host cell through additive mechanisms","authors":"Kevin Wang,&nbsp;Karissa J. Muñoz,&nbsp;Ming Tan,&nbsp;Christine Sütterlin","doi":"10.1111/cmi.13397","DOIUrl":"10.1111/cmi.13397","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <p>Based on epidemiology studies, <i>Chlamydia trachomatis</i> has been proposed as a co-factor for human papillomavirus (HPV) in the development of cervical cancer. These two intracellular pathogens have been independently reported to induce the production of extra centrosomes, or centrosome amplification, which is a hallmark of cancer cells. We developed a cell culture model to systematically measure the individual and combined effects of <i>Chlamydia</i> and HPV on the centrosome in the same host cell. We found that <i>C. trachomatis</i> caused centrosome amplification in a greater proportion of cells than HPV and that the effects of the two pathogens on the centrosome were additive. Furthermore, centrosome amplification induced by <i>Chlamydia</i>, but not by HPV, strongly correlated with multinucleation and required progression through mitosis. Our results suggest that <i>C. trachomatis</i> and HPV induce centrosome amplification through different mechanisms, with the chlamydial effect being largely due to a failure in cytokinesis that also results in multinucleation. Our findings provide support for <i>C. trachomatis</i> as a co-factor for HPV in carcinogenesis and offer mechanistic insights into how two infectious agents may cooperate to promote cancer.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Take Aways</h3>\u0000 \u0000 <p>• <i>Chlamydia</i> and HPV induce centrosome amplification in an additive manner.</p>\u0000 \u0000 <p>• <i>Chlamydia</i>-induced centrosome amplification is linked to host cell multinucleation.</p>\u0000 \u0000 <p>• <i>Chlamydia</i>-induced centrosome amplification requires cell cycle progression.</p>\u0000 \u0000 <p>• <i>Chlamydia</i> and HPV cause centrosome amplification through different mechanisms.</p>\u0000 \u0000 <p>• This study supports <i>Chlamydia</i> as a co-factor for HPV in carcinogenesis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":"23 12","pages":""},"PeriodicalIF":3.4,"publicationDate":"2021-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39842219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}