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Article: Enterotoxin genes, biofilm formation, and antimicrobial and disinfectant resistance of Bacillus cereus isolates from primary producing stages

Hwang, Daekeun / Oh, Tae Young / Baek, Seung-Yeob / Kang, Mi Seon / Hong, Seok-In / Kim, Hyun Jung

Food control. 2022 Nov., v. 141

2022

Abstract: In this study, we analyzed enterotoxin genes, biofilm formation, and resistance to sixteen antimicrobials and chlorine dioxide (ClO₂) in Bacillus cereus group isolates (n = 76) from samples (leaves, seeds, water and nutrients, and soil) from microgreen ... ...

Abstract	In this study, we analyzed enterotoxin genes, biofilm formation, and resistance to sixteen antimicrobials and chlorine dioxide (ClO₂) in Bacillus cereus group isolates (n = 76) from samples (leaves, seeds, water and nutrients, and soil) from microgreen primary producing farms. Most isolates possessed at least one enterotoxin gene, as well as resistance to β-lactam antimicrobials, and more than half of the isolates showed moderate to strong biofilm-forming ability. Several B. cereus isolates with strong biofilm-forming ability survived ClO₂ treatment, thereby preventing their decontamination in samples from microgreen producing farms. When the B. cereus group isolates were treated with ClO₂ for 5 min, antimicrobial resistance to rifampin and gentamicin increased. These results provide a useful insight into the development of risk management technologies to ensure the food safety of fresh produce, including microgreens, with a particular focus on the primary production stages.
Keywords	Bacillus cereus ; antibiotic resistance ; biofilm ; chlorine dioxide ; decontamination ; disinfectants ; enterotoxins ; food safety ; fresh produce ; genes ; gentamicin ; microgreens ; primary productivity ; rifampicin ; risk management ; soil
Language	English
Dates of publication	2022-11
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	1027805-9
ISSN	0956-7135
ISSN	0956-7135
DOI	10.1016/j.foodcont.2022.109196
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: p70S6K on astrocytes protects dopamine neurons from 1-methyl-4-phenylpyridinium neurotoxicity.

Kim, Kyoung In / Baek, Jeong Yeob / Chung, Young Cheul / Nam, Jin Han / Shin, Won-Ho / Jin, Byung Kwan

Glia

2021 Volume 69, Issue 9, Page(s) 2133–2145

Abstract: Our recent finding has demonstrated that astrocytes confer neuroprotection by endogenously producing ciliary neurotrophic factor (CNTF) via transient receptor potential vanilloid 1 (TRPV1) in Parkinson's disease (PD). In this study, the possible ... ...

Abstract	Our recent finding has demonstrated that astrocytes confer neuroprotection by endogenously producing ciliary neurotrophic factor (CNTF) via transient receptor potential vanilloid 1 (TRPV1) in Parkinson's disease (PD). In this study, the possible molecular target for TRPV1-mediated CNTF production and its neuroprotective effects on dopamine neurons were further investigated. For comparison, glial cell-line derived neurotrophic factor (GDNF) was also examined. The results show that TRPV1-ribosomal protein 70 S6 kinase (p70S6K) signaling on astrocytes produces endogenous CNTF in the SN of MPP
MeSH term(s)	1-Methyl-4-phenylpyridinium/metabolism ; 1-Methyl-4-phenylpyridinium/toxicity ; Animals ; Astrocytes/metabolism ; Dopaminergic Neurons/metabolism ; Glial Cell Line-Derived Neurotrophic Factor/metabolism ; Humans ; Neuroprotective Agents/pharmacology ; Rats ; Ribosomal Protein S6 Kinases, 70-kDa/metabolism ; Ribosomal Protein S6 Kinases, 70-kDa/pharmacology ; Substantia Nigra/metabolism
Chemical Substances	Glial Cell Line-Derived Neurotrophic Factor ; Neuroprotective Agents ; Ribosomal Protein S6 Kinases, 70-kDa (EC 2.7.11.1) ; 1-Methyl-4-phenylpyridinium (R865A5OY8J)
Language	English
Publishing date	2021-05-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.24013
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Article ; Online: Loss of Acot12 contributes to NAFLD independent of lipolysis of adipose tissue.

Park, Sujeong / Song, Jinsoo / Baek, In-Jeoung / Jang, Kyu Yun / Han, Chang Yeob / Jun, Dae Won / Kim, Peter K / Raught, Brian / Jin, Eun-Jung

Experimental & molecular medicine

2021 Volume 53, Issue 7, Page(s) 1159–1169

Abstract: In this study, we hypothesized that deregulation in the maintenance of the pool of coenzyme A (CoA) may play a crucial role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Specific deletion of Acot12 ( ... ...

Abstract	In this study, we hypothesized that deregulation in the maintenance of the pool of coenzyme A (CoA) may play a crucial role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Specific deletion of Acot12 (Acot12
MeSH term(s)	Acetyl Coenzyme A/metabolism ; Animals ; Cholesterol/biosynthesis ; Cholesterol/genetics ; Diet, High-Fat/adverse effects ; Female ; Humans ; Lipids/biosynthesis ; Lipids/genetics ; Lipogenesis/physiology ; Lipolysis/physiology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Obese ; Non-alcoholic Fatty Liver Disease/genetics ; Non-alcoholic Fatty Liver Disease/metabolism ; PPAR alpha/genetics ; PPAR alpha/metabolism ; Pregnancy ; Thiolester Hydrolases/genetics ; Thiolester Hydrolases/metabolism ; Mice
Chemical Substances	Lipids ; PPAR alpha ; Ppara protein, mouse ; Acetyl Coenzyme A (72-89-9) ; Cholesterol (97C5T2UQ7J) ; ACOT12 protein, human (EC 3.1.2.-) ; Thiolester Hydrolases (EC 3.1.2.-)
Language	English
Publishing date	2021-07-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1328915-9
ISSN	2092-6413 ; 1226-3613 ; 0378-8512
ISSN (online)	2092-6413
ISSN	1226-3613 ; 0378-8512
DOI	10.1038/s12276-021-00648-1
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Article ; Online: Fecal microbiota transplantation ameliorates atherosclerosis in mice with C1q/TNF-related protein 9 genetic deficiency.

Kim, Eun Sil / Yoon, Bo Hyun / Lee, Seung Min / Choi, Min / Kim, Eun Hye / Lee, Byong-Wook / Kim, Sang-Yeob / Pack, Chan-Gi / Sung, Young Hoon / Baek, In-Jeoung / Jung, Chang Hee / Kim, Tae-Bum / Jeong, Jin-Yong / Ha, Chang Hoon

Experimental & molecular medicine

2022 Volume 54, Issue 2, Page(s) 103–114

Abstract: Despite the strong influence of the gut microbiota on atherosclerosis, a causal relationship between atherosclerosis pathophysiology and gut microbiota is still unverified. This study was performed to determine the impact of the gut microbiota on the ... ...

Abstract	Despite the strong influence of the gut microbiota on atherosclerosis, a causal relationship between atherosclerosis pathophysiology and gut microbiota is still unverified. This study was performed to determine the impact of the gut microbiota on the pathogenesis of atherosclerosis caused by genetic deficiency. To elucidate the influence of the gut microbiota on atherosclerosis pathogenesis, an atherosclerosis-prone mouse model (C1q/TNF-related protein 9-knockout (CTRP9-KO) mice) was generated. The gut microbial compositions of CTRP9-KO and WT control mice were compared. Fecal microbiota transplantation (FMT) was performed to confirm the association between gut microbial composition and the progression of atherosclerosis. FMT largely affected the gut microbiota in both CTRP9-KO and WT mice, and all transplanted mice acquired the gut microbiotas of the donor mice. Atherosclerotic lesions in the carotid arteries were decreased in transplanted CTRP9-KO mice compared to CTRP9-KO mice prior to transplantation. Conversely, WT mice transplanted with the gut microbiotas of CTRP9-KO mice showed the opposite effect as that of CTRP9-KO mice transplanted with the gut microbiotas of WT mice. Here, we show that CTRP9 gene deficiency is related to the distribution of the gut microbiota in subjects with atherosclerosis. Transplantation of WT microbiotas into CTRP9-KO mice protected against the progression of atherosclerosis. Conversely, the transplantation of CTRP9-KO microbiotas into WT mice promoted the progression of atherosclerosis. Treating atherosclerosis by restoring gut microbial homeostasis may be an effective therapeutic strategy.
MeSH term(s)	Adiponectin/genetics ; Adiponectin/metabolism ; Animals ; Atherosclerosis/genetics ; Atherosclerosis/therapy ; Complement C1q ; Fecal Microbiota Transplantation ; Gastrointestinal Microbiome ; Glycoproteins/genetics ; Glycoproteins/metabolism ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Knockout
Chemical Substances	Adiponectin ; CTRP9 protein, mouse ; Glycoproteins ; Complement C1q (80295-33-6)
Language	English
Publishing date	2022-02-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1328915-9
ISSN	2092-6413 ; 1226-3613 ; 0378-8512
ISSN (online)	2092-6413
ISSN	1226-3613 ; 0378-8512
DOI	10.1038/s12276-022-00728-w
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Article: Delayed Treatment of Capsaicin Produces Partial Motor Recovery by Enhancing Dopamine Function in MPP

Kim, Kyoung In / Baek, Jeong Yeob / Jeong, Jae Yeong / Nam, Jin Han / Park, Eun Su / Bok, Eugene / Shin, Won-Ho / Chung, Young Cheul / Jin, Byung Kwan

Experimental neurobiology

2019 Volume 28, Issue 2, Page(s) 289–299

Abstract: Transient receptor potential vanilloid subtype 1 (TRPV1) on astrocytes prevents ongoing degeneration of nigrostriatal dopamine (DA) neurons in ... ...

Abstract	Transient receptor potential vanilloid subtype 1 (TRPV1) on astrocytes prevents ongoing degeneration of nigrostriatal dopamine (DA) neurons in MPP
Language	English
Publishing date	2019-03-20
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	2639017-6
ISSN	2093-8144 ; 1226-2560
ISSN (online)	2093-8144
ISSN	1226-2560
DOI	10.5607/en.2019.28.2.289
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Article ; Online: Inhibition of Microglia-Derived Oxidative Stress by Ciliary Neurotrophic Factor Protects Dopamine Neurons In Vivo from MPP + Neurotoxicity

Jeong Yeob Baek / Jae Yeong Jeong / Kyoung In Kim / So-Yoon Won / Young Cheul Chung / Jin Han Nam / Eun Ju Cho / Tae-Beom Ahn / Eugene Bok / Won-Ho Shin / Byung Kwan Jin

International Journal of Molecular Sciences, Vol 19, Iss 11, p

2018 Volume 3543

Abstract: We demonstrated that capsaicin (CAP), an agonist of transient receptor potential vanilloid subtype 1 (TRPV1), inhibits microglia activation and microglia-derived oxidative stress in the substantia nigra (SN) of MPP + -lesioned rat. However, the detailed ... ...

Abstract	We demonstrated that capsaicin (CAP), an agonist of transient receptor potential vanilloid subtype 1 (TRPV1), inhibits microglia activation and microglia-derived oxidative stress in the substantia nigra (SN) of MPP + -lesioned rat. However, the detailed mechanisms how microglia-derived oxidative stress is regulated by CAP remain to be determined. Here we report that ciliary neurotrophic factor (CNTF) endogenously produced by CAP-activated astrocytes through TRPV1, but not microglia, inhibits microglial activation and microglia-derived oxidative stress, as assessed by OX-6 and OX-42 immunostaining and hydroethidine staining, respectively, resulting in neuroprotection. The significant increase in levels of CNTF receptor alpha (CNTFRα) expression was evident on microglia in the MPP + -lesioned rat SN and the observed beneficial effects of CNTF was abolished by treatment with CNTF receptor neutralizing antibody. It is therefore likely that CNTF can exert its effect via CNTFRα on microglia, which rescues dopamine neurons in the SN of MPP + -lesioned rats and ameliorates amphetamine-induced rotations. Immunohistochemical analysis revealed also a significantly increased expression of CNTFRα on microglia in the SN from human Parkinson’s disease patients compared with age-matched controls, indicating that these findings may have relevance to the disease. These data suggest that CNTF originated from TRPV1 activated astrocytes may be beneficial to treat neurodegenerative disease associated with neuro-inflammation such as Parkinson’s disease.
Keywords	Parkinson’s disease ; Microglia ; Ciliary neurotrophic factor ; Ciliary neurotrophic factor receptor ; oxidative stress ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	333
Language	English
Publishing date	2018-11-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Inhibition of Microglia-Derived Oxidative Stress by Ciliary Neurotrophic Factor Protects Dopamine Neurons In Vivo from MPP⁺ Neurotoxicity.

Baek, Jeong Yeob / Jeong, Jae Yeong / Kim, Kyoung In / Won, So-Yoon / Chung, Young Cheul / Nam, Jin Han / Cho, Eun Ju / Ahn, Tae-Beom / Bok, Eugene / Shin, Won-Ho / Jin, Byung Kwan

International journal of molecular sciences

2018 Volume 19, Issue 11

Abstract	We demonstrated that capsaicin (CAP), an agonist of transient receptor potential vanilloid subtype 1 (TRPV1), inhibits microglia activation and microglia-derived oxidative stress in the substantia nigra (SN) of MPP⁺-lesioned rat. However, the detailed mechanisms how microglia-derived oxidative stress is regulated by CAP remain to be determined. Here we report that ciliary neurotrophic factor (CNTF) endogenously produced by CAP-activated astrocytes through TRPV1, but not microglia, inhibits microglial activation and microglia-derived oxidative stress, as assessed by OX-6 and OX-42 immunostaining and hydroethidine staining, respectively, resulting in neuroprotection. The significant increase in levels of CNTF receptor alpha (CNTFRα) expression was evident on microglia in the MPP⁺-lesioned rat SN and the observed beneficial effects of CNTF was abolished by treatment with CNTF receptor neutralizing antibody. It is therefore likely that CNTF can exert its effect via CNTFRα on microglia, which rescues dopamine neurons in the SN of MPP⁺-lesioned rats and ameliorates amphetamine-induced rotations. Immunohistochemical analysis revealed also a significantly increased expression of CNTFRα on microglia in the SN from human Parkinson's disease patients compared with age-matched controls, indicating that these findings may have relevance to the disease. These data suggest that CNTF originated from TRPV1 activated astrocytes may be beneficial to treat neurodegenerative disease associated with neuro-inflammation such as Parkinson's disease.
MeSH term(s)	1-Methyl-4-phenylpyridinium/toxicity ; Aged ; Animals ; Astrocytes/drug effects ; Astrocytes/metabolism ; Astrocytes/pathology ; Capsaicin/pharmacology ; Cell Survival/drug effects ; Ciliary Neurotrophic Factor/pharmacology ; Dopaminergic Neurons/drug effects ; Dopaminergic Neurons/metabolism ; Dopaminergic Neurons/pathology ; Female ; Gene Knockdown Techniques ; Humans ; Male ; Microglia/drug effects ; Microglia/metabolism ; Microglia/pathology ; Models, Biological ; Nerve Degeneration/pathology ; Neuroprotection/drug effects ; Neurotoxicity Syndromes/pathology ; Oxidative Stress/drug effects ; RNA, Small Interfering/metabolism ; Rats, Sprague-Dawley ; Reactive Oxygen Species/metabolism ; Receptor, Ciliary Neurotrophic Factor/metabolism ; Substantia Nigra/drug effects ; Substantia Nigra/metabolism ; Substantia Nigra/pathology ; TRPV Cation Channels/metabolism
Chemical Substances	Ciliary Neurotrophic Factor ; RNA, Small Interfering ; Reactive Oxygen Species ; Receptor, Ciliary Neurotrophic Factor ; TRPV Cation Channels ; TRPV1 receptor ; 1-Methyl-4-phenylpyridinium (R865A5OY8J) ; Capsaicin (S07O44R1ZM)
Language	English
Publishing date	2018-11-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms19113543
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Article ; Online: Correction to: Contribution of Zinc-Dependent Delayed Calcium Influx via TRPC5 in Oxidative Neuronal Death and its Prevention by Novel TRPC Antagonist.

Park, Sang Eun / Song, Ji Hoon / Hong, Chansik / Kim, Dong Eun / Sul, Jee-Won / Kim, Tae-Youn / Seo, Bo-Ra / So, Insuk / Kim, Sang-Yeob / Bae, Dong-Jun / Park, Mi-Ha / Lim, Hye Min / Baek, In-Jeoung / Riccio, Antonio / Lee, Joo-Yong / Shim, Woo Hyun / Park, Bumwoo / Koh, Jae-Young / Hwang, Jung Jin

Molecular neurobiology

2018 Volume 56, Issue 4, Page(s) 2836–2837

Abstract: After the publication of this work errors were noticed in Fig. 3b and 4d. ...

Abstract	After the publication of this work errors were noticed in Fig. 3b and 4d.
Language	English
Publishing date	2018-12-12
Publishing country	United States
Document type	Published Erratum
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-018-1447-4
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Zs.A 2411: Show issues

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Article: Interleukin-4 receptor-targeted delivery of Bcl-xL siRNA sensitizes tumors to chemotherapy and inhibits tumor growth

Guruprasath, Padmanaban / Jihoon Kim / Gowri Rangaswamy Gunassekaran / Lianhua Chi / Soyoun Kim / Rang-Woon Park / Sang-Hyun Kim / Moon-Chang Baek / Sang Mun Bae / Sang-Yeob Kim / Dong-Kyu Kim / In-Kyu Park / Won-Jong Kim / Byungheon Lee

Biomaterials. 2017 Oct., v. 142

2017

Abstract: IL-4 receptor (IL-4R) is commonly up-regulated on tumor cells, and interactions between the receptor and Interleukin-4 (IL-4) can induce the expression of anti-apoptotic proteins, including Bcl-xL. This contributes to tumor cell survival and their ... ...

Abstract	IL-4 receptor (IL-4R) is commonly up-regulated on tumor cells, and interactions between the receptor and Interleukin-4 (IL-4) can induce the expression of anti-apoptotic proteins, including Bcl-xL. This contributes to tumor cell survival and their resistance to chemotherapy. In this study, we exploited IL-4R-targeted delivery of Bcl-xL siRNA to IL-4R-expressing tumor cells in order to sensitize them to chemotherapy. To target IL-4R, an IL-4R-binding peptide, IL4RPep-1, was attached to branched polyethyleneimine-superparamagnetic iron oxide nanoparticles (BPEI-SPION). These nanoparticles were then complexed with Bcl-xL-targeting siRNA. IL-4R-targeted BPEI-SPION/Bcl-xL siRNA more efficiently reduced Bcl-xL gene expression and enhanced cytotoxicity of doxorubicin in MDA-MB231 breast tumor cells compared to untargeted BPEI-SPION/Bcl-xL siRNA. The siRNA was released from the complexes after 15Â h of incubation at pH 5.5 and was stable in the complexes up to 72Â h in the serum. The IL-4R-targeted BPEI-SPION/siRNA was internalized by cells through IL-4R, successfully escaped the endosomes, and was dispersed into the cytoplasm. Near-infrared fluorescence and magnetic resonance imaging demonstrated that inÂ vivo tumor homing and accumulation of IL-4R-targeted BPEI-SPION/siRNA were both higher than untargeted BPEI-SPION/siRNA. The IL-4R-targeted BPEI-SPION/Bcl-xL siRNA, in combination with doxorubicin, significantly inhibited tumor growth in mice compared to untargeted BPEI-SPION/Bcl-xL siRNA. These results suggest that the IL-4R-targeted delivery of Bcl-xL siRNA to IL-4R-expressing tumors can sensitize tumors to chemotherapy and enhance the efficacy of anti-tumor therapeutics.
Keywords	blood serum ; breast neoplasms ; cell viability ; cytotoxicity ; doxorubicin ; drug therapy ; endosomes ; fluorescence ; gene expression ; interleukin-4 ; iron oxides ; magnetic resonance imaging ; mice ; nanoparticles ; neoplasm cells ; pH ; pro-apoptotic proteins ; small interfering RNA
Language	English
Dates of publication	2017-10
Size	p. 101-111.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	603079-8
ISSN	0142-9612
ISSN	0142-9612
DOI	10.1016/j.biomaterials.2017.07.024
Database	NAL-Catalogue (AGRICOLA)

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Zs.B 2371: Show issues

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Article ; Online: Interleukin-4 receptor-targeted delivery of Bcl-xL siRNA sensitizes tumors to chemotherapy and inhibits tumor growth.

Guruprasath, Padmanaban / Kim, Jihoon / Gunassekaran, Gowri Rangaswamy / Chi, Lianhua / Kim, Soyoun / Park, Rang-Woon / Kim, Sang-Hyun / Baek, Moon-Chang / Bae, Sang Mun / Kim, Sang-Yeob / Kim, Dong-Kyu / Park, In-Kyu / Kim, Won-Jong / Lee, Byungheon

Biomaterials

2017 Volume 142, Page(s) 101–111

Abstract	IL-4 receptor (IL-4R) is commonly up-regulated on tumor cells, and interactions between the receptor and Interleukin-4 (IL-4) can induce the expression of anti-apoptotic proteins, including Bcl-xL. This contributes to tumor cell survival and their resistance to chemotherapy. In this study, we exploited IL-4R-targeted delivery of Bcl-xL siRNA to IL-4R-expressing tumor cells in order to sensitize them to chemotherapy. To target IL-4R, an IL-4R-binding peptide, IL4RPep-1, was attached to branched polyethyleneimine-superparamagnetic iron oxide nanoparticles (BPEI-SPION). These nanoparticles were then complexed with Bcl-xL-targeting siRNA. IL-4R-targeted BPEI-SPION/Bcl-xL siRNA more efficiently reduced Bcl-xL gene expression and enhanced cytotoxicity of doxorubicin in MDA-MB231 breast tumor cells compared to untargeted BPEI-SPION/Bcl-xL siRNA. The siRNA was released from the complexes after 15 h of incubation at pH 5.5 and was stable in the complexes up to 72 h in the serum. The IL-4R-targeted BPEI-SPION/siRNA was internalized by cells through IL-4R, successfully escaped the endosomes, and was dispersed into the cytoplasm. Near-infrared fluorescence and magnetic resonance imaging demonstrated that in vivo tumor homing and accumulation of IL-4R-targeted BPEI-SPION/siRNA were both higher than untargeted BPEI-SPION/siRNA. The IL-4R-targeted BPEI-SPION/Bcl-xL siRNA, in combination with doxorubicin, significantly inhibited tumor growth in mice compared to untargeted BPEI-SPION/Bcl-xL siRNA. These results suggest that the IL-4R-targeted delivery of Bcl-xL siRNA to IL-4R-expressing tumors can sensitize tumors to chemotherapy and enhance the efficacy of anti-tumor therapeutics.
Language	English
Publishing date	2017-10
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	603079-8
ISSN	1878-5905 ; 0142-9612
ISSN (online)	1878-5905
ISSN	0142-9612
DOI	10.1016/j.biomaterials.2017.07.024
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