Journal Articles
- Furan-based Chalcone Annihilates the Multi-Drug-Resistant Pseudomonas aeruginosa and Protects Zebra Fish Against its Infection
-
Santosh Pushpa Ramya Ranjan Nayak , Catharine Basty , Seenivasan Boopathi , Loganathan Sumathi Dhivya , Khaloud Mohammed Alarjani , Mohamed Ragab Abdel Gawwad , Raghda Hager , Muthu Kumaradoss Kathiravan , Jesu Arockiaraj
-
J. Microbiol. 2024;62(2):75-89. Published online February 21, 2024
-
DOI: https://doi.org/10.1007/s12275-024-00103-6
-
-
22
View
-
0
Download
-
3
Citations
-
Abstract
- The emergence of carbapenem-resistant Pseudomonas aeruginosa, a multi-drug-resistant bacteria, is becoming a serious
public health concern. This bacterium infects immunocompromised patients and has a high fatality rate. Both naturally and
synthetically produced chalcones are known to have a wide array of biological activities. The antibacterial properties of
synthetically produced chalcone were studied against P. aeruginosa. In vitro, study of the compound (chalcone derivative
named DKO1), also known as (2E)-1-(5-methylfuran-2-yl)-3-(4-nitrophenyl) prop-2-en-1-one, had substantial antibacterial
and biofilm disruptive action. DKO1 effectively shielded against P. aeruginosa-induced inflammation, oxidative stress, lipid
peroxidation, and apoptosis in zebrafish larvae. In adult zebrafish, the treatment enhanced the chances of survivability and
reduced the sickness-like behaviors. Gene expression, biochemical analysis, and histopathology studies found that proinflammatory
cytokines (TNF-α, IL-1β, IL-6, iNOS) were down regulated; antioxidant enzymes such as superoxide dismutase
(SOD) and catalase (CAT) levels increased, and histoarchitecture was restored in zebrafish. The data indicate that DKO1 is
an effective antibacterial agent against P. aeruginosa demonstrated both in vitro and in vivo.
- Ultrasonic Treatment Enhanced Astaxanthin Production of Haematococcus pluvialis
-
Yun Hwan Park , Jaewon Park , Jeong Sik Choi , Hyun Soo Kim , Jong Soon Choi , Yoon-E Choi
-
J. Microbiol. 2023;61(6):633-639. Published online June 13, 2023
-
DOI: https://doi.org/10.1007/s12275-023-00053-5
-
-
18
View
-
0
Download
-
2
Citations
-
Abstract
- In this study, effects of ultrasonic treatment on Haematococcus pluvialis (H. pluvialis) were investigated. It has been confirmed
that the ultrasonic stimulation acted as stress resources in the red cyst stage H. pluvialis cells containing astaxanthin,
result
ing in additional astaxanthin production. With the increase in production of astaxanthin, the average diameter of H.
pluvialis cells increased accordingly. In addition, to determine how ultrasonic stimulation had an effect on the further biosynthesis
of astaxanthin, genes related to astaxanthin synthesis and cellular ROS level were measured. As a result, it was
confirmed that astaxanthin biosynthesis related genes and cellular ROS levels were increased, and thus ultrasonic stimulation
acts as an oxidative stimulus. These results support the notion on the effect of the ultrasonic treatment, and we believe
our novel approach based on the ultrasonic treatment would help to enhance the astaxanthin production from H. pluvialis.
Review
- The crosstalk between bacteria and host autophagy: host defense or bacteria offense
-
Lin Zheng , Fang Wei , Guolin Li
-
J. Microbiol. 2022;60(5):451-460. Published online April 29, 2022
-
DOI: https://doi.org/10.1007/s12275-022-2009-z
-
-
22
View
-
0
Download
-
6
Citations
-
Abstract
- Xenophagy is a specific selective autophagy for the elimination
of intracellular bacteria. Current evidence suggests that the
processes for host autophagy system to recognize and eliminate
invading bacteria are complex, and vary according to
different pathogens. Although both ubiquitin-dependent and
ubiquitin-independent autophagy exist in host to defense invading
bacteria, successful pathogens have evolved diverse
strategies to escape from or paralyze host autophagy system.
In this review, we discuss the mechanisms of host autophagy
system to recognize and eliminate intracellular pathogens and
the mechanisms of different pathogens to escape from or paralyze
host autophagy system, with a particular focus on the
most extensively studied bacteria.
Journal Article
- [PROTOCOL]A Signature-Tagged Mutagenesis (STM)-based murine-infectivity assay for Cryptococcus neoformans
-
Kwang-Woo Jung , Kyung-Tae Lee , Yong-Sun Bahn
-
J. Microbiol. 2020;58(10):823-831. Published online September 29, 2020
-
DOI: https://doi.org/10.1007/s12275-020-0341-8
-
-
18
View
-
0
Download
-
1
Citations
-
Abstract
- Signature-tagged mutagenesis (STM) is a high-throughput
genetic technique that can be used to investigate the function
of genes by constructing a large number of mutant strains
with unique DNA identification tags, pooling them, and screening
them for a particular phenotypic trait. STM was first designed
for the identification of genes that contribute to the
virulence or infectivity of a pathogen in its host. Recently, this
method
has also been applied for the identification of mutants
with specific phenotypes, such as antifungal drug resistance
and proliferation. In the present study, we describe an STM
method
for the identification of genes contributing to the infectivity
of Cryptococcus neoformans using a mutant library,
in which each strain was tagged with a unique DNA sequence.
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
-
-
18
View
-
0
Download
-
7
Citations
-
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.
- Characterization of cell death in Escherichia coli mediated by XseA, a large subunit of exonuclease VII
-
Hyeim Jung , Junwei Liang , Yuna Jung , Dongbin Lim
-
J. Microbiol. 2015;53(12):820-828. Published online December 2, 2015
-
DOI: https://doi.org/10.1007/s12275-015-5304-0
-
-
16
View
-
0
Download
-
12
Citations
-
Abstract
- Exonuclease VII (ExoVII) of Escherichia coli is a single strandspecific
DNA nuclease composed of two different subunits:
the large subunit, XseA, and the small subunit, XseB. In
this study, we found that multicopy single-stranded DNAs
(msDNAs), Ec83 and Ec78, are the in vivo substrates of
ExoVII; the enzyme cuts the phosphodiester bond between
the fourth and fifth nucleotides from the 5′ end. We used
this msDNA cleavage to assess ExoVII activity in vivo. Both
subunits were required for enzyme activity. Expression of
XseA without XseB caused cell death, even though no ExoVII
activity was detected. The lethality caused by XseA was rescued
by surplus XseB. In XseA-induced death, cells were
elongated and multinucleated, and their chromosomes were
fragmented and condensed; these are the morphological
hallmarks of apoptotic cell death in bacteria. A putative caspase
recognition sequence (FVAD) was found in XseA, and
its hypothetical caspase product with 257 amino acids was
as active as the intact protein in inducing cell death. We propose
that under ordinary conditions, XseA protects chromosome
as a component of the ExoVII enzyme, but in some
conditions, the protein causes cell death; the destruction of
cell is probably carried out by the amino terminal fragment
derived from the cleavage of XseA by caspase-like enzyme.
- Anti-tumor effect of Cordyceps militaris in HCV-infected human hepatocarcinoma 7.5 cells
-
Seulki Lee , Hwan Hee Lee , Jisung Kim , Joohee Jung , Aree Moon , Choon-Sik Jeong , Hyojeung Kang , Hyosun Cho
-
J. Microbiol. 2015;53(7):468-474. Published online June 27, 2015
-
DOI: https://doi.org/10.1007/s12275-015-5198-x
-
-
12
View
-
0
Download
-
11
Citations
-
Abstract
- Cordyceps extract has been reported to have various pharmacological
activities including an anti-cancer effect. We
investigated the inhibitory effect of Cordyceps militaris on
hepatitis C virus-infected human hepatocarcinoma 7.5 cells
(J6/JFH1-huh 7.5 cells). The huh7.5 cells with or without
HCV infection were treated with various concentrations of
ethanol extract of Cordyceps militaris (CME) for 48 h and the
cytotoxicity was measured by CCK-8 assay. Both J6/JFH1-
huh7.5 cells and huh7.5 cells were highly susceptible to CME.
To examine the molecular mechanisms of the inhibitory effect
on huh7.5 cells, the effect of CME on cell apoptosis was
measured using flow cytometry and the expressions of p53,
Bim, Bax, PARP, (cleaved) caspase-9, and (cleaved) caspase-
3 in huh 7.5 cells were detected by western blot assays. CME
significantly increased early apoptosis and up-regulated the
expression of Bim, Bax, cleaved PARP, cleaved caspase 9
and cleaved caspase-3. We also found the decrease of HCV
Core or NS3 protein by CME in HCV-infected huh 7.5 cells.
- VvpM, an Extracellular Metalloprotease of Vibrio vulnificus, Induces Apoptotic Death of Human Cells
-
Mi-Ae Lee , Jeong-A Kim , Yu Jin Yang , Mee-Young Shin , Soon-Jung Park , Kyu-Ho Lee
-
J. Microbiol. 2014;52(12):1036-1043. Published online November 3, 2014
-
DOI: https://doi.org/10.1007/s12275-014-4531-0
-
-
13
View
-
0
Download
-
20
Citations
-
Abstract
- A pathogenic bacterium, Vibrio vulnificus produces various
extracellular proteases including the elastolytic metalloprotease,
VvpE. In silico analysis of its genome revealed a VvpEhomologous
protease, VvpM whose proteolytic activity was
abolished by specific inhibitors against metalloproteases. To
investigate whether this newly identified protease has pathogenic
role in host interaction in addition to proteolytic role,
human cell lines were incubated with recombinant VvpM
(rVvpM). rVvpM-challenged cells showed typical morphological
changes found in cells under apoptosis. Apoptotic
cell death was further evidenced by estimating the Annexin
V-stained cells, whose proportions were dependent upon
the concentrations of rVvpM treated to human cells. To elucidate
the signaling pathway for VvpM-induced apoptosis,
three MAPKs were tested if their activation were mediated by
rVvpM. ERK1/2 was phosphorylated by treatment of rVvpM
and rVvpM-induced cell death was blocked by a specific inhibitor
against ERK1/2. In rVvpM-treated cells, the cytosolic
levels of cytochrome c were increased in a VvpM concentration-
dependent manner, while the levels of cytochrome c in
mitochondria were decreased. Cell deaths were accompanied
by apparent cleavages of procaspases-9 and -3 to the active
caspases-9 and -3, respectively. Therefore, this study demonstrates
that an extracellular metalloprotease of V. vulnificus,
VvpM induces apoptosis of human cells via a pathway consisting
of ERK activation, cytochrome c release, and then
activation of caspases-9 and -3.
- Effects of Fengycin from Bacillus subtilis fmbJ on Apoptosis and Necrosis in Rhizopus stolonifer
-
Qunyong Tang , Xiaomei Bie , Zhaoxin Lu , Fengxia Lv , Yang Tao , Xiaoxu Qu
-
J. Microbiol. 2014;52(8):675-680. Published online August 1, 2014
-
DOI: https://doi.org/10.1007/s12275-014-3605-3
-
-
12
View
-
0
Download
-
75
Citations
-
Abstract
- The lipopeptide antibiotic fengycin, produced by Bacillus subtilis, strongly inhibits growth of filamentous fungi. In this study, we evaluated the effects of fengycin treatment on apoptosis and necrosis in Rhizopus stolonifer by means of cell staining and epifluorescence microscopy. At fengycin concentrations less than 50 μg/ml, treated fungal cells demonstrated a dose-dependent increase in apoptosis-associated markers compared with the untreated control. These markers included chromatin condensation, reactive oxygen species accumulation, mitochondrial membrane potential depolarization, phosphatidylserine externalization, and the occurrence of DNA strand breaks. These results showed that fungal cells were impaired in a number of important functions and entered apoptosis upon treatment with low concentrations of fengycin. In contrast, high concentrations (>50 μg/ml) induced necrosis, indicating that the fungicidal action of fengycin operates via two modes: apoptosis at low concentrations and necrosis at high concentrations. Additionally, the apoptotic effect that we have shown suggests that lower concentrations of fengycin than previously thought may be effective for food preservation.
- 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
-
-
16
View
-
0
Download
-
7
Citations
-
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.
Journal Article
- Porphyromonas gingivalis-Derived Lipopolysaccharide-Mediated Activation of MAPK Signaling Regulates Inflammatory Response and Differentiation in Human Periodontal Ligament Fibroblasts
-
Taegun Seo , Seho Cha , Tae-Il Kim , Hee-Jung Park , Jeong-Soon Lee , Kyung Mi Woo
-
J. Microbiol. 2012;50(2):311-319. Published online April 27, 2012
-
DOI: https://doi.org/10.1007/s12275-012-2146-x
-
-
6
View
-
0
Download
-
31
Citations
-
Abstract
- Porphyromonas gingivalis (P.g.), which is a potential pathogen
for periodontal diseases, contains lipopolysaccharide
(LPS), and this endotoxin stimulates a variety of cellular
responses. At present, P.g.-derived LPS-induced cellular responses
in human periodontal ligament fibroblasts (PDLFs)
are not well characterized. Here, we demonstrate that P.gderived
LPS regulates inflammatory responses, apoptosis
and differentiation in PDLFs. Interleukin-6 (IL-6) and -8
(IL-8) were effectively upregulated by treatment of P.g.-derived
LPS, and we confirmed apoptosis markers including
elevated cytochrome c levels, active caspase-3 and morphological
change in the presence of P.g.-derived LPS. Moreover,
when PDLFs were cultured with differentiation media, P.g.-
derived LPS reduced the expression of differentiation marker
genes, as well as reducing alkaline phosphatase (ALP) activity
and mineralization. P.g.-derived LPS-mediated these
cellular responses were effectively abolished by treatment
of mitogen-activated protein kinase (MAPK) inhibitors.
Taken together, our results suggest that P.g.-derived LPS
regulates several cellular responses via activation of MAPK
signaling pathways in PDLFs.
Research Support, Non-U.S. Gov't
- Functional Analysis of the Inhibitor of Apoptosis Genes in Antheraea pernyi Nucleopolyhedrovirus
-
Feng Yan , Xiaobei Deng , Junpeng Yan , Jiancheng Wang , Lunguang Yao , Songya lv , Yipeng Qi , Hua Xu
-
J. Microbiol. 2010;48(2):199-205. Published online May 1, 2010
-
DOI: https://doi.org/10.1007/s12275-010-9108-y
-
-
11
View
-
0
Download
-
14
Citations
-
Abstract
- The inhibitor of apoptosis proteins (IAP) plays an important role in cell apoptosis. We cloned two novel IAP family members, Ap-iap1 and Ap-iap2, from Antheraea pernyi nucleopolyhedrovirus (ApNPV) genome. Ap-IAP1 contains two baculoviral IAP repeat (BIR) domains followed by a RING domain, but Ap-IAP2 has only one BIR domain and RING. The result of transient expression in Spodoptera frugiperda (Sf21) showed that Ap-iap1 blocked cell apoptosis induced by actinomycin D treatment and also rescued the p35 deficient Autographa californica nucleopolyhedrovirus (AcNPV) to replicate in Sf9 cells, while Ap-iap2 does not have this function. Several Ap-IAP1 truncations were constructed to test the activity of BIRs or RING motif to inhibit cell apoptosis. The results indicated that BIRs or RING of Ap-IAP1 had equally function to inhibit cell apoptosis. Therefore deletion of above both of the above domains could not block apoptosis induced by actinomycin D or rescue the replication of AcMNPV△p35. We also screened two phage-display peptides that might interact with Ap-IAP1.
Journal Article
- Ethanol Extract of Fermented Soybean, Chungkookjang, Inhibits the Apoptosis of Mouse Spleen, and Thymus Cells
-
Han Bok Kim , Hye Sung Lee , Sook Jin Kim , Hyung Jae Yoo , Jae Sung Hwang , Gang Chen , Hyun Joo Youn
-
J. Microbiol. 2007;45(3):256-261.
-
DOI: https://doi.org/2534 [pii]
-
-
Abstract
- Apoptosis is a step of the cell cycle which is important in the regulation of immune cell populations. Chungkookjang is a Korean traditional fermented soybean containing microorganisms, enzymes, and bioactive compounds which was used in the treatment of mouse spleen as well as thymus cells (CH1-fermented soybean containing barley, wormwood, and sea tangle; CH2-fermented soybean) and was found to exhibit substantially reduced small DNA fragmentation. An MTT assay showed that the treatment of CH1 and CH2 into the mouse splenocytes and thymocytes sharply increased their survival. Moreover, a FACS analysis also showed that CH1 and CH2 are effective at suppressing the apoptosis of splenocytes and thymocytes. The fermented soybean isoflavone concentrations, which are implicated in lowering breast and prostate cancers, lowering the risk of cardiovascular diseases, and improving bone health, were determined using Capillary Electrophoresis-Electrochemical Detection (CE-ED). The amount of Daidzein in fermented soybean significantly increased by 44-fold dramatically, compared with those in unfermented soybean. In this study, we demonstrated that ethanol extracts of Chungkookjang promote the survival of the mouse spleen and thymus cells in culture by suppressing their apoptotic death. Future studies should investigate which genes are related to apoptosis of the immune cells.
Research Support, Non-U.S. Gov't
- Molecular Taxonomy of a Soil Actinomycete Isolate, KCCM10454 Showing Neuroprotective Activity by 16S rRNA and rpoB Gene Analysis
-
Bong-Hee Lee , Hong Kim , Hyun-Ju Kim , Yoon-Kyu Lim , Kyung-Hee Byun , Brian Hutchinson , Chang-Jin Kim , Young-Hwan Ko , Keun-Hwa Lee , Chang-Yong Cha , Yoon-Hoh Kook , Bum-Joon Kim
-
J. Microbiol. 2005;43(2):213-218.
-
DOI: https://doi.org/2158 [pii]
-
-
Abstract
- Epilepsy constitutes a significant public health problem, and even the newest drugs and neurosurgical techniques have proven unable to cure the disease. In order to select a group of isolates which could generate an active compound with neuroprotective or antiepileptic properties, we isolated 517 actinomycete strains from soil samples taken from Jeju Island, in South Korea. We then screened these strains for possible anti-apoptotic effects against serum deprivation-induced hippocampal cell death, using the 3-(4, 5-dimethylthiazol-2-yl)2,5-diphenyl-tetrazolium bromide (MTT) assay as an in vitro test. The excitotoxic glutamate analog, kainic acid (KA), was used to induce seizures in experimental mice in our in vivo tests. As a result of this testing, we located one strain which exhibited profound neuroprotective activity. This strain was identified as a Streptomyces species, and exhibited the rifampin-resistant genotype, Asn(AAC)^442, according to the results of 16S rRNA and rpoB gene analyses
- Hepatitis C Virus Core Protein Sensitizes Cells to Apoptosis Induced by Anti-Cancer Drug
-
Kang, Mun Il , Cho, Mong , Kim, Sun Hee , Kang, Chi Dug , Kim, Dong Wan
-
J. Microbiol. 1999;37(2):90-96.
-
-
-
Abstract
- The core protein of the hepatitis C virus (HCV) is a multifunctional protein. The HCV core protein was reported to regulate cellular gene expression and transform primary rat embryo fibroblast cells. However, the role of the core protein in the pathogenesis of HCV-associated liver diseases is not well understood. To investigate the functional role of the core protein in cytophathogenicity, we have constructed stable expression systems of full length or truncated HCV core protein lacking the C-terminal hyderophobic domains and established HepG2 cell clones constitutively expressing the core protein. The full length core protein was localized in the cytoplasm and the C-terminal truncated core protein was localized in the nucleus. HepG2 cells expressing nuclear, truncated core protein showed elevated cell death during cultivation compared to untransfected cells and full length core-expressing cells. In the treatment with bleomycin, both cell clones expressing full length or truncated core protein appeared to be more sensitive to bleomycin than the parental HepG2 cells. These results suggest that the core protein may play a role in HCV pathogenesis promoting apoptotic cell death of infected cells.