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Genetically Engineered CLDN18.2 CAR-T Cells Expressing Synthetic PD1/CD28 Fusion Receptors Produced Using a Lentiviral Vector
Heon Ju Lee, Seo Jin Hwang, Eun Hee Jeong, Mi Hee Chang
J. Microbiol. 2024;62(7):555-568.   Published online May 3, 2024
DOI: https://doi.org/10.1007/s12275-024-00133-0
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AbstractAbstract
This study aimed to develop synthetic Claudin18.2 (CLDN18.2) chimeric antigen receptor (CAR)-T (CAR-T) cells as a treatment for advanced gastric cancer using lentiviral vector genetic engineering technology that targets the CLDN18.2 antigen and simultaneously overcomes the immunosuppressive environment caused by programmed cell death protein 1 (PD-1). Synthetic CAR T cells are a promising approach in cancer immunotherapy but face many challenges in solid tumors. One of the major problems is immunosuppression caused by PD-1. CLDN18.2, a gastric-specific membrane protein, is considered a potential therapeutic target for gastric and other cancers. In our study, CLDN18.2 CAR was a second-generation CAR with inducible T-cell costimulatory (CD278), and CLDN18.2-PD1/CD28 CAR was a third-generation CAR, wherein the synthetic PD1/CD28 chimeric-switch receptor (CSR) was added to the second-generation CAR. In vitro, we detected the secretion levels of different cytokines and the killing ability of CAR-T cells. We found that the secretion of cytokines such as interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) secreted by three types of CAR-T cells was increased, and the killing ability against CLDN18.2-positive GC cells was enhanced. In vivo, we established a xenograft GC model and observed the antitumor effects and off-target toxicity of CAR-T cells. These results support that synthetic anti-CLDN18.2 CAR-T cells have antitumor effect and anti-CLDN18.2-PD1/CD28 CAR could provide a promising design strategy to improve the efficacy of CAR-T cells in advanced gastric cancer.
Comprehensive Analysis of Gut Microbiota Alteration in the Patients and Animal Models with Polycystic Ovary Syndrome
Jing Zhou , Xuemei Qiu , Xuejing Chen , Sihan Ma , Zhaoyang Chen , Ruzhe Wang , Ying Tian , Yufan Jiang , Li Fan , Jingjie Wang
J. Microbiol. 2023;61(9):821-836.   Published online October 12, 2023
DOI: https://doi.org/10.1007/s12275-023-00079-9
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AbstractAbstract
Polycystic ovary syndrome (PCOS) is a common disease of endocrine–metabolic disorder, and its etiology remains largely unknown. The gut microbiota is possibly involved in PCOS, while the association remains unclear. The comprehensive analysis combining gut microbiota with PCOS typical symptoms was performed to analyze the role of gut microbiota in PCOS in this study. The clinical patients and letrozole-induced animal models were determined on PCOS indexes and gut microbiota, and fecal microbiota transplantation (FMT) was conducted. Results indicated that the animal models displayed typical PCOS symptoms, including disordered estrous cycles, elevated testosterone levels, and ovarian morphological change; meanwhile, the symptoms were improved after FMT. Furthermore, the microbial diversity exhibited disordered, and the abundance of the genus Ruminococcus and Lactobacillus showed a consistent trend in PCOS rats and patients. The microbiota diversity and several key genera were restored subjected to FMT, and correlation analysis also supported relevant conclusions. Moreover, LEfSe analysis showed that Gemmiger, Flexispira, and Eubacterium were overrepresented in PCOS groups. Overall, the results indicate the involvement of gut microbiota in PCOS and its possible alleviation of endocrinal and reproductive dysfunctions through several special bacteria taxa, which can function as the biomarker or potential target for diagnosis and treatment. These results can provide the new insights for treatment and prevention strategies of PCOS.

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  • Gut Microbes in Polycystic Ovary Syndrome and Associated Comorbidities; Type 2 Diabetes, Non-Alcoholic Fatty Liver Disease (NAFLD), Cardiovascular Disease (CVD), and the Potential of Microbial Therapeutics
    Vineet Singh, Kanika Mahra, DaRyung Jung, Jae-Ho Shin
    Probiotics and Antimicrobial Proteins.2024; 16(5): 1744.     CrossRef
  • Potential therapeutic application and mechanism of gut microbiota-derived extracellular vesicles in polycystic ovary syndrome
    Liangliang Yang, Tingxiu Liu, Yan Liao, Yuehan Ren, Zheng Zheng, Mingyue Zhang, Yue Yu, Chang Liu, Chaoying Wang, Tong Chen, Lili Zhang, Dongxue Zheng, Haidan Zhao, Zhexin Ni, Xinmin Liu
    Biomedicine & Pharmacotherapy.2024; 180: 117504.     CrossRef
  • Research Advance on the Prevention and Treatment of Polycystic Ovary Syndrome Based on Dysbiosis of Gut Microbiota
    钰炜 王
    Advances in Clinical Medicine.2024; 14(08): 895.     CrossRef
The human symbiont Bacteroides thetaiotaomicron promotes diet-induced obesity by regulating host lipid metabolism
Sang-Hyun Cho , Yong-Joon Cho , Joo-Hong Park
J. Microbiol. 2022;60(1):118-127.   Published online December 29, 2021
DOI: https://doi.org/10.1007/s12275-022-1614-1
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  • 16 Web of Science
  • 15 Crossref
AbstractAbstract
The gut microbiome plays an important role in lipid metabolism. Consumption of a high-fat diet (HFD) alters the bacterial communities in the gut, leading to metabolic disorders. Several bacterial species have been associated with diet-induced obesity, nonalcoholic fatty liver disease, and metabolic syndrome. However, the mechanisms underlying the control of lipid metabolism by symbiotic bacteria remain elusive. Here, we show that the human symbiont Bacteroides thetaiotaomicron aggravates metabolic disorders by promoting lipid digestion and absorption. Administration of B. thetaiotaomicron to HFD-fed mice promoted weight gain, elevated fasting glucose levels, and impaired glucose tolerance. Furthermore, B. thetaiotaomicron treatment upregulated the gene expression of the fatty acid transporter and increased fatty acid accumulation in the liver. B. thetaiotaomicron inhibits expression of the gene encoding a lipoprotein lipase inhibitor, angiopoietin-like protein 4 (ANGPTL4), thereby increasing lipase activity in the small intestine. In particular, we found that B. thetaiotaomicron induced the expression of hepcidin, the master regulator of iron metabolism and an antimicrobial peptide, in the liver. Hepcidin treatment resulted in a decrease in ANGPTL4 expression in Caco-2 cells, whereas treatment with an iron chelator restored ANGPTL4 expression in hepcidin- treated cells. These results indicate that B. thetaiotaomicron- mediated regulation of iron storage in intestinal epithelial cells may contribute to increased fat deposition and impaired glucose tolerance in HFD-fed mice.

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  • Integrating transcriptomics and Microbiomics to unravel the regulatory effects of Anji white tea on lipid metabolism in HFD-induced obese mice
    Zhenyu Wang, Yifang Zhang, Xiaolei Shi, Xiaojun Li, Shangxiong Qi, Chunli Hu, Jin Zhao
    Food Research International.2025; 206: 116101.     CrossRef
  • Effects of dietary lipid and protein levels on metamorphosis, growth, metabolism and gut microbiota of tadpole (Lithobates catesbeianus)
    Bo Zhu, Lei Zhong, Chuang Shao, Wenjie Xu, Shuhui Xiang, Shuiquan Fu, Yi Hu
    Aquaculture.2024; 587: 740900.     CrossRef
  • Beneficial metabolic effects of PAHSAs depend on the gut microbiota in diet-induced obese mice but not in chow-fed mice
    Jennifer Lee, Kerry Wellenstein, Ali Rahnavard, Andrew T. Nelson, Marlena M. Holter, Bethany P. Cummings, Vladimir Yeliseyev, Angela Castoldi, Clary B. Clish, Lynn Bry, Dionicio Siegel, Barbara B. Kahn
    Proceedings of the National Academy of Sciences.2024;[Epub]     CrossRef
  • Anti-obesity activity of human gut microbiota Bacteroides stercoris KGMB02265
    Seoung Woo Ryu, Jeong Chan Moon, Byeong Seob Oh, Seung Yeob Yu, Jeong Eun Bak, Eun Seo Heo, Jae-Ho Jeong, Ju Huck Lee
    Archives of Microbiology.2024;[Epub]     CrossRef
  • Bacteroides thetaiotaomicron ameliorates mouse hepatic steatosis through regulating gut microbial composition, gut-liver folate and unsaturated fatty acids metabolism
    Hu Li, Xue-Kai Wang, Mei Tang, Lei Lei, Jian-Rui Li, Han Sun, Jing Jiang, Biao Dong, Hong-Ying Li, Jian-Dong Jiang, Zong-Gen Peng
    Gut Microbes.2024;[Epub]     CrossRef
  • Gut microbiota and metabolic modulation by supplementation of polysaccharide-producing Bacillus licheniformis from Tibetan Yaks: A comprehensive multi-omics analysis
    Zhibo Zeng, Chuxian Quan, Shimeng Zhou, Saisai Gong, Mudassar Iqbal, Muhammad Fakhar-e-Alam Kulyar, Shah Nawaz, Kewei Li, Jiakui Li
    International Journal of Biological Macromolecules.2024; 254: 127808.     CrossRef
  • Insights from metagenomics into gut microbiome associated with acute coronary syndrome therapy
    Yuee Guan, Shuru Zhao, Jing Li, Wenqian Zhang, Zhonghao Guo, Yi Luo, Xiaofei Jiang, Jun Li, Jianxiong Liu, Xi Chen, Zicheng Zhao, Zhe Zhang
    Frontiers in Microbiology.2024;[Epub]     CrossRef
  • Whole genome sequencing of mouse lines divergently selected for fatness (FLI) and leanness (FHI) revealed several genetic variants as candidates for novel obesity genes
    Martin Šimon, Špela Mikec, Santosh S. Atanur, Janez Konc, Nicholas M. Morton, Simon Horvat, Tanja Kunej
    Genes & Genomics.2024; 46(5): 557.     CrossRef
  • Extract of Gardenia jasminoides Ellis Attenuates High-Fat Diet-Induced Glycolipid Metabolism Disorder in Rats by Targeting Gut Microbiota and TLR4/Myd88/NF-κB Pathway
    Chenghao Lv, Xin Liu, Shiyun Chen, Yuhang Yi, Xinnian Wen, Tao Li, Si Qin
    Antioxidants.2024; 13(3): 293.     CrossRef
  • A microbial causal mediation analytic tool for health disparity and applications in body mass index
    Chan Wang, Jiyoung Ahn, Thaddeus Tarpey, Stella S. Yi, Richard B. Hayes, Huilin Li
    Microbiome.2023;[Epub]     CrossRef
  • Differences in dietary patterns related to metabolic health by gut microbial enterotypes of Korean adults
    Hwan-Hee Jang, Hwayoung Noh, Gichang Kim, Su-Yeon Cho, Hyeon-Jeong Kim, Jeong-Sook Choe, Jeongseon Kim, Augustin Scalbert, Marc J. Gunter, Oran Kwon, Hyesook Kim
    Frontiers in Nutrition.2023;[Epub]     CrossRef
  • Impact of diet and host genetics on the murine intestinal mycobiome
    Yask Gupta, Anna Lara Ernst, Artem Vorobyev, Foteini Beltsiou, Detlef Zillikens, Katja Bieber, Simone Sanna-Cherchi, Angela M. Christiano, Christian D. Sadik, Ralf J. Ludwig, Tanya Sezin
    Nature Communications.2023;[Epub]     CrossRef
  • Effects of OsomeFood Clean Label plant-based meals on the gut microbiome
    Dwiyanto Jacky, Chia Bibi, Look Melvin Chee Meng, Fong Jason, Tan Gwendoline, Lim Jeremy, Chong Chun Wie
    BMC Microbiology.2023;[Epub]     CrossRef
  • Consumption of Antioxidant-Rich “Cerrado” Cashew Pseudofruit Affects Hepatic Gene Expression in Obese C57BL/6J High Fat-Fed Mice
    Mariana Buranelo Egea, Gavin Pierce, Si-Hong Park, Sang-In Lee, Fabienne Heger, Neil Shay
    Foods.2022; 11(17): 2543.     CrossRef
  • Host—microbial interactions in metabolic diseases: from diet to immunity
    Ju-Hyung Lee, Joo-Hong Park
    Journal of Microbiology.2022; 60(6): 561.     CrossRef
Lactobacillus plantarum-derived metabolites sensitize the tumorsuppressive effects of butyrate by regulating the functional expression of SMCT1 in 5-FU-resistant colorectal cancer cells
Hye-Ju Kim , JaeJin An , Eun-Mi Ha
J. Microbiol. 2022;60(1):100-117.   Published online December 29, 2021
DOI: https://doi.org/10.1007/s12275-022-1533-1
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AbstractAbstract
A critical obstacle to the successful treatment of colorectal cancer (CRC) is chemoresistance. Chemoresistant CRC cells contribute to treatment failure by providing a mechanism of drug lethargy and modifying chemoresistance-associated molecules. The gut microbiota provide prophylactic and therapeutic effects by targeting CRC through anticancer mechanisms. Among them, Lactobacillus plantarum contributes to the health of the host and is clinically effective in treating CRC. This study confirmed that 5-fluorouracil (5-FU)-resistant CRC HCT116 (HCT116/5FUR) cells acquired butyrateinsensitive properties. To date, the relationship between 5- FU-resistant CRC and butyrate resistance has not been elucidated. Here, we demonstrated that the acquisition of butyrate resistance in HCT116/5FUR cells was strongly correlated with the inhibition of the expression and function of SMCT1, a major transporter of butyrate in colonocytes. L. plantarum-cultured cell-free supernatant (LP) restored the functional expression of SMCT1 in HCT116/5FUR cells, leading to butyrate-induced antiproliferative effect and apoptosis. These results suggest that LP has a synergistic effect on the SMCT1/butyrate-mediated tumor suppressor function and is a potential chemosensitizer to overcome dual 5-FU and butyrate resistance in HCT116 cells.

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  • The role of gut microbiota and metabolites in cancer chemotherapy
    Shiyu Li, Shuangli Zhu, Jun Yu
    Journal of Advanced Research.2024; 64: 223.     CrossRef
  • Sodium Butyrate Inhibits the Expression of Thymidylate Synthase and Induces Cell Death in Colorectal Cancer Cells
    Nayeon Kim, Changwon Yang
    International Journal of Molecular Sciences.2024; 25(3): 1572.     CrossRef
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    Babak Pakbin, Samaneh Allahyari, Shaghayegh Pishkhan Dibazar, Amir Peymani, Mozhdeh Khajeh Haghverdi, Khadijeh Taherkhani, Maryam Javadi, Razzagh Mahmoudi
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    Karla Vagnerová, Tomáš Hudcovic, Martin Vodička, Peter Ergang, Petra Klusoňová, Petra Petr Hermanová, Dagmar Šrůtková, Jiří Pácha
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    Pharmacological Research.2024; 208: 107373.     CrossRef
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    Suki Ha, Xiang Zhang, Jun Yu
    Chinese Medical Journal.2024; 137(1): 8.     CrossRef
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    Hye Ji Jang, Na-Kyoung Lee, Hyun-Dong Paik
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    Karolina Kaźmierczak-Siedlecka, Nikola Bulman, Paweł Ulasiński, Bartosz Kamil Sobocki, Karol Połom, Luigi Marano, Leszek Kalinowski, Karolina Skonieczna-Żydecka
    Gut Microbes.2023;[Epub]     CrossRef
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    Amino Acids.2023; 55(10): 1223.     CrossRef
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    Yali Liu, Harry Cheuk-Hay Lau, Jun Yu
    Gut Microbes.2023;[Epub]     CrossRef
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    Sihyun Jeong, Yuju Kim, Soyeong Park, Doyeon Lee, Juho Lee, Shwe Phyu Hlaing, Jin-Wook Yoo, Sang Hoon Rhee, Eunok Im
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    Biomedicine & Pharmacotherapy.2023; 169: 115812.     CrossRef
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    Yali Liu, Harry Cheuk-Hay Lau, Wing Yin Cheng, Jun Yu
    Genomics, Proteomics & Bioinformatics.2023; 21(1): 84.     CrossRef
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    Xiang Lin, Xinyu Yang, Yushang Yang, Hangbin Zhang, Xuan Huang
    Frontiers in Oncology.2023;[Epub]     CrossRef
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    Jia-Jie Zhu, Hai-Yan Liu, Liang-Jun Yang, Zheng Fang, Rui Fu, Jia-Bin Chen, Shan Liu, Bao-Ying Fei
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    Christina Thoda, Maria Touraki
    Microorganisms.2023; 11(8): 1898.     CrossRef
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  • Determination of the effect of L. plantarum AB6-25, L. plantarum MK55 and S. boulardii T8-3C microorganisms on colon, cervix, and breast cancer cell lines: Molecular docking, and molecular dynamics study
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    Journal of Molecular Structure.2022; 1261: 132939.     CrossRef
  • Extracellular vesicles derived from Lactobacillus plantarum restore chemosensitivity through the PDK2-mediated glucose metabolic pathway in 5-FU-resistant colorectal cancer cells
    JaeJin An, Eun-Mi Ha
    Journal of Microbiology.2022; 60(7): 735.     CrossRef
WasC, a WASP family protein, is involved in cell adhesion and migration through regulation of F-actin polymerization in Dictyostelium
Pyeonghwa Jeon , Taeck Joong Jeon
J. Microbiol. 2020;58(8):696-702.   Published online June 10, 2020
DOI: https://doi.org/10.1007/s12275-020-0138-9
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AbstractAbstract
The actin cytoskeleton is involved in the regulation of cell morphology and migration. Wiskott-Aldrich Syndrome proteins (WASPs) play an important role in controlling actin polymerization by activating the Arp2/3 complex. The present study investigated the roles of WasC, one of the 3 WASPs in Dictyostelium, in cellular processes. Cells lacking WasC displayed strong cell adhesion and approximately 1.5-fold increase in F-actin levels as compared to the wild-type cells. Loss of wasC caused defects in phagocytosis and decreased the migration speed in chemoattractant-mediated cell migration but did not affect directionality. WasC was localized to the protruding region in migrating cells and, transiently and rapidly translocated to the cell cortex in response to chemoattractant stimulation, in an F-actin dependent manner. Our
results
suggest that WasC is involved in cell adhesion and migration by regulating F-actin polymerization at the leading edge of migrating cells, probably as a negative regulator. The increased strength of adhesion in wasC null cells is likely to decrease the migration speed but not the directionality.

Citations

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  • Wiskott-Aldrich syndrome gene as a prognostic biomarker correlated with immune infiltrates in clear cell renal cell carcinoma
    Guixin Ding, Tianqi Wang, Shangjing Liu, Zhongbao Zhou, Jian Ma, Jitao Wu
    Frontiers in Immunology.2023;[Epub]     CrossRef
  • Dual regulation of the actin cytoskeleton by CARMIL-GAP
    Goeh Jung, Miao Pan, Christopher J. Alexander, Tian Jin, John A. Hammer
    Journal of Cell Science.2022;[Epub]     CrossRef
  • Regulation of the Actin Cytoskeleton via Rho GTPase Signalling in Dictyostelium and Mammalian Cells: A Parallel Slalom
    Vedrana Filić, Lucija Mijanović, Darija Putar, Antea Talajić, Helena Ćetković, Igor Weber
    Cells.2021; 10(7): 1592.     CrossRef
Antagonistic effect of peptidoglycan of Streptococcus sanguinis on lipopolysaccharide of major periodontal pathogens
Sung-Hoon Lee
J. Microbiol. 2015;53(8):553-560.   Published online July 31, 2015
DOI: https://doi.org/10.1007/s12275-015-5319-6
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AbstractAbstract
Streptococcus sanguinis is often found in subgingival biofilm including periodontopathogens, and is correlated with a delay in colonization by periodontopathogens. However, the effect of S. sanguinis on inflammation induced by periodontopathogens is poorly understood. Thus, this study investigated the effect of S. sanguinis peptidoglycan (PGN) on induction of TNF-α, IL-6, and IL-8 expression by lipopolysaccharide (LPS) of periodontal pathogens. LPS was extracted from Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Tannerella forsythia, and PGN was isolated from S. sanguinis. THP-1 cells, a monocytic cell-line, were cotreated with LPS of the periodontal pathogens and S. sanguinis PGN, and then the expression of inflammatory cytokines was analyzed by real-time RT-PCR. To analyze the underlying mechanism, the binding assay of the LPS to CD14 or LPS-binding protein (LBP) was performed in the presence or absence of the PGN after coating recombinant human CD14 and LBP on EIA plate. The PGN inhibited the binding of LPS to CD14 and LBP in a dose-dependent manner. Also, THP-1 cells were co-treated with the LPS in the presence of N-acetylmuramic acid and N-acetylglucosamine, as components of PGN, and the competition binding assay to CD14 and LBP was performed. N-acetylmuramic acid inhibited the induction of inflammatory cytokine expression by LPS and the binding of LPS to CD14 or LBP whereas Nacetylglucosamine did not show such effect. Collectively, the
results
suggest that S. sanguinis PGN inhibited the cytokine expression induced by the LPS of periodontopathogens due to the inhibition of LPS binding to LBP and CD14. N-acetylmuramic acid of PGN may play a role in inhibition of the LPS binding of periodontopathogens to CD14 and LBP.

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Review
REVIEW] Perturbation of Pulmonary Immune Functions by Carbon Nanotubes and Susceptibility to Microbial Infection
Brent E. Walling , Gee W. Lau
J. Microbiol. 2014;52(3):227-234.   Published online March 1, 2014
DOI: https://doi.org/10.1007/s12275-014-3695-y
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AbstractAbstract
Occupational and environmental pulmonary exposure to carbon nanotubes (CNT) is considered to be a health risk with a very low threshold of tolerance as determined by the United States Center for Disease Control. Immortalized airway epithelial cells exposed to CNTs show a diverse range of effects including reduced viability, impaired proliferation, and elevated reactive oxygen species generation. Additionally, CNTs inhibit internalization of targets in multiple macrophage cell lines. Mice and rats exposed to CNTs often develop pulmonary granulomas and fibrosis. Furthermore, CNTs have immunomodulatory properties in these animal models. CNTs themselves are proinflammatory and can exacerbate the allergic response. However, CNTs may also be immunosuppressive, both locally and systemically. Studies that examined the relationship of CNT exposure prior to pulmonary infection have reached different conclusions. In some cases, pre-exposure either had no effect or enhanced clearance of infections while other studies showed CNTs inhibited clearance. Interestingly, most studies exploring this relationship use pathogens which are not considered primary pulmonary pathogens. Moreover, harmony across studies is difficult as different types of CNTs have dissimilar biological effects. We used Pseudomonas aeruginosa as model pathogen to study how helical multi-walled carbon nanotubes (HCNTs) affected internalization and clearance of the pulmonary pathogen. The results showed that, although HCNTs can inhibit internalization through multiple processes, bacterial clearance was not altered, which was attributed to an enhanced inflammatory response caused by pre-exposure to HCNTs. We compare and contrast our findings in relation to other studies to gauge the modulation of pulmonary immune response by CNTs.

Citations

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    Environmental Science: Nano.2023; 10(3): 855.     CrossRef
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Research Support, Non-U.S. Gov'ts
Tularemia Progression Accompanied with Oxidative Stress and Antioxidant Alteration in Spleen and Liver of BALB/c Mice
Miroslav Pohanka , Oto Pavlis , Branislav Ruttkay-Nedecky , Jiri Sochor , Jakub Sobotka , Jiri Pikula , Vojtech Adam , Rene Kizek
J. Microbiol. 2012;50(3):401-408.   Published online June 30, 2012
DOI: https://doi.org/10.1007/s12275-012-1621-8
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AbstractAbstract
Francisella tularensis is the causative agent of tularemia. It is an intracellular pathogen with the ability to survive within phagosomes and induce pyroptotic cell death. In this study, we attempted to prove whether oxidative imbalance plays a significant role in tularemia pathogenesis. In our experimental model, we subcutaneously infected female BALB/c mice (dose 105 CFU of F. tularensis LVS). Liver, spleen, and blood were collected from mice at regular intervals from days 1–15 after infection. The bacterial burden was assessed by a cultivation test. The burden was unchanging from the 2nd to 6th day after infection. The bacterial burden corresponded to the plasmatic level of IFN-γ, IL-6, and liver malondialdehyde. After the phase of acute bacteraemia and the innate immunity reaction, the levels of reduced glutathione and total low molecular weight antioxidants decreased significantly and the activity of caspase-3 increased in the liver. The level of reduced glutathione decreased to 25% of the original level, and the total level of low molecular weight antioxidants was less than 50% of the initial amount. The demonstrated effects of tularemia-induced pathology had a more extensive impact on the liver than on the spleen.
Modulation of Immune Response by Interleukin-10 in Systemic Corynebacterium kutscheri Infection in Mice
Eui-Suk Jeong , Kyoung-Sun Lee , Seung-Ho Heo , Jin-Hee Seo , Yang-Kyu Choi
J. Microbiol. 2012;50(2):301-310.   Published online April 27, 2012
DOI: https://doi.org/10.1007/s12275-012-1298-z
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AbstractAbstract
Interleukin (IL)-10 is an anti-inflammatory cytokine that modulates sepsis by decreasing pro-inflammatory cytokine production and chemokine expression. In this study, IL- 10-deficient and wild-type (WT) mice were infected with Corynebacterium kutscheri to determine if the absence of IL-10 altered the protective immunity and pathogenesis. After infection, IL-10 knockout (KO) mice had a higher survival rate than WT mice. The decrease of body weight and the increased weight of organs such as liver and spleen were greater in WT mice. Bacterial counts were significantly increased after inoculation in WT mice over those in IL-10 KO mice. WT mice had more granulomatous inflammation and coagulative necrosis in the liver and spleen, lymphocyte depletion in lymphoid follicles, and apoptosis of immune cells in the spleen. WT mice had significantly higher plasma concentrations of aspartate aminotransferase and alanine aminotransferase. Furthermore, more upregulation of tumor necrosis factor-α and IL-4 in the plasma, macrophage inflammatory protein-2, keratinocyte-derived chemokine, inducible nitric oxide synthase, and interferoninducible protein 10 mRNA in the spleen were observed in WT mice after inoculation. These results suggest that the lack of IL-10 contributes to an increase in the systemic clearance of C. kutscheri, and that IL-10 plays a detrimental role in controlling systemic C. kutscheri infection.
Neovastat(Æ-941) inhibits the airway inflammation and hyperresponsiveness in a murine model of asthma
Sook-Young Lee , Soon-Young Paik , Su-Mi Chung ,
J. Microbiol. 2005;43(1):11-16.
DOI: https://doi.org/2145 [pii]
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AbstractAbstract
Matrix metalloproteinase (MMP)-9 plays an important role in the pathogenesis of bronchial asthma. Neovastat, having significant antitumor and antimetastatic properties, is classified as a naturally occurring multifunctional antiangiogenic agent. We evaluated the therapeutic effect of Neovastat on airway inflammation in a mouse model of asthma. BALB/c mice were immunized subcutaneously with ovalbumin (OVA) on days 0, 7, 14, and 21 and challenged with inhaled OVA on days 26, 29, and 31. Neovastat was administrated by gavage (5 mg/kg body weight) three times with 12 h intervals, beginning 30 min before OVA inhalation. On day 32, mice were challenged with inhaled methacholine, and enhanced pause (Penh) was measured as an index of airway hyperresponsiveness. The severity of airway inflammation was determined by differential cell count of bronchoalveolar lavage (BAL) fluid. The MMP-9 concentration in BAL fluid samples was measured by ELISA, and MMP-9 activity was measured by zymography. The untreated asthma group showed an increased inflammatory cell count in BAL fluid and Penh value compared with the normal control group. Mice treated with Neovastat had significantly reduced Penh values and inflammatory cell counts in BAL fluid compared with untreated asthmatic mice. Furthermore, mice treated with Neovastat showed significantly reduced MMP-9 concentrations and activity in BAL fluid. These results demonstrate that Neovastat might have new therapeutic potential for airway asthmatic inflammation. <br><br><br>
Published Erratum
Erratum to: Fungal Catastrophe of a Specimen Room: Just One Week is Enough to Eradicate Traces of Thousands of Animals
Ji Seon Kim , Yoonhee Cho , Chang Wan Seo , Ki Hyeong Park , Shinnam Yoo , Jun Won Lee , Sung Hyun Kim , Wonjun Lee , Young Woon Lim
J. Microbiol. 2023;61(6):653-653.
DOI: https://doi.org/10.1007/s12275-023-00060-6
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AbstractAbstract
Correction to: Journal of Microbiology (2023) 61:189–197 https://doi.org/10.1007/s12275-023-00017-9 In this article two author names are given erroneaously: Written incorrectly: Ki Hyung Park · Shin Nam Yoo It should be read: Ki Hyeong Park · Shinnam Yoo

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