Journal of Microbiology

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Pycnogenol reduces the expression of P. aeruginosa T3SS and inflammatory response in NCI-H292 cells: Seung-Ho Kim, Da Yun Seo, Sang-Bae Han, Un-Hwan Ha, Ji-Won Park, Kyung-Seop Ahn; Received March 4, 2025 Accepted July 31, 2025 Published online September 19, 2025; DOI: https://doi.org/10.71150/jm.2503004 [Epub ahead of print]

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Abstract PDF Supplementary Material: Nosocomial infections caused by Pseudomonas aeruginosa (P. aeruginosa) have become increasingly common, particularly among immunocompromised individuals, who experience high mortality rates and prolonged treatment durations due to the limited availability of effective therapies. In this study, we screened for anti-ExoS compounds targeting P. aeruginosa and identified pycnogenol (PYC) as a potent inhibitor of the type III secretion system (T3SS), a major virulence mechanism responsible for the translocation of effectors such as ExoS. Using ELISA, western blotting, and real-time PCR analyses in both P. aeruginosa and infected H292 cells, we found that PYC significantly reduced T3SS activity. Mechanistically, PYC suppressed the transcription of T3SS-related genes by downregulating exsA expression in P. aeruginosa. Furthermore, pretreatment with PYC attenuated the cytotoxic effects and reduced the expression of proinflammatory cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), and interleukin-18 (IL-18), in P. aeruginosa-infected H292 cells. These effects were associated with the inhibition of NF-κB signaling and inflammasome activation. Taken together, our findings suggest that PYC may serve as a promising therapeutic candidate against P. aeruginosa infections by targeting T3SS-mediated virulence and modulating host inflammatory responses.

Alizarin, which reduces ExoS, attenuates inflammation by P. aeruginosa in H292 cells: Seung-Ho Kim, Hye In Ahn, Jae-Hoon Oh, Da Yun Seo, Jung-Hee Kim, Ok-kyoung Kwon, Ji-Won Park, Kyung-Seop Ahn; J. Microbiol. 2025;63(5):e2411012. Published online May 27, 2025; DOI: https://doi.org/10.71150/jm.2411012

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Pseudomonas aeruginosa (P. aeruginosa) is resistant to several drugs as well as antibiotics and is thus classified as multidrug resistant and extensively drug resistant. These bacteria have a secretion system called the "type 3 secretion system (T3SS)", which facilitates infection by delivering an effector protein. ExoenzymeS (ExoS) is known to induce cell death and activate caspase-1. In particular, patients infected with P. aeruginosa develop diseases associated with high mortality, such as pneumonia, because no drug targets an ExoS or T3SS. We selected natural compounds to treat T3SS-mediated pneumonia and chose alizarin, a red dye. We confirmed the effects of alizarin on T3SS by bacterial PCR and ELISA. It was confirmed that alizarin regulates ExoS by inhibiting exsA but also popD and pscF. Furthermore, in infected H292 cells, it not only attenuates inflammation by inhibiting lipopolysaccharide (LPS)-induced phosphorylation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65 but also interferes with the level of ExoS delivered into the host and modulates caspase-1. We confirmed this result and determined that it led to decreases in proinflammatory cytokines such as Interleukin-1beta (IL-1β), Interleukin-6 (IL-6), and Interleukin-18 (IL-18). Therefore, we suggest that alizarin is a suitable drug for treating pneumonia caused by P. aeruginosa because it helps to attenuate inflammation by regulating T3SS and NF-κB signaling.

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Beyond pathogenicity: applications of the type III secretion system (T3SS) of Pseudomonas aeruginosa
Tianqi Su, Lin Zhang, Jie Shen, Danyu Qian, Yulei Guo, Zhenpeng Li
Frontiers in Microbiology.2025;[Epub] CrossRef

Journal Articles

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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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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Characteristics of Gut Microbiota in Patients with Polycystic Ovary Syndrome and Its Association with Metabolic Abnormalities: A Review
Shuang Liu, Linqi Cheng, Sen Li
International Journal of Women's Health.2025; Volume 17: 2165. CrossRef
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Research Advance on the Prevention and Treatment of Polycystic Ovary Syndrome Based on Dysbiosis of Gut Microbiota
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Genome Sequencing Highlights the Plant Cell Wall Degrading Capacity of Edible Mushroom Stropharia rugosoannulata: Mengpei Guo , Xiaolong Ma , Yan Zhou , Yinbing Bian , Gaolei Liu , Yingli Cai , Tianji Huang , Hongxia Dong , Dingjun Cai , Xueji Wan , Zhihong Wang , Yang Xiao , Heng Kang; J. Microbiol. 2023;61(1):83-93. Published online February 1, 2023; DOI: https://doi.org/10.1007/s12275-022-00003-7

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The basidiomycetous edible mushroom Stropharia rugosoannulata has excellent nutrition, medicine, bioremediation, and biocontrol properties. S. rugosoannulata has been widely and easily cultivated using agricultural by-products showing strong lignocellulose degradation capacity. However, the unavailable high-quality genome information has hindered the research on gene function and molecular breeding of S. rugosoannulata. This study provided a high-quality genome assembly and annotation from S. rugosoannulata monokaryotic strain QGU27 based on combined Illumina-Nanopore data. The genome size was about 47.97 Mb and consisted of 20 scaffolds, with an N50 of 3.73 Mb and a GC content of 47.9%. The repetitive sequences accounted for 17.41% of the genome, mostly long terminal repeats (LTRs). A total of 15,726 coding gene sequences were putatively identified with the BUSCO score of 98.7%. There are 142 genes encoding plant cell wall degrading enzymes (PCWDEs) in the genome, and 52, 39, 30, 11, 8, and 2 genes related to lignin, cellulose, hemicellulose, pectin, chitin, and cutin degradation, respectively. Comparative genomic analysis revealed that S. rugosoannulata is superior in utilizing aldehyde-containing lignins and is possible to utilize algae during the cultivation.

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Analysis of Gene Regulatory Network and Transcription Factors in Different Tissues of the Stropharia rugosoannulata Fruiting Body
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Journal of Fungi.2025; 11(2): 123. CrossRef
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Isolation and Structural Characterization of Melanins from Red and Yellow Varieties of Stropharia rugosoannulata
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Miao Gu, Qiang Chen, Yan Zhang, Yongchang Zhao, Li Wang, Xiangli Wu, Mengran Zhao, Wei Gao
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Research Support, Non-U.S. Gov'ts

Innate signaling mechanisms controlling Mycobacterium chelonae-mediated CCL2 and CCL5 expression in macrophages: Yi Sak Kim , Ji Hye Kim , Minjeong Woo , Tae-sung Kim Kim , Kyung Mok Sohn , Young-Ha Lee , Eun-Kyeong Jo , Jae-Min Yuk; J. Microbiol. 2015;53(12):864-874. Published online December 2, 2015; DOI: https://doi.org/10.1007/s12275-015-5348-1

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Abstract

Mycobacterium chelonae (Mch) is an atypical rapidly growing mycobacterium (RGM) that belongs to the M. chelonae complex, which can cause a variety of human infections. During this type of mycobacterial infection, macrophagederived chemokines play an important role in the mediation of intracellular communication and immune surveillance by which they orchestrate cellular immunity. However, the intracellular signaling pathways involved in the macrophage- induced chemokine production during Mch infections remain unknown. Thus, the present study aimed to determine the molecular mechanisms by which Mch activates the gene expressions of chemokine (C-C motif) ligand 2 (CCL2) and CCL5 in murine bone marrow-derived macrophages (BMDMs) and in vivo mouse model. Toll-like receptor 2 (TLR2)-deficient mice showed increased bacterial burden in spleen and lung and decreased protein expression of CCL2 and CCL5 in serum. Additionally, Mch infection triggered the mRNA and protein expression of CCL2 and CCL5 in BMDMs via TLR2 and myeloid differentiation primary response gene 88 (MyD88) signaling and that it rapidly activated nuclear factor (NF)-κB signaling, which is required for the Mch-induced expressions of CCL2 and CCL5 in BMDMs. Moreover, while the innate receptor Dectin-1 was only partly involved in the Mch-induced expression of the CCL2 and CCL5 chemokines in BMDMs, the generation of intracellular reactive oxygen species (ROS) was an important contributor to these processes. Taken together, the present data indicate that the TLR2, MyD88, and NF-κB pathways, Dectin-1 signaling, and intracellular ROS generation contribute to the Mch-mediated expression of chemokine genes in BMDMs.

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The Rise of Non-Tuberculosis Mycobacterial Lung Disease
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Huili Li, Boguang Sun, Xianhui Ning, Shuai Jiang, Li Sun
International Journal of Molecular Sciences.2019; 20(22): 5724. CrossRef
Abnormal Microglia and Enhanced Inflammation-Related Gene Transcription in Mice with Conditional Deletion ofCtcfinCamk2a-Cre-Expressing Neurons
Bryan E. McGill, Ruteja A. Barve, Susan E. Maloney, Amy Strickland, Nicholas Rensing, Peter L. Wang, Michael Wong, Richard Head, David F. Wozniak, Jeffrey Milbrandt
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Characterization of the rapamycin-inducible EBV LMP1 activation system: Sang Yong Kim , Jung-Eun Kim , Jiyeon Won , Yoon-Jae Song; J. Microbiol. 2015;53(10):732-738. Published online October 2, 2015; DOI: https://doi.org/10.1007/s12275-015-5455-z

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Abstract

Epstein-Barr virus (EBV) latent infection membrane protein 1 (LMP1) is required for EBV-mediated B lymphocyte transformation into proliferating lymphoblastoid cell lines (LCL). LMP1 oligomerizes spontaneously in membrane lipid rafts via its transmembrane domain and constitutively activates signal transduction pathways, including NF-κB, p38 Mitogen-Activated Protein Kinase (MAPK), and c-Jun N-terminal Kinase (JNK). Since LMP1 mimics the tumor necrosis factor receptor (TNFR), CD40, it may be effectively utilized to study the effects of constitutive activation of signal transduction pathways on cellular physiology. On the other hand, LMP1 presents a disadvantage in terms of determining the sequential events and factors involved in signaling pathways. A CD40-LMP1 chimeric molecule has been generated to overcome this limitation but does not represent the authentic and physiological nature of LMP1. In the current study, a ligand-dependent activation system for LMP1 using rapamycin-inducible dimerization was generated to delineate the LMP1 signaling pathway.

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Intestinal Intraepithelial TCRγδ+ T Cells are Activated by Normal Commensal Bacteria: Sang Phil Jeong , Jung-Ah Kang , Sung-Gyoo Park; J. Microbiol. 2012;50(5):837-841. Published online November 4, 2012; DOI: https://doi.org/10.1007/s12275-012-2468-8

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Abstract

TCRγδ+ T cells play a critical role in protecting the intestinal mucosa against pathogenic infection. In the absence of infection, TCRγδ+ T cell activation must be continuously regulated by T regulatory cells (Treg) to prevent the development of colitis. However, the activation of intestinal TCRγδ+ T cells under normal conditions has not been clearly resolved. In order to determine TCRγδ+ T cell activation in vivo, we designed an NF-κB based reporter system. Using the recombinant lentiviral method, we delivered the NF-κB reporter to isolated TCRγδ+ T cells, which were then adoptively transferred into normal mice. Our data indicate that the NF-κB activation level in TCRγδ+ T cells is higher in the intestinal intraepithelial layer than in the lamina propria region. In addition, the surface expression level of lymphocyte activation marker CD69 in TCRγδ+ T cells is also higher in the intestinal intraepithelial layer and this activation was reduced by Sulfatrim treatment which removes of commensal bacteria. Collectively, our data indicate that the TCRγδ+ T cell population attached to the intestinal lumen is constitutively activated even by normal commensal bacteria.

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