Journal of Microbiology

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Adenoviral Vector System: A Comprehensive Overview of Constructions, Therapeutic Applications and Host Responses: Anyeseu Park, Jeong Yoon Lee; J. Microbiol. 2024;62(7):491-509. Published online July 22, 2024; DOI: https://doi.org/10.1007/s12275-024-00159-4

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Adenoviral vectors are crucial for gene therapy and vaccine development, offering a platform for gene delivery into host cells. Since the discovery of adenoviruses, first-generation vectors with limited capacity have evolved to third-generation vectors flacking viral coding sequences, balancing safety and gene-carrying capacity. The applications of adenoviral vectors for gene therapy and anti-viral treatments have expanded through the use of in vitro ligation and homologous recombination, along with gene editing advancements such as CRISPR-Cas9. Current research aims to maintain the efficacy and safety of adenoviral vectors by addressing challenges such as pre-existing immunity against adenoviral vectors and developing new adenoviral vectors from rare adenovirus types and non-human species. In summary, adenoviral vectors have great potential in gene therapy and vaccine development. Through continuous research and technological advancements, these vectors are expected to lead to the development of safer and more effective treatments.

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Journal Article

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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Abstract: 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.

Research Support, Non-U.S. Gov'ts

Changes in Arbuscular Mycorrhizal Fungus Community Along an Exotic Plant Eupatorium adenophorum Invasion in a Chinese Secondary Forest: Xin Sun , Cheng Gao , Liang-Dong Guo; J. Microbiol. 2013;51(3):295-300. Published online June 28, 2013; DOI: https://doi.org/10.1007/s12275-013-3169-7

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Abstract: Knowledge of the changes in arbuscular mycorrhizal (AM) fungi is fundamental for understanding the success of exotic plant invasions in natural ecosystems. In this study, AM fungal colonization and spore community were examined along an invasive gradient of the exotic plant Eupatorium adenophorum in a secondary forest in southwestern China. With increasing E. adenophorum invasion, the density of arbuscules in the roots of E. adenophorum significantly increased, but the AM root colonization rate and the densities of vesicles and hyphal coils in roots of E. adenophorum were not significantly different. A total of 29 AM fungi belonging to nine genera were identified based on spore morphology. Claroideoglomus etunicatum, Funneliformis geosporus, and Glomus aggregatum were the most common AM fungal species. The E. adenophorum invasion significantly decreased the AM fungal spore density in the soil. Furthermore, with increasing of E. adenophorum invasion the spore densities of C. etunicatum, G. aggregatum, and G. arenarium significantly decreased, whereas F. geosporus significantly increased. Nonmetric multidimensional scaling demonstrated that the AM fungus community composition was significantly different (P=0.003) in the different invasive levels of E. adenophorum, and significantly correlated with plant species richness, soil total P, and soil NO3--N. The results suggest that the alteration in AM fungus community might be caused by E. adenophorum invasion via changing the local plant community and soil properties in a Chinese secondary forest ecosystem.

SP0454, A Putative Threonine Dehydratase, Is Required For Pneumococcal Virulence In Mice: WenJuan Yan , Hong Wang , WenChun Xu , KaiFeng Wu , Run Yao , XiuYu Xu , Jie Dong , YanQing Zhang , Wen Zhong , XueMei Zhang; J. Microbiol. 2012;50(3):511-517. Published online June 30, 2012; DOI: https://doi.org/10.1007/s12275-012-2014-8

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Abstract: Increasing pressure in antibiotic resistance and the requirement for the design of new vaccines are the objectives of clarifying the putative virulence factors in pneumococcal infection. In this study, the putative threonine dehydratase sp0454 was inactivated by erythromycin-resistance cassette replacement in Streptococcus pneumoniae CMCC 31203 strain. The sp0454 mutant was tested for cell growth, adherence, colonization, and virulence in a murine model. The Δsp0454 mutant showed decreased ability for colonization and impaired ability to adhere to A549 cells. However, the SP0454 polypeptide or its antiserum did not affect pneumococcal CMCC 31203 adhesion to A549 cells. The sp0454 deletion mutant was less virulent in a murine intranasal infection model. Real-time RT-PCR analysis revealed significant decrease of the pneumococcal surface antigen A expression in the sp0454 mutant. These results suggest that SP0454 contributes to virulence and colonization, which could be explained in part by modulating the expression of other virulence factors, such as psaA in pneumococcal infection.

Interaction of Acinetobacter baumannii 19606 and 1656-2 with Acanthamoeba castellanii: Migma Dorji Tamang , Shukho Kim , Sung-Min Kim , Hyun-Hee Kong , Jungmin Kim; J. Microbiol. 2011;49(5):841-846. Published online November 9, 2011; DOI: https://doi.org/10.1007/s12275-011-1063-8

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9 Scopus

Abstract: Acinetobacter baumannii is virtually avirulent for healthy people but maintains a high virulence among critically ill patients or immuno-compromised individuals. The ability of A. baumannii to adhere to cells and persist on surfaces as biofilms could be central to its pathogenicity. In the present study, we compared the virulence of the A. baumannii 1656-2 clinical strain, which is able to form a thick biofilm, with the virulence of the A. baumannii type strain (ATCC 19606T). Acanthamoeba castellanii, a single-celled organism, was used as the host model system to study the virulence of A. baumannii. Compared to A. baumannii ATCC 19606T, A. baumannii 1656-2 exhibited a higher ability to adhere and invade A. castellanii cells and had a higher killing rate of A. castellanii cells. Furthermore, co-incubation of the amoeba cells and the cell-free supernatant of A. baumannii resulted in the cell death of the amoebae. Heat inactivation or proteinase K treatment of the supernatant did not eliminate its cytotoxicity, suggesting heat stable non-protein factors are responsible for its cytotoxicity to A. castellanii cells. In conclusion, this study for the first time has revealed the capacity of the A. baumannii strain and/or its metabolic products to induce cytotoxicity in A. castellanii cells.

Berberine Inhibits HEp-2 Cell Invasion Induced by Chlamydophila pneumoniae Infection: Li Jun Zhang , Li Jun Zhang , Wei Quan , Bei Bei Wang , Bing Ling Shen , Teng Teng Zhang , Yi Kang; J. Microbiol. 2011;49(5):834-840. Published online November 9, 2011; DOI: https://doi.org/10.1007/s12275-011-1051-z

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Abstract: This study investigated the inhibitory effects of berberine on Chlamydophila (Chlamydia) pneumoniae infection-induced HEp-2 cell invasion and explored the possible mechanisms involved in this process. C. pneumoniae infection resulted in a significant increase in HEp-2 cell invasion when compared with the control cells (P<0.01) in a Matrigel invasion assay. This enhanced cell invasion was strongly suppressed by berberine (50 μM) (P<0.01). In a cell adhesion assay, the infection-induced HEp-2 cell adhesion to Matrigel was also significantly inhibited by berberine (P<0.01). C. pneumoniae infection was found to promote HEp-2 cell migration remarkably (P<0.01), which was markedly suppressed by berberine (P<0.01) in the cell migration assays. There were no statistically significant differences in the expression of matrix metalloproteinase-1 (MMP-1) and MMP-9 in the infected cells and berberine did not change the expression of MMP-1 and MMP-9. These data suggest that berberine inhibits C. pneumoniae infection-induced HEp-2 cell invasion through suppressing HEp-2 cell adhesion and migration, but not through changing the expression of MMP-1 and MMP-9.

Effect of Acidic pH on the Invasion Efficiency and the Type III Secretion System of Burkholderia thailandensis: Siroj Jitprasutwit , Wisansanee Thaewpia , Veerachat Muangsombut , Aroonlug Lulitanond , Chanvit Leelayuwat , Ganjana Lertmemongkolchai , Sunee Korbsrisate; J. Microbiol. 2010;48(4):526-532. Published online August 20, 2010; DOI: https://doi.org/10.1007/s12275-010-0078-x

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Abstract: Burkholderia thailandensis is a close relative of Burkholderia pseudomallei. These organisms are very similar, but B. thailandensis is far less virulent than B. pseudomallei. Nucleotide sequencing and analysis of 14 B. thailandensis isolates revealed variation in the regions coding for the type III secreted BipD protein. The degree of B. thailandensis BipD sequence variation was greater than that found in B. pseudomallei. Western blot analysis indicated that, unlike B. pseudomallei, B. thailandensis type III secreted proteins including BipD and BopE could not be detected in the supernatant of culture medium unless induced by acidic conditions. In addition, culturing B. thailandensis under acidic growth conditions (pH 4.5) can induce the ability of this bacterium to invade human respiratory epithelial cells A549. The identification of an environmental stimulus that increases the invasion capability of B. thailandensis invasion is of value for those who would like to use this bacterium as a model to study B. pseudomallei virulence.

Penetration of HEp-2 and Chinese Hamster Ovary Epithelial Cells by Escherichia coli Harbouring the Invasion-Conferring Genomic Region from Salmonella typhimurium: Jeong Uck Park , Sang-Gu Hwang , Ja-Young Moon , Yong-Kweon Cho , Dong Wan Kim , Yong Kee Jeong , andKwang-Ho Rhee; J. Microbiol. 2000;38(4):270-274.

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Abstract: Pathogenic Salmonella typhimurium can invade the intestinal epithelium and cause a wide range of diseases including gastroenteritis and bacteremia in human and animals. To identify the genes involved in the infection, the invasion determinant was obtained from S. typhimurium 82/6915 and was subcloned into pGEM-7Z. A subclone DH1 (pSV6235) invaded HEp-2 and Chinese hamster ovary epithelial cells and contained a 4.4 kb fragment of S. typhimurium genomic region. Compared with the host strain E. coli DH1, the subclone DH1 (pSV6235) invaded cultured HEp-2 and Chinese hamster ovary cells at least 75- and 68-fold higher, respectively. The invasion rate of E. coli DH1 for the cells significantly increased by harbouring the genomic region derived from pathogenic S. typhimurium 82/6915.

Salmonella Invasion Gene Regulation: A Story of Environmental Awareness: Bradley D. Jones; J. Microbiol. 2005;43(1):110-117.

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Abstract: Salmonella enterica serovar Typhimurium causes human gastroenteritis and a systemic typhoid-like infection in mice. A critical virulence determinant of Salmonella is the ability to invade mammalian cells. The expression of genes required for invasion is tightly regulated by environmental conditions and a variety of regulatory genes. The hilA regulator encodes an OmpR/ToxR family transcriptional regulator that activates the expression of invasion genes in response to both environmental and genetic regulatory factors. Work from several laboratories has highlighted that regulation of hilA expression is a key point for controlling expression of the invasive phenotype. A number of positive regulators of hilA expression have been identified including csrAB, sirA/barA, pstS, hilC/sirC/sprA, fis, and hilD. HilD, an AraC/XylS type transcriptional regulator, is of particular importance as a mutation in hilD results in a 14-fold decrease in chromosomal hilA::Tn5lacZY-080 expression and a 53-fold decrease in invasion of HEp-2 cells. It is believed that HilD directly regulates hilA expression as it has been shown to bind to hilA promoter sequences. In addition, our research group, and others, have identified genes (hilE, hha, pag, and lon) that negatively affect hilA transcription. HilE appears to be an important Salmonella-specific regulator that plays a critical role in inactivating hilA expression. Recent work in our lab has been directed at understanding how environmental signals that affect hilA expression may be processed through a hilE pathway to modulate expression of hilA and the invasive phenotype. The current understanding of this complex regulatory system is reviewed.

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