Han Li, Mingshuang Tang, Tao Zheng, Ming Yang, Youning Wang, Yating Shuai, Yan Li, Yibo Zhang, Dongfang Ma
Fusarium head blight (FHB) is a serious disease of wheat that threatens wheat production worldwide. In this study, high-throughput sequencing technology was used to analyze the rhizosphere soil microbial metagenomes of 4 wheat cultivars with different levels of resistance to FHB. The results showed that there were differences in the diversity, structure, and composition of rhizosphere microorganisms between resistant and sensitive varieties. The rhizosphere soil bacterial diversity of the resistant wheat varieties Su Mai 3 and Yang Mai 16 was higher than that of the susceptible wheat varieties Zheng Mai 9023 and Zhou Mai 20. The diversity of rhizosphere fungi in resistant varieties was lower than that in susceptible varieties, but the abundance was higher than that in susceptible varieties. Variety was found to alter the community structure of wheat rhizosphere microorganisms. Resistant varieties SM3 and YM16 and moderately susceptible variety ZM9023 had similar microbial community structure, while highly susceptible variety ZM20 was significantly different from other varieties. The study is aimed at analyzing the effects of wheat varieties of different resistance to FHB on the composition and abundance of rhizosphere soil microbial community to screen out bacteria or fungi that can be used to control FHB, providing the theoretical basis for FHB biological control.
小麦赤霉病(Fusarium head blight, FHB)是一种严重威胁小麦生产的小麦病害。本研究采用高通量测序技术对4个不同抗赤霉病水平小麦品种的根际土壤微生物宏基因组进行分析。结果表明，抗性品种和敏感品种在根际微生物的多样性、结构和组成上存在差异。抗性小麦品种苏麦3号和杨麦16根际土壤细菌多样性高于敏感小麦品种郑麦9023和周麦20。抗性品种的根际真菌多样性低于感病品种，但丰度高于感病品种。品种改变了小麦根际微生物的群落结构。耐药品种SM3、YM16与中感品种ZM9023微生物群落结构相似，而高感品种ZM20与其他品种差异显著。本研究旨在分析不同抗赤霉病小麦品种对根际土壤微生物群落组成及丰度的影响，筛选出可用于防治赤霉病的细菌或真菌，为赤霉病生物防治提供理论依据。
{"title":"Differences in Rhizosphere Microbial Community Structure and Composition in Resistance and Susceptible Wheat to Fusarium Head Blight","authors":"Han Li, Mingshuang Tang, Tao Zheng, Ming Yang, Youning Wang, Yating Shuai, Yan Li, Yibo Zhang, Dongfang Ma","doi":"10.1155/2023/9963635","DOIUrl":"https://doi.org/10.1155/2023/9963635","url":null,"abstract":"Fusarium head blight (FHB) is a serious disease of wheat that threatens wheat production worldwide. In this study, high-throughput sequencing technology was used to analyze the rhizosphere soil microbial metagenomes of 4 wheat cultivars with different levels of resistance to FHB. The results showed that there were differences in the diversity, structure, and composition of rhizosphere microorganisms between resistant and sensitive varieties. The rhizosphere soil bacterial diversity of the resistant wheat varieties Su Mai 3 and Yang Mai 16 was higher than that of the susceptible wheat varieties Zheng Mai 9023 and Zhou Mai 20. The diversity of rhizosphere fungi in resistant varieties was lower than that in susceptible varieties, but the abundance was higher than that in susceptible varieties. Variety was found to alter the community structure of wheat rhizosphere microorganisms. Resistant varieties SM3 and YM16 and moderately susceptible variety ZM9023 had similar microbial community structure, while highly susceptible variety ZM20 was significantly different from other varieties. The study is aimed at analyzing the effects of wheat varieties of different resistance to FHB on the composition and abundance of rhizosphere soil microbial community to screen out bacteria or fungi that can be used to control FHB, providing the theoretical basis for FHB biological control.","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":"6 4","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135869727","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}
Timothy R. Ganderton, Daniel Ghete, Karen Hogg, Graeme J. Park, Christoph G. Baumann, Anthony J. Wilkinson, Paul R. Pryor
Rhodococcus equi is a Gram-positive facultative intracellular pathogen associated with life-threatening bronchopneumonial disease in foals. Key to R. equi’s intracellular survival in host macrophages is the production of virulence associated proteins (Vaps). Numerous vap genes are found on virulence plasmids isolated from different species, and the Vaps share a high degree of sequence identity. VapA has been extensively studied, and although vapK and vapN genes from other R. equi virulence plasmids have been shown to be essential for R. equi intracellular survival, their mode of action is less characterised. We, therefore, examined whether VapK and VapN worked mechanistically in the same way as VapA. Indeed, like VapA, VapK and VapN neutralised lysosomal pH and reduced lysosomal hydrolase activity. A loss of VapA and R. equi virulence could be regained by the presence of either VapK or VapN. The acid-neutralisation activity was also observed to a lesser extent with VapB. There was a differential activity across these virulence-promoting Vaps with the most “acid-neutralising” activity found with VapN, then VapA and K, and finally VapB. These data suggest that VapA production, which is often found in equine infections, can be substituted by VapK and B (produced by plasmids often found in porcine species) or VapN (produced by plasmids often isolated in bovine and human samples). These data imply that the molecular mechanism(s) that VapA uses to neutralise lysosomal acidity should also be seen in VapN and K which will help guide researchers in identifying their precise mode of action and aid the future development of targeted therapeutics.
{"title":"Commonality of Virulence-Promoting Function in Rhodococcus equi Virulence Associated Proteins (Vaps)","authors":"Timothy R. Ganderton, Daniel Ghete, Karen Hogg, Graeme J. Park, Christoph G. Baumann, Anthony J. Wilkinson, Paul R. Pryor","doi":"10.1155/2023/9141112","DOIUrl":"https://doi.org/10.1155/2023/9141112","url":null,"abstract":"Rhodococcus equi is a Gram-positive facultative intracellular pathogen associated with life-threatening bronchopneumonial disease in foals. Key to R. equi’s intracellular survival in host macrophages is the production of virulence associated proteins (Vaps). Numerous vap genes are found on virulence plasmids isolated from different species, and the Vaps share a high degree of sequence identity. VapA has been extensively studied, and although vapK and vapN genes from other R. equi virulence plasmids have been shown to be essential for R. equi intracellular survival, their mode of action is less characterised. We, therefore, examined whether VapK and VapN worked mechanistically in the same way as VapA. Indeed, like VapA, VapK and VapN neutralised lysosomal pH and reduced lysosomal hydrolase activity. A loss of VapA and R. equi virulence could be regained by the presence of either VapK or VapN. The acid-neutralisation activity was also observed to a lesser extent with VapB. There was a differential activity across these virulence-promoting Vaps with the most “acid-neutralising” activity found with VapN, then VapA and K, and finally VapB. These data suggest that VapA production, which is often found in equine infections, can be substituted by VapK and B (produced by plasmids often found in porcine species) or VapN (produced by plasmids often isolated in bovine and human samples). These data imply that the molecular mechanism(s) that VapA uses to neutralise lysosomal acidity should also be seen in VapN and K which will help guide researchers in identifying their precise mode of action and aid the future development of targeted therapeutics.","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":"35 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136294886","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}
Jing Wu, Yuee Liu, M. Xie, Yanzhi Cui, Yaona Wei, Yan Cheng, Jing Yang, Hongxia Zhang, Lei Wang
The aim of this study is to analyze the distribution characteristics of specific allergens based on the immunoglobulin E (IgE) test, performed using the sera of patients with allergic diseases in the Shanxi region of China. Sera from 3141 patients with allergic diseases were analyzed with immunoblotting for IgE antibodies specific to inhaled and ingested allergens. The distribution of allergens and association with factors such as disease profile, sex, age, and cosensitization of the patients who tested positive were analyzed. The most common positive rate of IgE specific to inhaled allergens was mugwort, followed by dust mite mix and common ragweed. The most common positive rate of IgE specific to ingested allergens was crab, followed by egg white and sea fish mix. When analyzed according to disease profile, mugwort was the most common allergen in asthma, rhinitis, and asthma combined with rhinitis. When analyzed by season, the allergens with the highest positive rates included tree mix (willow/poplar/elm), common ragweed, mugwort, and hop pollen from July through September. When analyzed by age, the allergens with the highest positive rates were tree mix, common ragweed, hop, house dust, cow’s milk, mutton/lamb, and peanut in participants aged 0–18 years and egg white in those aged ≥60 years. The radar charts showed cosensitization to multiple allergens. In the Shanxi region, the primary inhaled allergens were mugwort, dust mite mix (1: house dust mite/dust mite), and common ragweed. The primary ingested allergens were crab, egg white, and sea fish mix. There were differences in the positive rates of the allergens between genders, age groups, and seasons, and multiple allergens can cosensitize patients.
{"title":"Analysis of Specific Allergens in the Serum of Patients with Allergic Diseases in the Shanxi Region of China","authors":"Jing Wu, Yuee Liu, M. Xie, Yanzhi Cui, Yaona Wei, Yan Cheng, Jing Yang, Hongxia Zhang, Lei Wang","doi":"10.1155/2023/1460961","DOIUrl":"https://doi.org/10.1155/2023/1460961","url":null,"abstract":"The aim of this study is to analyze the distribution characteristics of specific allergens based on the immunoglobulin E (IgE) test, performed using the sera of patients with allergic diseases in the Shanxi region of China. Sera from 3141 patients with allergic diseases were analyzed with immunoblotting for IgE antibodies specific to inhaled and ingested allergens. The distribution of allergens and association with factors such as disease profile, sex, age, and cosensitization of the patients who tested positive were analyzed. The most common positive rate of IgE specific to inhaled allergens was mugwort, followed by dust mite mix and common ragweed. The most common positive rate of IgE specific to ingested allergens was crab, followed by egg white and sea fish mix. When analyzed according to disease profile, mugwort was the most common allergen in asthma, rhinitis, and asthma combined with rhinitis. When analyzed by season, the allergens with the highest positive rates included tree mix (willow/poplar/elm), common ragweed, mugwort, and hop pollen from July through September. When analyzed by age, the allergens with the highest positive rates were tree mix, common ragweed, hop, house dust, cow’s milk, mutton/lamb, and peanut in participants aged 0–18 years and egg white in those aged ≥60 years. The radar charts showed cosensitization to multiple allergens. In the Shanxi region, the primary inhaled allergens were mugwort, dust mite mix (1: house dust mite/dust mite), and common ragweed. The primary ingested allergens were crab, egg white, and sea fish mix. There were differences in the positive rates of the allergens between genders, age groups, and seasons, and multiple allergens can cosensitize patients.","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2023-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45479341","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}
Yurong Zhang, Dianlun Qian, Xiangfeng Bai, Shibo Sun
Ferroptosis is a new type of iron-dependent cell death caused by lipid peroxide (LPO) accumulation and involved in disease of pulmonary infection. The dysregulation of iron metabolism, the accumulation of LPO, and the inactivation and consumption of glutathione peroxidase 4 (GPX4) are the crucial cause of ferroptosis. Pulmonary infectious diseases caused by Pseudomonas aeruginosa (PA), Mycobacterium tuberculosis (MTB), and severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) are associated with ferroptosis. Ferroptosis may be a potential therapeutic target for pulmonary infectious diseases. However, the mechanisms by which these infections are involved in ferroptosis and whether pulmonary infectious diseases caused by Staphylococcus aureus, Klebsiella pneumoniae, and Leishmania spp are related to ferroptosis are unclear. Accordingly, more researches are needed.
{"title":"Ferroptosis Is a Potential Therapeutic Target for Pulmonary Infectious Diseases","authors":"Yurong Zhang, Dianlun Qian, Xiangfeng Bai, Shibo Sun","doi":"10.1155/2023/3875897","DOIUrl":"https://doi.org/10.1155/2023/3875897","url":null,"abstract":"Ferroptosis is a new type of iron-dependent cell death caused by lipid peroxide (LPO) accumulation and involved in disease of pulmonary infection. The dysregulation of iron metabolism, the accumulation of LPO, and the inactivation and consumption of glutathione peroxidase 4 (GPX4) are the crucial cause of ferroptosis. Pulmonary infectious diseases caused by Pseudomonas aeruginosa (PA), Mycobacterium tuberculosis (MTB), and severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) are associated with ferroptosis. Ferroptosis may be a potential therapeutic target for pulmonary infectious diseases. However, the mechanisms by which these infections are involved in ferroptosis and whether pulmonary infectious diseases caused by Staphylococcus aureus, Klebsiella pneumoniae, and Leishmania spp are related to ferroptosis are unclear. Accordingly, more researches are needed.","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2023-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44373940","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}
M. Vassey, Rininta Firdaus, A. Aslam, L. Wheldon, N. Oldfield, D. Ala'aldeen, K. Wooldridge
Neisseria meningitidis is the most frequent cause of bacterial meningitis and is one of the few bacterial pathogens that can breach the blood-brain barrier (BBB). The 37/67 kDa laminin receptor (LamR) was previously identified as a receptor mediating meningococcal binding to rodent and human brain microvascular endothelial cells, which form part of the BBB. The meningococcal surface proteins PorA and PilQ were identified as ligands for this receptor. Subsequently, the fourth extracellular loop of PorA (PorA-Loop4) was identified as the LamR-binding moiety. Here, we show that PorA-Loop4 targets the 37 kDa laminin receptor precursor (37LRP) on the cell surface by demonstrating that deletion of this loop abrogates the recruitment of 37LRP under meningococcal colonies. Using a circularized peptide corresponding to PorA-Loop4, as well as defined meningococcal mutants, we demonstrate that host cell interaction with PorA-Loop4 results in perturbation of p-CDK4 and Cyclin D1. These changes in cell cycle control proteins are coincident with cellular responses including inhibition of cell migration and a G1 cell cycle arrest. Modulation of the cell cycle of host cells is likely to contribute to the pathogenesis of meningococcal disease.
{"title":"G1 Cell Cycle Arrest Is Induced by the Fourth Extracellular Loop of Meningococcal PorA in Epithelial and Endothelial Cells","authors":"M. Vassey, Rininta Firdaus, A. Aslam, L. Wheldon, N. Oldfield, D. Ala'aldeen, K. Wooldridge","doi":"10.1155/2023/7480033","DOIUrl":"https://doi.org/10.1155/2023/7480033","url":null,"abstract":"Neisseria meningitidis is the most frequent cause of bacterial meningitis and is one of the few bacterial pathogens that can breach the blood-brain barrier (BBB). The 37/67 kDa laminin receptor (LamR) was previously identified as a receptor mediating meningococcal binding to rodent and human brain microvascular endothelial cells, which form part of the BBB. The meningococcal surface proteins PorA and PilQ were identified as ligands for this receptor. Subsequently, the fourth extracellular loop of PorA (PorA-Loop4) was identified as the LamR-binding moiety. Here, we show that PorA-Loop4 targets the 37 kDa laminin receptor precursor (37LRP) on the cell surface by demonstrating that deletion of this loop abrogates the recruitment of 37LRP under meningococcal colonies. Using a circularized peptide corresponding to PorA-Loop4, as well as defined meningococcal mutants, we demonstrate that host cell interaction with PorA-Loop4 results in perturbation of p-CDK4 and Cyclin D1. These changes in cell cycle control proteins are coincident with cellular responses including inhibition of cell migration and a G1 cell cycle arrest. Modulation of the cell cycle of host cells is likely to contribute to the pathogenesis of meningococcal disease.","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2023-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47272920","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}
Objective. Smoking is a primary hazard factor for chronic obstructive pulmonary disease (COPD), which induced a decrease in intestinal Akkermansia muciniphila abundance and Th17 imbalance in COPD. This study analyzed the changes of gut microbiota metabolism and Akkermansia abundance in patients with smoking-related COPD and explored the potential function of Akkermansia muciniphila in smoke-induced COPD mice. Methods. Gut microbiota diversity and metabolic profile were analyzed by 16S rRNA sequence and metabolomics in COPD patients. The IL-1β, IL-17, TNF-α, and IL-6 levels were tested by ELISA. Lung tissue damage was observed by HE staining. The expression of cleave-caspase 3, trophoblast antigen 2 (TROP2), and LC3 in lung tissues were analyzed by IHC or IF. The p-mTOR, mTOR, p62, and LC3 expression in lung tissues were tested by western blot. Results. The levels of IL-17, IL-1β, TNF-α, and IL-6 in the peripheral blood of COPD patients increased significantly. The number and alpha diversity of gut microbiota were decreased in COPD patients. The abundance of Akkermansia muciniphila in gut of COPD patients was decreased, and the metabolic phenotype and retinol metabolism were changed. In the retinol metabolism, the retinol and retinal were significantly changed. Akkermansia muciniphila could improve the alveolar structure and inflammatory cell infiltration in lung tissue, reduce the IL-17, TNF-α, and IL-6 levels in peripheral blood, promote the p-mTOR expression, and inhibit the expression of autophagy-related proteins in smoke-induced COPD mice. Conclusion. The number and alpha diversity of gut microbiota were decreased in patients with smoking-related COPD, accompanied by decreased abundance of Akkermansia muciniphila, and altered retinol metabolism function. Gut Akkermansia muciniphila ameliorated lung injury in smoke-induced COPD mice by inflammation and autophagy.
{"title":"Akkermansia muciniphila Ameliorates Lung Injury in Smoke-Induced COPD Mice by IL-17 and Autophagy","authors":"Li Zhang, Junjuan Lu, Caihong Liu","doi":"10.1155/2023/4091825","DOIUrl":"https://doi.org/10.1155/2023/4091825","url":null,"abstract":"Objective. Smoking is a primary hazard factor for chronic obstructive pulmonary disease (COPD), which induced a decrease in intestinal Akkermansia muciniphila abundance and Th17 imbalance in COPD. This study analyzed the changes of gut microbiota metabolism and Akkermansia abundance in patients with smoking-related COPD and explored the potential function of Akkermansia muciniphila in smoke-induced COPD mice. Methods. Gut microbiota diversity and metabolic profile were analyzed by 16S rRNA sequence and metabolomics in COPD patients. The IL-1β, IL-17, TNF-α, and IL-6 levels were tested by ELISA. Lung tissue damage was observed by HE staining. The expression of cleave-caspase 3, trophoblast antigen 2 (TROP2), and LC3 in lung tissues were analyzed by IHC or IF. The p-mTOR, mTOR, p62, and LC3 expression in lung tissues were tested by western blot. Results. The levels of IL-17, IL-1β, TNF-α, and IL-6 in the peripheral blood of COPD patients increased significantly. The number and alpha diversity of gut microbiota were decreased in COPD patients. The abundance of Akkermansia muciniphila in gut of COPD patients was decreased, and the metabolic phenotype and retinol metabolism were changed. In the retinol metabolism, the retinol and retinal were significantly changed. Akkermansia muciniphila could improve the alveolar structure and inflammatory cell infiltration in lung tissue, reduce the IL-17, TNF-α, and IL-6 levels in peripheral blood, promote the p-mTOR expression, and inhibit the expression of autophagy-related proteins in smoke-induced COPD mice. Conclusion. The number and alpha diversity of gut microbiota were decreased in patients with smoking-related COPD, accompanied by decreased abundance of Akkermansia muciniphila, and altered retinol metabolism function. Gut Akkermansia muciniphila ameliorated lung injury in smoke-induced COPD mice by inflammation and autophagy.","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2023-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42165692","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}
The influenza virus induces cellular apoptosis during viral propagation, and controlling this virus-induced apoptosis process has been shown to have significant antiviral effects. The proapoptotic BH3-only protein Noxa is a strong inducer of apoptosis that can be activated by this virus, suggesting that Noxa has the potential as an anti-influenza target. To assess the value of Noxa as an antiviral target, we utilized CRISPR/Cas9 technology to produce a Noxa-knockout cell line. We found that the knockout of Noxa resulted in a dramatic reduction in the cytopathic effect induced by the influenza virus. Moreover, Noxa knockout decreased the expression of influenza viral proteins (NP, M2, HA, and NS2). In addition, Noxa deficiency triggered a complete autophagic flux to weaken influenza virus-induced autophagosome accumulation, indicating that Noxa may be a promising antiviral target for controlling influenza virus infections.
{"title":"Knockout of Noxa with CRISPR/Cas9 Increases Host Resistance to Influenza Virus Infection","authors":"Ao Zhou, Wenhua Zhang, Baoxin Wang, Xia Dong, Jing Zhang, Hongbo Chen","doi":"10.1155/2023/3877614","DOIUrl":"https://doi.org/10.1155/2023/3877614","url":null,"abstract":"The influenza virus induces cellular apoptosis during viral propagation, and controlling this virus-induced apoptosis process has been shown to have significant antiviral effects. The proapoptotic BH3-only protein Noxa is a strong inducer of apoptosis that can be activated by this virus, suggesting that Noxa has the potential as an anti-influenza target. To assess the value of Noxa as an antiviral target, we utilized CRISPR/Cas9 technology to produce a Noxa-knockout cell line. We found that the knockout of Noxa resulted in a dramatic reduction in the cytopathic effect induced by the influenza virus. Moreover, Noxa knockout decreased the expression of influenza viral proteins (NP, M2, HA, and NS2). In addition, Noxa deficiency triggered a complete autophagic flux to weaken influenza virus-induced autophagosome accumulation, indicating that Noxa may be a promising antiviral target for controlling influenza virus infections.","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":"1 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2023-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42002335","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}
J. Joseph, Amy L. Leestemaker-Palmer, S. Kazemi, L. Danelishvili, L. Bermudez
Mycobacterium avium subsp. hominissuis (M. avium) is an opportunistic environmental pathogen that typically infects patients with existing lung conditions such as cystic fibrosis or COPD. Pulmonary M. avium infection generates peribronchial granulomas that contain infected macrophages and multinucleated giant cells (MGCs). While granuloma formation with MGCs is a common feature of mycobacterial infection, the role of MGCs within the granulomas as well as in the host-pathogen interaction is poorly understood. To shed light on the role of MGCs, we established a novel in vitro model utilizing THP-1 cells stimulated with a combination of IFN-γ and TNF-α. In this study, we show that MGCs can take up M. avium, which replicates intracellularly before leaving the cell. Bacteria that escape the MGC exhibit a highly invasive phenotype, which warrants further evaluation. Characterization of MGCs with transmission electron microscopy revealed an accumulation of cytoplasmic lipid droplets, autophagic activity, and multiple nuclei. Autophagy markers are upregulated in both uninfected and infected MGCs early in infection, measured by RT-qPCR analysis of Beclin-1 and LC3. Inhibition of autophagy with siRNA significantly reduced M. avium survival significantly in THP-1 macrophages. Depletion of host cholesterol and sphingomyelin in MGCs also resulted in decreased survival of M. avium. These processes potentially contribute to the formation of a supportive intracellular environment for the pathogen. Collectively, our results suggest that M. avium is adapted to replicate in MGCs and utilize them as a springboard for local spread.
{"title":"Mycobacterium avium Infection of Multinucleated Giant Cells Reveals Association of Bacterial Survival to Autophagy and Cholesterol Utilization","authors":"J. Joseph, Amy L. Leestemaker-Palmer, S. Kazemi, L. Danelishvili, L. Bermudez","doi":"10.1155/2023/5064371","DOIUrl":"https://doi.org/10.1155/2023/5064371","url":null,"abstract":"Mycobacterium avium subsp. hominissuis (M. avium) is an opportunistic environmental pathogen that typically infects patients with existing lung conditions such as cystic fibrosis or COPD. Pulmonary M. avium infection generates peribronchial granulomas that contain infected macrophages and multinucleated giant cells (MGCs). While granuloma formation with MGCs is a common feature of mycobacterial infection, the role of MGCs within the granulomas as well as in the host-pathogen interaction is poorly understood. To shed light on the role of MGCs, we established a novel in vitro model utilizing THP-1 cells stimulated with a combination of IFN-γ and TNF-α. In this study, we show that MGCs can take up M. avium, which replicates intracellularly before leaving the cell. Bacteria that escape the MGC exhibit a highly invasive phenotype, which warrants further evaluation. Characterization of MGCs with transmission electron microscopy revealed an accumulation of cytoplasmic lipid droplets, autophagic activity, and multiple nuclei. Autophagy markers are upregulated in both uninfected and infected MGCs early in infection, measured by RT-qPCR analysis of Beclin-1 and LC3. Inhibition of autophagy with siRNA significantly reduced M. avium survival significantly in THP-1 macrophages. Depletion of host cholesterol and sphingomyelin in MGCs also resulted in decreased survival of M. avium. These processes potentially contribute to the formation of a supportive intracellular environment for the pathogen. Collectively, our results suggest that M. avium is adapted to replicate in MGCs and utilize them as a springboard for local spread.","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2023-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42021136","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}
Objectives. The effects of Kluyveromyces marxianus on high-fat diet- (HFD-) induced kidney injury (KI) were explored. Methods. HFD-induced KI model was established using male C57BL/6 mice and treated with K. marxianus JLU-1016 and acid-resistant (AR) strain JLU-1016A. Glucose tolerance was evaluated via an oral glucose tolerance test (OGTT). KI was measured using Hematoxylin and Eosin (H&E) staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) analysis. The chemical indexes were analyzed, including lipid profiles, inflammatory cytokines, and creatinine. The levels of Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) or phospho-NF-κB p65 (Ser536) and alpha inhibitor of NF-κB (IκBα) were measured using qPCR and Western blot. The gut microbiota was sequenced using high-throughput sequencing. Results. HFD induction increased OGTT value, KI severity, oxidative stress, inflammatory cytokines, oxidative stress, apoptotic rate, creatinine levels, and the expression of TLR4/NF-κB, phospho-NF-κB p65 (Ser536), and IκBα deteriorated lipid profiles ( P < 0.05 ) and reduced gut microbiota abundance. K. marxianus treatment ameliorated HFD-induced metabolic disorders and reversed these parameters ( P < 0.05 ). Compared with the control, HFD induction increased the proportion of Firmicutes but reduced the proportion of Bacteroidetes and Lactobacillus. K. marxianus JLU-1016 and AR strain JLU-1016A treatments improved gut microbiota by reducing the proportion of Firmicutes and increasing the proportion of Bacteroidetes and Lactobacillus in the KI model ( P < 0.0001 ). Helicobacter has been identified with many infectious diseases and was increased after HFD induction and inhibited after K. marxianus JLU-1016 and AR strain JLU-1016A treatments. The strain JLU-1016A exhibited better results possibly with acid-tolerance properties to pass through an acidic environment of the stomach. Conclusions. K. marxianus may have a beneficial effect on KI by improving gut microbiota and inhibiting TLR4/NF-κB pathway activation.
{"title":"Kluyveromyces marxianus Ameliorates High-Fat-Diet-Induced Kidney Injury by Affecting Gut Microbiota and TLR4/NF-κB Pathway in a Mouse Model","authors":"Na Li, Guanjie Zhao, Mingzhu Xu","doi":"10.1155/2023/2822094","DOIUrl":"https://doi.org/10.1155/2023/2822094","url":null,"abstract":"Objectives. The effects of Kluyveromyces marxianus on high-fat diet- (HFD-) induced kidney injury (KI) were explored. Methods. HFD-induced KI model was established using male C57BL/6 mice and treated with K. marxianus JLU-1016 and acid-resistant (AR) strain JLU-1016A. Glucose tolerance was evaluated via an oral glucose tolerance test (OGTT). KI was measured using Hematoxylin and Eosin (H&E) staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) analysis. The chemical indexes were analyzed, including lipid profiles, inflammatory cytokines, and creatinine. The levels of Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) or phospho-NF-κB p65 (Ser536) and alpha inhibitor of NF-κB (IκBα) were measured using qPCR and Western blot. The gut microbiota was sequenced using high-throughput sequencing. Results. HFD induction increased OGTT value, KI severity, oxidative stress, inflammatory cytokines, oxidative stress, apoptotic rate, creatinine levels, and the expression of TLR4/NF-κB, phospho-NF-κB p65 (Ser536), and IκBα deteriorated lipid profiles ( P < 0.05 ) and reduced gut microbiota abundance. K. marxianus treatment ameliorated HFD-induced metabolic disorders and reversed these parameters ( P < 0.05 ). Compared with the control, HFD induction increased the proportion of Firmicutes but reduced the proportion of Bacteroidetes and Lactobacillus. K. marxianus JLU-1016 and AR strain JLU-1016A treatments improved gut microbiota by reducing the proportion of Firmicutes and increasing the proportion of Bacteroidetes and Lactobacillus in the KI model ( P < 0.0001 ). Helicobacter has been identified with many infectious diseases and was increased after HFD induction and inhibited after K. marxianus JLU-1016 and AR strain JLU-1016A treatments. The strain JLU-1016A exhibited better results possibly with acid-tolerance properties to pass through an acidic environment of the stomach. Conclusions. K. marxianus may have a beneficial effect on KI by improving gut microbiota and inhibiting TLR4/NF-κB pathway activation.","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2023-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46914924","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}
H. Yin, Jiaoli Zhu, Yi Jiang, Yijing Mao, Chenquan Tang, Hui Cao, Yufang Huang, Huijun Zhu, Jianping Luo, Qingjiang Jin, Q. Jin, Yingjun Xue, Xin Wang
In clinical practice, urinary tract infections (UTIs) are second only to respiratory infections in terms of infectious diseases. In recent years, drug resistance of Escherichia coli (E. coli) has increased significantly. The therapeutic effects of Shionone on UTI were assessed by modelling UTI in SD rats and SV-HUC-1 cells with E. coli solution. After treatment of Shionone, the UTI rat model showed a decrease in wet weight/body weight of bladder, as well as a reduction in cellular inflammatory infiltration of bladder tissue and a decrease in urinary levels of IL-6, IL-1β, and TNF-α. In addition, the levels of proinflammatory factors were significantly reduced in a dose-dependent manner in UTI cell model treated with different doses of Shionone (5, 10, and 20 μg/kg). The results of immunofluorescence analysis in both in vivo and in vitro experiments revealed that Shionone reduced bacterial load and the number of E. coli colonies growing on the plates was greatly reduced. These results suggested that Shionone has a good therapeutic effect on UTI, achieved by reducing bacterial load in bladder epithelial cells. The data presented here provide a basis for further research into the treatment of UTI.
{"title":"Shionone Relieves Urinary Tract Infections by Removing Bacteria from Bladder Epithelial Cells","authors":"H. Yin, Jiaoli Zhu, Yi Jiang, Yijing Mao, Chenquan Tang, Hui Cao, Yufang Huang, Huijun Zhu, Jianping Luo, Qingjiang Jin, Q. Jin, Yingjun Xue, Xin Wang","doi":"10.1155/2023/3201540","DOIUrl":"https://doi.org/10.1155/2023/3201540","url":null,"abstract":"In clinical practice, urinary tract infections (UTIs) are second only to respiratory infections in terms of infectious diseases. In recent years, drug resistance of Escherichia coli (E. coli) has increased significantly. The therapeutic effects of Shionone on UTI were assessed by modelling UTI in SD rats and SV-HUC-1 cells with E. coli solution. After treatment of Shionone, the UTI rat model showed a decrease in wet weight/body weight of bladder, as well as a reduction in cellular inflammatory infiltration of bladder tissue and a decrease in urinary levels of IL-6, IL-1β, and TNF-α. In addition, the levels of proinflammatory factors were significantly reduced in a dose-dependent manner in UTI cell model treated with different doses of Shionone (5, 10, and 20 μg/kg). The results of immunofluorescence analysis in both in vivo and in vitro experiments revealed that Shionone reduced bacterial load and the number of E. coli colonies growing on the plates was greatly reduced. These results suggested that Shionone has a good therapeutic effect on UTI, achieved by reducing bacterial load in bladder epithelial cells. The data presented here provide a basis for further research into the treatment of UTI.","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2023-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46164264","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}
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