Journal of Microbiology

Journal Articles

Comparative Transcriptomic Analysis of Flagellar‑Associated Genes in Salmonella Typhimurium and Its rnc Mutant: Seungmok Han , Ji-Won Byun , Minho Lee; J. Microbiol. 2024;62(1):33-48. Published online January 5, 2024; DOI: https://doi.org/10.1007/s12275-023-00099-5

85 View
0 Download
3 Web of Science
2 Crossref

Salmonella enterica serovar Typhimurium (S. Typhimurium) is a globally recognized foodborne pathogen that affects both animals and humans. Endoribonucleases mediate RNA processing and degradation in the adaptation of bacteria to environmental changes and have been linked to the pathogenicity of S. Typhimurium. Not much is known about the specific regulatory mechanisms of these enzymes in S. Typhimurium, particularly in the context of environmental adaptation. Thus, this study carried out a comparative transcriptomic analysis of wild-type S. Typhimurium SL1344 and its mutant (Δrnc), which lacks the rnc gene encoding RNase III, thereby elucidating the detailed regulatory characteristics that can be attributed to the rnc gene. Global gene expression analysis revealed that the Δrnc strain exhibited 410 upregulated and 301 downregulated genes (fold-change > 1.5 and p < 0.05), as compared to the wild-type strain. Subsequent bioinformatics analysis indicated that these differentially expressed genes are involved in various physiological functions, in both the wild-type and Δrnc strains. This study provides evidence for the critical role of RNase III as a general positive regulator of flagellar-associated genes and its involvement in the pathogenicity of S. Typhimurium.

Citations

Citations to this article as recorded by

CspA regulates stress resistance, flagellar motility and biofilm formation in Salmonella Enteritidis
Xiang Li, Yan Cui, Xiaohui Sun, Chunlei Shi, Shoukui He, Xianming Shi
Food Bioscience.2025; 66: 106237. CrossRef
Influence of Flagella on Salmonella Enteritidis Sedimentation, Biofilm Formation, Disinfectant Resistance, and Interspecies Interactions
Huixue Hu, Jingguo Xu, Jingyu Chen, Chao Tang, Tianhao Zhou, Jun Wang, Zhuangli Kang
Foodborne Pathogens and Disease.2024;[Epub] CrossRef

Potent antibacterial and antibiofilm activities of TICbf-14, a peptide with increased stability against trypsin: Liping Wang , Xiaoyun Liu , Xinyue Ye , Chenyu Zhou , Wenxuan Zhao , Changlin Zhou , Lingman Ma; J. Microbiol. 2022;60(1):89-99. Published online December 29, 2021; DOI: https://doi.org/10.1007/s12275-022-1368-9

72 View
0 Download
2 Web of Science
2 Crossref

Abstract

The poor stability of peptides against trypsin largely limits their development as potential antibacterial agents. Here, to obtain a peptide with increased trypsin stability and potent antibacterial activity, TICbf-14 derived from the cationic peptide Cbf-14 was designed by the addition of disulfide-bridged hendecapeptide (CWTKSIPPKPC) loop. Subsequently, the trypsin stability and antimicrobial and antibiofilm activities of this peptide were evaluated. The possible mechanisms underlying its mode of action were also clarified. The results showed that TICbf-14 exhibited elevated trypsin inhibitory activity and effectively mitigated lung histopathological damage in bacteria-infected mice by reducing the bacterial counts, further inhibiting the systemic dissemination of bacteria and host inflammation. Additionally, TICbf-14 significantly repressed bacterial swimming motility and notably inhibited biofilm formation. Considering the mode of action, we observed that TICbf-14 exhibited a potent membrane-disruptive mechanism, which was attributable to its destructive effect on ionic bridges between divalent cations and LPS of the bacterial membrane. Overall, TICbf-14, a bifunctional peptide with both antimicrobial and trypsin inhibitory activity, is highly likely to become an ideal candidate for drug development against bacteria.

Citations

Citations to this article as recorded by

Modified polymeric biomaterials with antimicrobial and immunomodulating properties
Katarzyna Szałapata, Mateusz Pięt, Martyna Kasela, Marcin Grąz, Justyna Kapral-Piotrowska, Aleksandra Mordzińska-Rak, Elżbieta Samorek, Paulina Pieniądz, Jolanta Polak, Monika Osińska-Jaroszuk, Roman Paduch, Bożena Pawlikowska-Pawlęga, Anna Malm, Anna Jar
Scientific Reports.2024;[Epub] CrossRef
Epinecidin-1, a marine antifungal peptide, inhibits Botrytis cinerea and delays gray mold in postharvest peaches
Li Fan, Yingying Wei, Yi Chen, Shu Jiang, Feng Xu, Chundan Zhang, Hongfei Wang, Xingfeng Shao
Food Chemistry.2023; 403: 134419. CrossRef

Interaction between hypoviral-regulated fungal virulence factor laccase3 and small heat shock protein Hsp24 from the chestnut blight fungus Cryphonectria parasitica: Jeesun Chun† , Yo-Han Ko† , Dae-Hyuk Kim; J. Microbiol. 2022;60(1):57-62. Published online November 26, 2021; DOI: https://doi.org/10.1007/s12275-022-1498-0

59 View
0 Download
5 Web of Science
3 Crossref

Abstract

Laccase3 is an important virulence factor of the fungus Cryphonectria parasitica. Laccase3 gene (lac3) transcription is induced by tannic acid, a group of phenolic compounds found in chestnut trees, and its induction is regulated by the hypovirus CHV1 infection. CpHsp24, a small heat shock protein gene of C. parasitica, plays a determinative role in stress adaptation and pathogen virulence. Having uncovered in our previous study that transcriptional regulation of the CpHsp24 gene in response to tannic acid supplementation and CHV1 infection was similar to that of the lac3, and that conserved phenotypic changes of reduced virulence were observed in mutants of both genes, we inferred that both genes were implicated in a common pathway. Building on this finding, in this paper we examined whether the CpHsp24 protein (CpHSP24) was a molecular chaperone for the lac3 protein (LAC3). Our pull-down experiment indicated that the protein products of the two genes directly interacted with each other. Heterologous co-expression of CpHsp24 and lac3 genes using Saccharomyces cerevisiae resulted in more laccase activity in the cotransformant than in a parental lac3-expresssing yeast strain. These findings suggest that CpHSP24 is, in fact, a molecular chaperone for the LAC3, which is critical component of fungal pathogenesis.

Citations

Citations to this article as recorded by

Characteristics and expression of heat shock gene Lghsp17.4 in Lenzites gibbosa, a white rot fungus of wood
Lianrong Feng, Yujie Chi, Jian Zhang, Xuxin Yang, Shuying Han
Journal of Forestry Research.2024;[Epub] CrossRef
Hypovirus infection induces proliferation and perturbs functions of mitochondria in the chestnut blight fungus
Jinzi Wang, Rui Quan, Xipu He, Qiang Fu, Shigen Tian, Lijiu Zhao, Shuangcai Li, Liming Shi, Ru Li, Baoshan Chen
Frontiers in Microbiology.2023;[Epub] CrossRef
Applying molecular and genetic methods to trees and their fungal communities
Markus Müller, Ursula Kües, Katharina B. Budde, Oliver Gailing
Applied Microbiology and Biotechnology.2023; 107(9): 2783. CrossRef

PROTOCOL] Applications of different solvents and conditions for differential extraction of lipopolysaccharide in Gram-negative bacteria: Mai Phuong Nguyen , Le Viet Ha Tran , Hyun Namgoong , Yong-Hak Kim; J. Microbiol. 2019;57(8):644-654. Published online May 23, 2019; DOI: https://doi.org/10.1007/s12275-019-9116-5

59 View
0 Download
6 Web of Science
6 Crossref

Abstract

Lipopolysaccharide (LPS) is one of the major components in the outer membrane of Gram-negative bacteria. However, its heterogeneity and variability in different bacteria and differentiation conditions make it difficult to extract all of the structural variants. We designed a solution to improve quality and biological activity of LPS extracted from various bacteria with different types of LPS, as compared to conventional
methods
. We introduced a quality index as a simple measure of LPS purity in terms of a degree of polysaccharide content detected by absorbance at 204 nm. Further experiments using gel electrophoresis, endotoxin test, and macrophage activation test were performed to evaluate the performance and reliability of a proposed ‘T-sol’ method and the biological effectiveness and character of the LPS products. We presented that the T-sol method had differential effects on extraction of a RAW 264.7 cell-activating LPS, which was effective in the macrophage activation with similar effects in stimulating the production of TNF-alpha. In conclusion, the T-sol method provides a simple way to improve quality and biological activity of LPS with high yield.

Citations

Citations to this article as recorded by

Effective Modalities of Periodontitis Induction in Rat Model
Fazle Khuda, Badiah Baharin, Nur Najmi Mohamad Anuar, Bellen Sharon Fred Satimin, Nurrul Shaqinah Nasruddin
Journal of Veterinary Dentistry.2024; 41(1): 49. CrossRef
LPS-Induced Mortality in Zebrafish: Preliminary Characterisation of Common Fish Pathogens
Rafaela A. Santos, Cláudia Cardoso, Neide Pedrosa, Gabriela Gonçalves, Jorge Matinha-Cardoso, Filipe Coutinho, António P. Carvalho, Paula Tamagnini, Aires Oliva-Teles, Paulo Oliveira, Cláudia R. Serra
Microorganisms.2023; 11(9): 2205. CrossRef
Heterogeneity of Lipopolysaccharide as Source of Variability in Bioassays and LPS-Binding Proteins as Remedy
Alexandra C. Fux, Cristiane Casonato Melo, Sara Michelini, Benjamin J. Swartzwelter, Andreas Neusch, Paola Italiani, Martin Himly
International Journal of Molecular Sciences.2023; 24(9): 8395. CrossRef
Identification workflow of endotoxins by pyrolysis–gas chromatography–mass spectrometry based on a database and chemometrics
Jackie Jackie, Chun Kiang Chua, Norrapat Shih, Sam Fong Yau Li
Journal of Analytical and Applied Pyrolysis.2022; 165: 105547. CrossRef
Exploring the Lipidome: Current Lipid Extraction Techniques for Mass Spectrometry Analysis
Julian Aldana, Adriana Romero-Otero, Mónica P. Cala
Metabolites.2020; 10(6): 231. CrossRef
The outer membrane glycolipids of bacteria from cold environments: isolation, characterization, and biological activity
Angela Casillo, Ermenegilda Parrilli, Maria Luisa Tutino, Maria Michela Corsaro
FEMS Microbiology Ecology.2019;[Epub] CrossRef

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

A small hairpin RNA targeting myeloid cell leukemia-1 enhances apoptosis in host macrophages infected with Mycobacterium tuberculosis: Fei-yu Wang , Yu-qing Zhang , Xin-min Wang , Chan Wang , Xiao-fang Wang , Jiang-dong Wu , Fang Wu , Wan-jiang Zhang , Le Zhang; J. Microbiol. 2016;54(4):330-337. Published online April 1, 2016; DOI: https://doi.org/10.1007/s12275-016-5627-5

61 View
0 Download
5 Crossref

Abstract

Myeloid cell leukemia-1 (Mcl-1) plays an important role in various cell survival pathways. Some studies indicated that the expression of Mcl-1 was upregulated in host cells during infection with the virulent Mycobacterium tuberculosis strain, H37Rv. The present study was designed to investigate the effect of inhibiting Mcl-1 expression both in vivo and in vitro on apoptosis of host macrophages infected with M. tuberculosis using a small hairpin (sh)RNA. Mcl-1 expression was detected by the real time-polymerase chain reaction, western blotting, and immunohistochemistry. Flow cytometry and transmission electron microscopy were used to measure host macrophage apoptosis. We found elevated Mcl-1 levels in host macrophages infected with M. tuberculosis H37Rv. The expression of Mcl-1 was downregulated efficiently in H37Rv-infected host macrophages using shRNA. Knockdown of Mcl-1 enhanced the extent of apoptosis in H37Rv-infected host macrophages significantly. The increased apoptosis correlated with a decrease in M. tuberculosis colony forming units recovered from H37Rv-infected cells that were treated with Mcl-1-shRNA. Reducing Mcl-1 accumulation by shRNA also reduced accumulation of the anti-apoptotic gene, Bcl-2, and increased expression of the pro-apoptotic gene, Bax, in H37Rv-infected host macrophages. Our results showed that specific knockdown of Mcl-1 expression increased apoptosis of host macrophages significantly and decreased the intracellular survival of a virulent strain of M. tuberculosis. These data indicate that interference with Mcl-1 expression may provide a new avenue for tuberculosis therapy.

Citations

Citations to this article as recorded by

Tolerance of Listeria monocytogenes to biocides used in food processing environments
Sanelisiwe Thinasonke Duze, Musa Marimani, Mrudula Patel
Food Microbiology.2021; 97: 103758. CrossRef
Regulatory role and mechanism of the inhibition of the Mcl-1 pathway during apoptosis and polarization of H37Rv-infected macrophages
Ling Han, Yang Lu, Xiaofang Wang, Shujun Zhang, Yingzi Wang, Fang Wu, Wanjiang Zhang, Xinmin Wang, Le Zhang
Medicine.2020; 99(42): e22438. CrossRef
Current and emerging therapies to combat persistent intracellular pathogens
Philip Arandjelovic, Marcel Doerflinger, Marc Pellegrini
Current Opinion in Pharmacology.2019; 48: 33. CrossRef
PPARγ is critical for Mycobacterium tuberculosis induction of Mcl-1 and limitation of human macrophage apoptosis
Eusondia Arnett, Ashlee M. Weaver, Kiersten C. Woodyard, Maria J. Montoya, Michael Li, Ky V. Hoang, Andrew Hayhurst, Abul K. Azad, Larry S. Schlesinger, Thomas R. Hawn
PLOS Pathogens.2018; 14(6): e1007100. CrossRef
Effect of gap junctions on RAW264.7 macrophages infected with H37Rv
Yang Lu, Xin-min Wang, Pu Yang, Ling Han, Ying-zi Wang, Zhi-hong Zheng, Fang Wu, Wan-jiang Zhang, Le Zhang
Medicine.2018; 97(35): e12125. CrossRef

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

56 View
0 Download
3 Crossref

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.

Citations

Citations to this article as recorded by

The Rise of Non-Tuberculosis Mycobacterial Lung Disease
Champa N. Ratnatunga, Viviana P. Lutzky, Andreas Kupz, Denise L. Doolan, David W. Reid, Matthew Field, Scott C. Bell, Rachel M. Thomson, John J. Miles
Frontiers in Immunology.2020;[Epub] CrossRef
A Comparative Analysis of Edwardsiella tarda-Induced Transcriptome Profiles in RAW264.7 Cells Reveals New Insights into the Strategy of Bacterial Immune Evasion
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
The Journal of Neuroscience.2018; 38(1): 200. CrossRef

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

46 View
0 Download
5 Crossref

Abstract

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

Citations to this article as recorded by

Activation of Kruppel-like factor 6 by multi-walled carbon nanotubes in a diameter-dependent manner in THP-1 macrophages in vitro and bronchoalveolar lavage cells in vivo
Fengmei Song, Xiaomin Tang, Weichao Zhao, Chaobo Huang, Xuyan Dai, Yi Cao
Environmental Science: Nano.2023; 10(3): 855. CrossRef
Comparative analysis of lung and blood transcriptomes in mice exposed to multi-walled carbon nanotubes
Timur O. Khaliullin, Naveena Yanamala, Mackenzie S. Newman, Elena R. Kisin, Liliya M. Fatkhutdinova, Anna A. Shvedova
Toxicology and Applied Pharmacology.2020; 390: 114898. CrossRef
Non-Malignant Respiratory Illnesses in Association with Occupational Exposure to Asbestos and Other Insulating Materials: Findings from the Alberta Insulator Cohort
Subhabrata Moitra, Ali Farshchi Tabrizi, Kawtar Idrissi Machichi, Samineh Kamravaei, Noushin Miandashti, Linda Henderson, Manali Mukherjee, Fadi Khadour, Muhammad T. Naseem, Paige Lacy, Lyle Melenka
International Journal of Environmental Research and Public Health.2020; 17(19): 7085. CrossRef
The curious case of how mimicking physiological complexity in in vitro models of the human respiratory system influences the inflammatory responses. A preliminary study focused on gold nanoparticles
Dania Movia, Luisana Di Cristo, Roaa Alnemari, Joseph E. McCarthy, Hanane Moustaoui, Marc Lamy de la Chapelle, Jolanda Spadavecchia, Yuri Volkov, Adriele Prina‐Mello
Journal of Interdisciplinary Nanomedicine.2017; 2(2): 110. CrossRef
Molecular microbiology in antibacterial research
You-Hee Cho
Journal of Microbiology.2014; 52(3): 185. CrossRef

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

Lithium Inhibits Growth of Intracellular Mycobacterium kansasii through Enhancement of Macrophage Apoptosis: Hosung Sohn , Kwangwook Kim , Kil-Soo Lee , Han-Gyu Choi , Kang-In Lee , A-Rum Shin , Jong-Seok Kim , Sung Jae Shin , Chang-Hwa Song , Jeong-Kyu Park , Hwa-Jung Kim; J. Microbiol. 2014;52(4):299-306. Published online February 17, 2014; DOI: https://doi.org/10.1007/s12275-014-3469-6

64 View
0 Download
7 Crossref

Abstract

Mycobacterium kansasii (Mk) is an emerging pathogen that causes a pulmonary disease similar to tuberculosis. Macrophage apoptosis contributes to innate host defense against mycobacterial infection. Recent studies have suggested that lithium significantly enhances the cytotoxic activity of death stimuli in many cell types. We examined the effect of lithium on the viability of host cells and intracellular Mk in infected macrophages. Lithium treatment resulted in a substantial reduction in the viability of intracellular Mk in macrophages. Macrophage cell death was significantly enhanced after adding lithium to Mk-infected cells but not after adding to uninfected macrophages. Lithium-enhanced cell death was due to an apoptotic response, as evidenced by augmented DNA fragmentation and caspase activation. Reactive oxygen species were essential for lithium-induced apoptosis. Intracellular scavenging by N-acetylcysteine abrogated the lithiummediated decrease in intracellular Mk growth as well as apoptosis. These data suggest that lithium is associated with control of intracellular Mk growth through modulation of the apoptotic response in infected macrophages.

Citations

Citations to this article as recorded by

Recombinant Rv0753c Protein of Mycobacterium tuberculosis Induces Apoptosis Through Reactive Oxygen Species-JNK Pathway in Macrophages
Kang-In Lee, Seunga Choi, Han-Gyu Choi, Sintayehu Gurmessa Kebede, Thi Binh Dang, Yong Woo Back, Hye-Soo Park, Hwa-Jung Kim
Journal of Bacteriology and Virology.2020; 50(4): 246. CrossRef
Investigating the Role of Everolimus in mTOR Inhibition and Autophagy Promotion as a Potential Host-Directed Therapeutic Target in Mycobacterium tuberculosis Infection
Stephen Cerni, Dylan Shafer, Kimberly To, Vishwanath Venketaraman
Journal of Clinical Medicine.2019; 8(2): 232. CrossRef
Mycobacterium abscessus glycopeptidolipids inhibit macrophage apoptosis and bacterial spreading by targeting mitochondrial cyclophilin D
Jake Whang, Yong Woo Back, Kang-In Lee, Nagatoshi Fujiwara, Seungwha Paik, Chul Hee Choi, Jeong-Kyu Park, Hwa-Jung Kim
Cell Death & Disease.2017; 8(8): e3012. CrossRef
Invasion of Mammalian Cells by Rough Variant ofMycobacterium abscessus
Jake Whang, Young Woo Back, Gang-In Lee, Hwa-Jung Kim
Journal of Bacteriology and Virology.2016; 46(4): 193. CrossRef
Mycobacterium tuberculosis effectors interfering host apoptosis signaling
Minqiang Liu, Wu Li, Xiaohong Xiang, Jianping Xie
Apoptosis.2015; 20(7): 883. CrossRef
Targeting Batf2 for infectious diseases and cancer
Reto Guler, Sugata Roy, Harukazu Suzuki, Frank Brombacher
Oncotarget.2015; 6(29): 26575. CrossRef
Extended stability of cyclin D1 contributes to limited cell cycle arrest at G1-phase in BHK-21 cells with Japanese encephalitis virus persistent infection
Ji Young Kim, Soo Young Park, Hey Rhyoung Lyoo, Eung Seo Koo, Man Su Kim, Yong Seok Jeong
Journal of Microbiology.2015; 53(1): 77. CrossRef

Nucleotide-Binding Oligomerization Domain 2 (Nod2) Is Dispensable for the Innate Immune Responses of Macrophages against Yersinia enterocolitica: Yu-Jin Jeong , Chang-Hwan Kim , Eun-Jung Song , Min-Jung Kang , Jee-Cheon Kim , Sang-Muk Oh , Kyung-Bok Lee , Jong-Hwan Park; J. Microbiol. 2012;50(3):489-495. Published online June 30, 2012; DOI: https://doi.org/10.1007/s12275-012-1534-6

33 View
0 Download
8 Scopus

Abstract: Nucleotide-binding oligomerization domain 2 (Nod2) is a cytosolic sensor for muramyl dipeptide, a component of bacterial peptidoglycan. In this study, we have examined whether Nod2 mediates the immune response of macrophages against Yersinia enterocolitica. Bone-marrow-derived macrophages (BMDMs) were isolated from WT and Nod2-deficient mice and were infected with various strains of Y. enterocolitica. ELISA showed that the production of IL-6 and TNF-α in BMDMs infected with Y. enterocolitica was not affected by the Nod2 deficiency. iNOS mRNA expression was induced in both WT and Nod2-deficienct BMDMs in response to Y. enterocolitica, beginning 2 h after infection. Nitric oxide (NO) production by Y. enterocolitica did not differ between WT and Nod2-deficient BMDMs. Western blot analysis revealed that Y. enterocolitica induces activation of NF-κB, p38, and ERK MAPK through a Nod2-independent pathway. Neither LDH release by Y. enterocolitica nor the phagocytic activity of the macrophages was altered by Nod2 deficiency. An in vivo experiment showed that bacterial clearance ability and production of IL-6 and KC in serum were comparable in WT and Nod2-deficient mice infected with Y. enterocolitica. These findings suggest that Nod2 may not be critical for initiating the innate immune response of macrophages against Yersinia infection.

NOTE] IL-10 Suppresses Bactericidal Response of Macrophages against Salmonella Typhimurium: Kyoung-Sun Lee , Eui-Suk Jeong , Seung-Ho Heo , Jin-Hee Seo , Dong-Gu Jeong , Yang-Kyu Choi; J. Microbiol. 2011;49(6):1050-1053. Published online December 28, 2011; DOI: https://doi.org/10.1007/s12275-011-1043-z

32 View
0 Download
23 Scopus

Abstract: We report, herein, an attempt to determine whether an IL-10-induced immunological state affects the response of macrophages against Salmonella Typhimurium (ST). Pretreatment with mrIL-10 induced the intracellular invasion of ST into macrophages in a dose-dependent manner. It also activated AKT phosphorylation, cyclin D1, Bcl-XL, and COX-2 upon ST infection, which may correlate with Salmonella’s survival within the macrophages. However, I-κB phosphorylation was shown to be inhibited, along with the expression of TNF-α and MIP-2α mRNA. Therefore, IL-10 not only suppresses the bactericidal response of macrophages against ST, but also ultimately causes infected macrophages to function as hosts for ST replication.

Journal Article

Screening-Level Assays for Potentially Human-Infectious Environmental Legionella spp.: Helen Y. Buse , Abby Brehm , Jorge W. Santo Domingo , Nicholas J. Ashbolt; J. Microbiol. 2011;49(2):200-207. Published online May 3, 2011; DOI: https://doi.org/10.1007/s12275-011-0233-z

42 View
0 Download
7 Scopus

Abstract: In spite of the fact that various Legionella species are isolated from nonclinical water settings, there is no standard method to determine whether environmental legionellae may be infectious to humans. Here we provide a screening-level approach based on an in vivo murine (A/J mouse) model and three in vitro proliferation assays using Acanthamoeba polyphaga, and THP-1 human and J774 murine macrophage cell lines to identify potentially human-infectious legionellae. As an initial demonstration the infectivity potential of three clinical (Legionella pneumophila, L. longbeacheae, and L. micdadei) and three environmental (L. dumoffii, L. maceachernii, and L. sainthelensi) legionellae were evaluated. A/J mice were intranasally infected and by 6 h post infection (p.i.), there were significant bacterial titers in the lungs. L. pneumophila, L. dumoffii, and L. micdadei densities were higher than L. longbeacheae, L. maceacherni, and L. sainthelensi at 24 h p.i. However, only L. pneumophila and L. micdadei persisted in the lungs after 48 h, indicating that the other isolates were rapidly cleared. Results from the in vitro assays showed that only L. pneumophila significantly multiplied within A. polyphaga, THP-1 and J774 cells after 72 h, but lysis of any of the in vitro hosts also flagged the strains for potential concern (e.g. L. dumoffii and L. micdadei). The results demonstrate the value of using multiple approaches to assess the potential level of pathogenicity of Legionella strains isolated from different environmental matrices.

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

Virulence Attenuation of Streptococcus pneumoniae clpP Mutant by Sensitivity to Oxidative Stress in Macrophages via an NO-Mediated Pathway: Chul-Yong Park , Eun-Hye Kim , Sang-Yoon Choi , Thao Dang-Hien Tran , In-Hye Kim , Su-Nam Kim , Suhkneung Pyo , Dong-Kwon Rhee; J. Microbiol. 2010;48(2):229-235. Published online May 1, 2010; DOI: https://doi.org/10.1007/s12275-010-9300-0

43 View
0 Download
18 Crossref

Abstract

ClpP protease is essential for virulence and survival under stress conditions in several pathogenic bacteria. The clpP mutation in a murine infection model has demonstrated both attenuation of virulence and a sensitivity to hydrogen peroxide. However, the underlying mechanisms for these changes have not been resolved. Because macrophages play a major role in immune response and activated macrophages can kill microbes via oxygen-dependant mechanisms, we investigated the effect of the clpP mutation on its sensitivity to macrophage-mediated oxygen-dependant mechanisms. The clpP mutant derived from D39 (serotype 2) exhibited a higher sensitivity to oxidative stresses such as reactive oxygen intermediates, reactive nitrogen intermediates, and H2O2, but no sensitivity to osmotic stress (NaCl) and pH. Moreover, viability of the clpP mutant was significantly increased in murine macrophage cells by treatment with S-methylisothiourea sulfate, which inhibits inducible nitric oxide synthase (iNOS) activity and subsequently elicits lower level secretions of nitric oxide (NO). However, viability of wild type was unchanged. Taken together, these results indicate that ClpP is involved in the resistance to oxidative stresses after entrapment by macrophages and subsequently contributes to virulence via NO mediated pathway.

Citations

Citations to this article as recorded by

The oxidative stress response of Streptococcus pneumoniae: its contribution to both extracellular and intracellular survival
Mirelys Hernandez-Morfa, Nadia B. Olivero, Victoria E. Zappia, German E. Piñas, Nicolas M. Reinoso-Vizcaino, Melina B. Cian, Mariana Nuñez-Fernandez, Paulo R. Cortes, Jose Echenique
Frontiers in Microbiology.2023;[Epub] CrossRef
Pathogenicity and virulence ofStreptococcus pneumoniae: Cutting to the chase on proteases
Mary E. Marquart
Virulence.2021; 12(1): 766. CrossRef
ClpP participates in stress tolerance, biofilm formation, antimicrobial tolerance, and virulence of Enterococcus faecalis
Jinxin Zheng, Yang Wu, Zhiwei Lin, Guangfu Wang, Sibo Jiang, Xiang Sun, Haopeng Tu, Zhijian Yu, Di Qu
BMC Microbiology.2020;[Epub] CrossRef
Las proteasas de serina bacterianas y su implicación en la fisiopatología de la infección
Gerardo García-González, Gloria María González, José P. Palma-Nicolás
Revista del Laboratorio Clínico.2019; 12(3): 137. CrossRef
ClpP Protease, a Promising Antimicrobial Target
Carlos Moreno-Cinos, Kenneth Goossens, Irene G. Salado, Pieter Van Der Veken, Hans De Winter, Koen Augustyns
International Journal of Molecular Sciences.2019; 20(9): 2232. CrossRef
Identification and Characterization of Approved Drugs and Drug-Like Compounds as Covalent Escherichia coli ClpP Inhibitors
Elisa Sassetti, Cristina Durante Cruz, Päivi Tammela, Mathias Winterhalter, Koen Augustyns, Philip Gribbon, Björn Windshügel
International Journal of Molecular Sciences.2019; 20(11): 2686. CrossRef
α-Amino Diphenyl Phosphonates as Novel Inhibitors of Escherichia coli ClpP Protease
Carlos Moreno-Cinos, Elisa Sassetti, Irene G. Salado, Gesa Witt, Siham Benramdane, Laura Reinhardt, Cristina D. Cruz, Jurgen Joossens, Pieter Van der Veken, Heike Brötz-Oesterhelt, Päivi Tammela, Mathias Winterhalter, Philip Gribbon, Björn Windshügel, Koe
Journal of Medicinal Chemistry.2019; 62(2): 774. CrossRef
Characterization of Pectobacterium carotovorum proteins differentially expressed during infection of Zantedeschia elliotiana in vivo and in vitro which are essential for virulence
Huan Wang, Zhongling Yang, Shuo Du, Lin Ma, Yao Liao, Yujie Wang, Ian Toth, Jiaqin Fan
Molecular Plant Pathology.2018; 19(1): 35. CrossRef
Biological and Chemical Adaptation to Endogenous Hydrogen Peroxide Production in Streptococcus pneumoniae D39
John P. Lisher, Ho-Ching Tiffany Tsui, Smirla Ramos-Montañez, Kristy L. Hentchel, Julia E. Martin, Jonathan C. Trinidad, Malcolm E. Winkler, David P. Giedroc, Craig D. Ellermeier
mSphere.2017;[Epub] CrossRef
An ensemble-guided approach identifies ClpP as a major regulator of transcript levels in nitric oxide-stressed Escherichia coli
Jonathan L. Robinson, Mark P. Brynildsen
Metabolic Engineering.2015; 31: 22. CrossRef
Stress responses in Streptococcus species and their effects on the host
Cuong Thach Nguyen, Sang-Sang Park, Dong-Kwon Rhee
Journal of Microbiology.2015; 53(11): 741. CrossRef
Overexpression and Enzymatic Assessment of Antigenic Fragments of Hyaluronidase Recombinant Protein from Streptococcus pyogenes
Shabnam Sadoogh Abbasian, Ehsanollah Ghaznavi Rad, Neda Akbari, Mohammad Reza Zolfaghari, Iraj pakzad, Hamid Abtahi
Jundishapur Journal of Microbiology.2014;[Epub] CrossRef
Streptococcus pneumoniae and reactive oxygen species: an unusual approach to living with radicals
Hasan Yesilkaya, Vahid Farshchi Andisi, Peter W. Andrew, Jetta J.E. Bijlsma
Trends in Microbiology.2013; 21(4): 187. CrossRef
Streptococcus pneumoniae ClpP protease induces apoptosis via caspase-independent pathway in human neuroblastoma cells: Cytoplasmic relocalization of p53
Jun-Oh Lee, Ji-Yun Kim, Dong-Kwon Rhee, Suhkneung Pyo
Toxicon.2013; 70: 142. CrossRef
Alveolar macrophages in pulmonary host defence – the unrecognized role of apoptosis as a mechanism of intracellular bacterial killing
J D Aberdein, J Cole, M A Bewley, H M Marriott, D H Dockrell
Clinical and Experimental Immunology.2013; 174(2): 193. CrossRef
The Role of ClpP in Protein Expression of Streptococcus pneumoniae
Qun Zhang, Yuanshuai Huang, Hong Wang, Wenchun Xu, Lan Liu, Yibing Yin, Xuemei Zhang
Current Microbiology.2012; 64(3): 294. CrossRef
Pneumococcal Gene Complex Involved in Resistance to Extracellular Oxidative Stress
Vahid Farshchi Andisi, Cecilia A. Hinojosa, Anne de Jong, Oscar P. Kuipers, Carlos J. Orihuela, Jetta J. E. Bijlsma, J. N. Weiser
Infection and Immunity.2012; 80(3): 1037. CrossRef
A proteome analysis of the response of a Pseudomonas aeruginosa oxyR mutant to iron limitation
Tiffany Vinckx, Qing Wei, Sandra Matthijs, Jean-Paul Noben, Ruth Daniels, Pierre Cornelis
BioMetals.2011; 24(3): 523. CrossRef

Expression of c-Myc Is Related to Host Cell Death Following Salmonella typhimurium Infection in Macrophage: Jihyoun Seong , Hong Hua Piao , Phil Yeoul Ryu , Youn Uck Kim , Hyon E Choy , Yeongjin Hong; J. Microbiol. 2009;47(2):214-219. Published online May 2, 2009; DOI: https://doi.org/10.1007/s12275-008-0308-7

42 View
0 Download
5 Scopus

Abstract: It has been known that ornithine decarboxylase (ODC) induced by the binding of c-Myc to odc gene is closely linked to cell death. Here, we investigated the relationship between their expressions and cell death in macrophage cells following treatment with Salmonella typhimurium or lipopolysaccharide (LPS). ODC expression was increased by bacteria or LPS and repressed by inhibitors against mitogen-activated protein kinases (MAPKs) in Toll-like receptor 4 (TLR4) signaling pathway. In contrast, c-Myc protein level was increased after treatment with bacteria, but not by treatment with LPS or heat-killed bacteria although both bacteria and LPS increased the levels of c-myc mRNA to a similar extent. c-Myc protein level is dependent upon bacterial invasion because treatment with cytochalasin D (CCD), inhibitors of endocytosis, decreased c-Myc protein level. The cell death induced by bacteria was significantly decreased after treatment of CCD or c-Myc inhibitor, indicating that cell death by S. typhimurium infection is related to c-Myc, but not ODC. Consistent with this conclusion, treatment with bacteria mutated to host invasion did not increase c-Myc protein level and cell death rate. Taken together, it is suggested that induction of c-Myc by live bacterial infection is directly related to host cell death.

Journal Articles

Induction of Cytokines and Nitric Oxide in Murine Macrophages Stimulated with Enzymatically Digested Lactobacillus Strains: Dong Woon Kim , Sung Back Cho , Cheol Heui Yun , Ha Yeon Jeong , Wan Tae Chung , Chang Weon Choi , Hyun Jeong Lee , In Sik Nam , Guk Hyun Suh , Sang Suk Lee , Byong Seak Lee; J. Microbiol. 2007;45(5):373-378.; DOI: https://doi.org/2601 [pii]

40 View
0 Download

Abstract: Based on observations that lactic acid bacteria have the ability to activate macrophages, we assessed the potential effects of eight different Lactobacillus strains treated with gastrointestinal enzymes on the production of nitric oxide and various cytokines in macrophages. RAW 264.7 murine macrophage cells were cultured with either precipitates or supernatants of Lactobacillus strains digested with pepsin followed by pancreatin. The increased production of nitric oxide and interleukin (IL)-1β, IL-6, IL-12 and tumour necrosis factor (TNF)-α were observed when cultured with precipitates, and this effect was largely strain-dependent. In contrast, the exposure of RAW 264.7 cells to supernatants produced weaker or nearly undetectable effects in comparison to the effects of exposure to precipitates. The induction of nitric oxide appeared to be unaffected. These results demonstrate that nitric oxide and cytokines were effectively induced when the bacterial precipitate was treated with macrophages. The results of the present study also indicate that Lactobacillus strains treated with digestive enzymes are capable of stimulating the production of nitric oxide and cytokines in macrophages, which may modulate the gastrointestinal immune function of the host when it is given as a feed additive.

Comparison of Cytokine and Nitric Oxide Induction in Murine Macrophages between Whole Cell and Enzymatically Digested Bifidobacterium sp. Obtained from Monogastric Animals: Dong Woon Kim , Sung Back Cho , Hyun Jeong Lee , Wan Tae Chung , Kyoung Hoon Kim , Jong Hwangbo , In Sik Nam , Young Il Cho , Mhan Pyo Yang , Il Byung Chung; J. Microbiol. 2007;45(4):305-310.; DOI: https://doi.org/2568 [pii]

43 View
0 Download

Abstract: The principal objective of this study was to compare the effects of whole and hydrolyzed cells (bifidobacteria) treated with gastrointestinal digestive enzymes on the activation of cloned macrophages. Seven different strains of Bifidobacterium obtained from swine, chickens, and rats, were digested with pepsin followed by pancreatin and the precipitate (insoluble fraction) and supernatant (soluble fraction) obtained via centrifugation. The RAW 264.7 murine macrophages were incubated with either whole cells, the precipitate, or supernatant at various concentrations. Pronounced increases in the levels of nitric oxide (NO), interleukin (IL)-1β, IL-6, IL-12, and tumor necrosis factor (TNF)-α were observed in the whole cells and precipitates, but these effects were less profound in the supernatants. The precipitates also evidenced a slight, but significant, inductive activity for NO and all tested cytokines, with the exception of TNF-α in the macrophage model as compared with the whole cells. By way of contrast, TNF-α production when cultured with whole cells (100 ng/ml) resulted in marked increases as compared with what was observed with the precipitates. The results of this study indicated, for the first time, that digested Bifidobacterium sp. can induce the production of NO and several cytokines in RAW 264.7 murine macrophage cells. In the current study, it was demonstrated that Bifidobacterium strains treated with digestive enzymes, as compared with whole cells, are capable of stimulating the induction of macrophage mediators, which reflects that they may be able to modulate the gastrointestinal immune functions of the host.

First
Prev
Page of 2
Next
Last

Search