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Article ; Online: Caspase-4 Mediates Restriction of Burkholderia pseudomallei in Human Alveolar Epithelial Cells.

Srisaowakarn, Chanya / Pudla, Matsayapan / Ponpuak, Marisa / Utaisincharoen, Pongsak

2020 Volume 88, Issue 3

Abstract: Melioidosis is an infectious disease with a high mortality rate responsible for community-acquired sepsis in Southeast Asia and Northern Australia. The causative agent of this disease ... ...

Abstract	Melioidosis is an infectious disease with a high mortality rate responsible for community-acquired sepsis in Southeast Asia and Northern Australia. The causative agent of this disease is
MeSH term(s)	Alveolar Epithelial Cells/physiology ; Animals ; Burkholderia pseudomallei/pathogenicity ; Burkholderia pseudomallei/physiology ; Caspases, Initiator/physiology ; Melioidosis/immunology ; Melioidosis/microbiology ; Mice
Chemical Substances	CASP4 protein, human (EC 3.4.22.-) ; Caspases, Initiator (EC 3.4.22.-)
Language	English
Publishing date	2020-02-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/IAI.00868-19
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Article: Deficit of female sex hormones desensitizes rat cardiac mitophagy.

Kampaengsri, Theerachat / Ponpuak, Marisa / Wattanapermpool, Jonggonnee / Bupha-Intr, Tepmanas

The Chinese journal of physiology

2021 Volume 64, Issue 2, Page(s) 72–79

Abstract: Long-term deprivation of female sex hormones has been shown to mediate accumulation of damaged mitochondria in ventricular muscle leading to cardiovascular dysfunction. Therefore, the roles of female sex hormones in mitochondrial quality control are ... ...

Abstract	Long-term deprivation of female sex hormones has been shown to mediate accumulation of damaged mitochondria in ventricular muscle leading to cardiovascular dysfunction. Therefore, the roles of female sex hormones in mitochondrial quality control are closely focused. In the present study, depletion of female sex hormones impairing mitochondrial autophagy in the heart was hypothesized. Cardiac mitophagy was therefore investigated in the heart of 10-week ovariectomized (OVX) and sham-operated (SHAM) rats. By using isolated mitochondria preparation, results demonstrated an increase in mitochondrial PTEN-induced kinase 1 accumulation in the sample of OVX rats indicating mitochondrial outer membrane dysfunction. However, no change in p62 and LC3-II translocation to mitochondria was observed between two groups indicating unresponsiveness of mitophagosome formation in the OVX rat heart. This loss might be resulted from significant decreases in Parkin and Bcl2l13 expression, but not Bnip3 activation. In summary, results suggest that mitochondrial abnormality in the heart after deprivation of female sex hormones could consequently be due to desensitization of mitophagy process.
MeSH term(s)	Animals ; Autophagy ; Female ; Gonadal Steroid Hormones ; Heart ; Mitochondria ; Mitophagy ; Rats
Chemical Substances	Gonadal Steroid Hormones
Language	English
Publishing date	2021-05-03
Publishing country	India
Document type	Journal Article
ZDB-ID	966112-8
ISSN	0304-4920 ; 0300-8525
ISSN	0304-4920 ; 0300-8525
DOI	10.4103/cjp.cjp_102_20
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Article ; Online: TLR9 Negatively Regulates Intracellular Bacterial Killing by Pyroptosis in Burkholderia pseudomallei

Pudla, Matsayapan / Sanongkiet, Sucharat / Ekchariyawat, Peeraya / Luangjindarat, Chularat / Ponpuak, Marisa / Utaisincharoen, Pongsak

Microbiology spectrum

2022 Volume 10, Issue 5, Page(s) e0348822

Abstract: Melioidosis is a serious infectious disease caused by Burkholderia pseudomallei. This bacterium is able to survive and multiply inside the immune cells such as macrophages. It is well established that Toll-like receptors (TLRs), particularly surface TLRs ...

Abstract	Melioidosis is a serious infectious disease caused by Burkholderia pseudomallei. This bacterium is able to survive and multiply inside the immune cells such as macrophages. It is well established that Toll-like receptors (TLRs), particularly surface TLRs such as TLR2, TLR4, and TLR5, play an essential role in defending against this bacterial infection. However, the involvement of endosomal TLRs in the infection has not been elucidated. In this study, we demonstrated that the number of intracellular bacteria is reduced in TLR9-depleted RAW264.7 cells infected with B. pseudomallei, suggesting that TLR9 is involved in intracellular bacterial killing in macrophages. As several reports have previously demonstrated that pyroptosis is essential for restricting intracellular bacterial killing, particularly in B. pseudomallei infection, we also observed an increased release of cytosolic enzyme lactate dehydrogenase (LDH) in TLR9-depleted cells infected with B. pseudomallei, suggesting TLR9 involvement in pyroptosis in this context. Consistently, the increases in caspase-11 and gasdermind D (GSDMD) activations, which are responsible for the LDH release, were also detected. Moreover, we demonstrated that the increases in pyroptosis and bacterial killing in B. pseudomallei
MeSH term(s)	Mice ; Animals ; Burkholderia pseudomallei/metabolism ; Toll-Like Receptor 9/metabolism ; Toll-Like Receptor 2/metabolism ; Pyroptosis ; Toll-Like Receptor 4/metabolism ; Toll-Like Receptor 5/metabolism ; Melioidosis/metabolism ; Melioidosis/microbiology ; Macrophages ; Cell Line ; Toll-Like Receptors/genetics ; Toll-Like Receptors/metabolism ; Cytokines/metabolism ; Caspases/metabolism ; Lactate Dehydrogenases/metabolism
Chemical Substances	Toll-Like Receptor 9 ; Toll-Like Receptor 2 ; Toll-Like Receptor 4 ; Toll-Like Receptor 5 ; Toll-Like Receptors ; Cytokines ; Caspases (EC 3.4.22.-) ; Lactate Dehydrogenases (EC 1.1.-) ; Tlr9 protein, mouse
Language	English
Publishing date	2022-10-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2807133-5
ISSN	2165-0497 ; 2165-0497
ISSN (online)	2165-0497
ISSN	2165-0497
DOI	10.1128/spectrum.03488-22
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Article ; Online: BORC complex specific components and Kinesin-1 mediate autophagy evasion by the autophagy-resistant Mycobacterium tuberculosis Beijing strain.

Tunganuntarat, Janpen / Kanjanasirirat, Phongthon / Khumpanied, Tanawadee / Benjaskulluecha, Salisa / Wongprom, Benjawan / Palaga, Tanapat / Siregar, Tegar Adriansyah Putra / Borwornpinyo, Suparerk / Chaiprasert, Angkana / Palittapongarnpim, Prasit / Ponpuak, Marisa

Scientific reports

2023 Volume 13, Issue 1, Page(s) 1663

Abstract: Autophagy induction by starvation has been shown to enhance lysosomal delivery to mycobacterial phagosomes, resulting in the restriction of the Mycobacterium tuberculosis reference strain H37Rv. In contrast to H37Rv, our previous study showed that ... ...

Abstract	Autophagy induction by starvation has been shown to enhance lysosomal delivery to mycobacterial phagosomes, resulting in the restriction of the Mycobacterium tuberculosis reference strain H37Rv. In contrast to H37Rv, our previous study showed that strains belonging to the notorious M. tuberculosis Beijing genotype could evade autophagic elimination. Our recent RNA-Seq analysis also discovered that the autophagy-resistant M. tuberculosis Beijing strain (BJN) evaded autophagic control by upregulating the expression of Kxd1, a BORC complex component, and Plekhm2, both of which function in lysosome positioning towards the cell periphery in host macrophages, thereby suppressing enhanced lysosomal delivery to its phagosome and sparing the BJN from elimination as a result. In this work, we further characterised the other specific components of the BORC complex, BORC5-8, and Kinesin proteins in autophagy resistance by the BJN. Depletion of BORCS5-8 and Kinesin-1, but not Kinesin-3, reverted autophagy avoidance by the BJN, resulting in increased lysosomal delivery to the BJN phagosomes. In addition, the augmented lysosome relocation towards the perinuclear region could now be observed in the BJN-infected host cells depleted in BORCS5-8 and Kinesin-1 expressions. Taken together, the data uncovered new roles for BORCS5-8 and Kinesin-1 in autophagy evasion by the BJN.
MeSH term(s)	Humans ; Autophagy/genetics ; Autophagy/immunology ; Beijing ; Carrier Proteins/genetics ; Carrier Proteins/immunology ; Kinesins/genetics ; Kinesins/immunology ; Mycobacterium tuberculosis/genetics ; Mycobacterium tuberculosis/immunology ; Tuberculosis/genetics ; Tuberculosis/immunology ; Macrophages/immunology
Chemical Substances	Carrier Proteins ; Kinesins (EC 3.6.4.4) ; KXD1 protein, human
Language	English
Publishing date	2023-01-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-28983-5
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Article ; Online: Novel Potent Autophagy Inhibitor Ka-003 Inhibits Dengue Virus Replication.

Limthongkul, Jitra / Akkarasereenon, Kornkamon / Yodweerapong, Tanpitcha / Songthammawat, Poramate / Tong-Ngam, Pirut / Tubsuwan, Alisa / Kunkaew, Nawapol / Kanjanasirirat, Phongthon / Khumpanied, Tanawadee / Wannalo, Warawuth / Ubol, Sukathida / Borwornpinyo, Suparerk / Ploypradith, Poonsakdi / Ponpuak, Marisa

Viruses

2023 Volume 15, Issue 10

Abstract: Every year, dengue virus (DENV) affects millions of people. Currently, there are no approved drugs for the treatment of DENV infection. Autophagy is a conserved degradation process that was shown to be induced by DENV infection and required for optimal ... ...

Abstract	Every year, dengue virus (DENV) affects millions of people. Currently, there are no approved drugs for the treatment of DENV infection. Autophagy is a conserved degradation process that was shown to be induced by DENV infection and required for optimal DENV replication. The modulation of autophagy is, therefore, considered an attractive target to treat DENV infection. This study carried out a high-content image screen analysis using Crispr-Cas9 GFP-LC3 knocked-in HeLa cells of a compound library synthesized from or inspired by natural products and their biocongener precursors to discover novel autophagy inhibitors. The screen identified Ka-003 as the most effective compound for decreasing the number of autophagic vacuoles inside cells upon autophagy induction. Ka-003 could inhibit autophagy in a dose-dependent manner at low micromolar concentrations. More importantly, Ka-003 demonstrated the concentration-dependent inhibition of DENV production in Crispr-Cas9 GFP-LC3 knocked-in THP-1 monocytes. The core structure of Ka-003, which is a methyl cyclohexene derivative, resembles those found in mulberry plants, and could be synthetically prepared in a bioinspired fashion. Taken together, data indicate that Ka-003 hampered autophagy and limited DENV replication. The low cytotoxicity of Ka-003 suggests its therapeutic potential, which warrants further studies for the lead optimization of the compound for dengue treatment.
MeSH term(s)	Humans ; Dengue Virus/physiology ; HeLa Cells ; Autophagy/physiology ; Dengue ; Virus Replication
Language	English
Publishing date	2023-09-27
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v15102012
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Article ; Online: ECDD-S16 targets vacuolar ATPase: A potential inhibitor compound for pyroptosis-induced inflammation.

Ekchariyawat, Peeraya / Saengfak, Rattatammanoon / Sanongkiet, Sucharat / Charoenwongpaiboon, Thanapon / Khongpraphan, Suphasuta / Mala, Supaporn / Luangjindarat, Chularat / Munyoo, Bumrung / Chabang, Napason / Charoensutthivarakul, Sitthivut / Borwornpinyo, Suparerk / Tuchinda, Patoomratana / Ponpuak, Marisa / Pudla, Matsayapan / Utaisincharoen, Pongsak

PloS one

2023 Volume 18, Issue 11, Page(s) e0292340

Abstract: Background: Cleistanthin A (CA), extracted from Phyllanthus taxodiifolius Beille, was previously reported as a potential V-ATPase inhibitor relevant to cancer cell survival. In the present study, ECDD-S16, a derivative of cleistanthin A, was ... ...

Abstract	Background: Cleistanthin A (CA), extracted from Phyllanthus taxodiifolius Beille, was previously reported as a potential V-ATPase inhibitor relevant to cancer cell survival. In the present study, ECDD-S16, a derivative of cleistanthin A, was investigated and found to interfere with pyroptosis induction via V-ATPase inhibition. Objective: This study examined the ability of ECDD-S16 to inhibit endolysosome acidification leading to the attenuation of pyroptosis in Raw264.7 macrophages activated by both surface and endosomal TLR ligands. Methods: To elucidate the activity of ECDD-S16 on pyroptosis-induced inflammation, Raw264.7 cells were pretreated with the compound before stimulation with surface and endosomal TLR ligands. The release of lactate dehydrogenase (LDH) was determined by LDH assay. Additionally, the production of cytokines and the expression of pyroptosis markers were examined by ELISA and immunoblotting. Moreover, molecular docking was performed to demonstrate the binding of ECDD-S16 to the vacuolar (V-)ATPase. Results: This study showed that ECDD-S16 could inhibit pyroptosis in Raw264.7 cells activated with surface and endosomal TLR ligands. The attenuation of pyroptosis by ECDD-S16 was due to the impairment of endosome acidification, which also led to decreased Reactive Oxygen Species (ROS) production. Furthermore, molecular docking also showed the possibility of inhibiting endosome acidification by the binding of ECDD-S16 to the vacuolar (V-)ATPase in the region of V0. Conclusion: Our findings indicate the potential of ECDD-S16 for inhibiting pyroptosis and prove that vacuolar H+ ATPase is essential for pyroptosis induced by TLR ligands.
MeSH term(s)	Humans ; Vacuolar Proton-Translocating ATPases/metabolism ; Pyroptosis ; Molecular Docking Simulation ; Inflammation
Chemical Substances	Vacuolar Proton-Translocating ATPases (EC 3.6.1.-) ; cleistanthin (25047-48-7)
Language	English
Publishing date	2023-11-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0292340
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Article: Therapeutic Implications of Ceritinib in Cholangiocarcinoma beyond ALK Expression and Mutation.

Myint, Kyaw Zwar / Balasubramanian, Brinda / Venkatraman, Simran / Phimsen, Suchada / Sripramote, Supisara / Jantra, Jeranan / Choeiphuk, Chaiwat / Mingphruedhi, Somkit / Muangkaew, Paramin / Rungsakulkij, Narongsak / Tangtawee, Pongsatorn / Suragul, Wikran / Farquharson, Watoo Vassanasiri / Wongprasert, Kanokpan / Chutipongtanate, Somchai / Sanvarinda, Pimtip / Ponpuak, Marisa / Poungvarin, Naravat / Janvilisri, Tavan /

Suthiphongchai, Tuangporn / Yacqub-Usman, Kiren / Grabowska, Anna M / Bates, David O / Tohtong, Rutaiwan

Pharmaceuticals (Basel, Switzerland)

2024 Volume 17, Issue 2

Abstract: Cholangiocarcinoma (CCA) is a difficult-to-treat cancer, with limited therapeutic options and surgery being the only curative treatment. Standard chemotherapy involves gemcitabine-based therapies combined with cisplatin, oxaliplatin, capecitabine, or 5- ... ...

Abstract	Cholangiocarcinoma (CCA) is a difficult-to-treat cancer, with limited therapeutic options and surgery being the only curative treatment. Standard chemotherapy involves gemcitabine-based therapies combined with cisplatin, oxaliplatin, capecitabine, or 5-FU with a dismal prognosis for most patients. Receptor tyrosine kinases (RTKs) are aberrantly expressed in CCAs encompassing potential therapeutic opportunity. Hence, 112 RTK inhibitors were screened in KKU-M213 cells, and ceritinib, an approved targeted therapy for ALK-fusion gene driven cancers, was the most potent candidate. Ceritinib's cytotoxicity in CCA was assessed using MTT and clonogenic assays, along with immunofluorescence, western blot, and qRT-PCR techniques to analyze gene expression and signaling changes. Furthermore, the drug interaction relationship between ceritinib and cisplatin was determined using a ZIP synergy score. Additionally, spheroid and xenograft models were employed to investigate the efficacy of ceritinib in vivo. Our study revealed that ceritinib effectively killed CCA cells at clinically relevant plasma concentrations, irrespective of ALK expression or mutation status. Ceritinib modulated multiple signaling pathways leading to the inhibition of the PI3K/Akt/mTOR pathway and activated both apoptosis and autophagy. Additionally, ceritinib and cisplatin synergistically reduced CCA cell viability. Our data show ceritinib as an effective treatment of CCA, which could be potentially explored in the other cancer types without ALK mutations.
Language	English
Publishing date	2024-02-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph17020197
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Article ; Online: Synthesis of synthetic mannan backbone polysaccharides found on the surface of Mycobacterium tuberculosis as a vaccine adjuvant and their immunological properties.

Wattanasiri, Chakree / Paha, Jiraporn / Ponpuak, Marisa / Ruchirawat, Somsak / Boonyarattanakalin, Siwarutt

Carbohydrate polymers

2017 Volume 175, Page(s) 746–755

Abstract: Surface components of Mycobacterium tuberculosis (Mtb) play crucial roles in modulating host immune responses. Thorough understandings of immunological properties of the Mtb's surface components are essential for the development of tuberculosis treatment ...

Abstract	Surface components of Mycobacterium tuberculosis (Mtb) play crucial roles in modulating host immune responses. Thorough understandings of immunological properties of the Mtb's surface components are essential for the development of tuberculosis treatment and prevention. Unfortunately, the accessibility to the molecules on the surface of Mtb is limited by the structural complexity due to their various macromolecular nature and the hazard of culturing Mtb. In this study, we reveal a practical synthesis of lipomannan (LM) backbone polysaccharides - the core glycans found on Mtb's surface. A rapid synthetic approach based on a controlled polymerization was developed for the chemical synthesis of mannopyranans, the core structure of LM. The size of the LM glycans can be controlled by using specific monomer concentrations in addition to stereo- and regioselectivity derived from the versatile tricyclic orthoester mannose monomer. The immunological properties of the synthesized mannopyranans were investigated and their adjuvant potential was revealed. The adjuvanticity mechanism of the synthetic mannopyranans appears to involve the NF-κB and inflammasome pathways.
MeSH term(s)	Adjuvants, Immunologic/chemical synthesis ; Animals ; Cytokines/metabolism ; Lipopolysaccharides/chemical synthesis ; Lipopolysaccharides/immunology ; Mice ; Mycobacterium tuberculosis/chemistry ; Polysaccharides, Bacterial/chemical synthesis ; Polysaccharides, Bacterial/immunology ; RAW 264.7 Cells ; Vaccines
Chemical Substances	Adjuvants, Immunologic ; Cytokines ; Lipopolysaccharides ; Polysaccharides, Bacterial ; Vaccines ; lipomannan
Language	English
Publishing date	2017-11-01
Publishing country	England
Document type	Journal Article
ZDB-ID	1501516-6
ISSN	1879-1344 ; 0144-8617
ISSN (online)	1879-1344
ISSN	0144-8617
DOI	10.1016/j.carbpol.2017.07.045
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Article ; Online: The autophagy-resistant Mycobacterium tuberculosis Beijing strain upregulates KatG to evade starvation-induced autophagic restriction.

Siregar, Tegar Adriansyah Putra / Prombutara, Pinidphon / Kanjanasirirat, Phongthon / Kunkaew, Nawapol / Tubsuwan, Alisa / Boonmee, Atsadang / Palaga, Tanapat / Khumpanied, Tanawadee / Borwornpinyo, Suparerk / Chaiprasert, Angkana / Utaisincharoen, Pongsak / Ponpuak, Marisa

Pathogens and disease

2022 Volume 80, Issue 1

Abstract: Mycobacterium tuberculosis utilizes several mechanisms to block phagosome-lysosome fusion to evade host cell restriction. However, induction of host cell autophagy by starvation was shown to overcome this block, resulting in enhanced lysosomal delivery ... ...

Abstract	Mycobacterium tuberculosis utilizes several mechanisms to block phagosome-lysosome fusion to evade host cell restriction. However, induction of host cell autophagy by starvation was shown to overcome this block, resulting in enhanced lysosomal delivery to mycobacterial phagosomes and the killing of the M. tuberculosis reference strain H37Rv. Nevertheless, our previous studies found that strains belonging to the M. tuberculosis Beijing genotype can resist starvation-induced autophagic elimination, though the mycobacterial factors involved remain unclear. In this study, we showed that KatG expression is upregulated in the autophagy-resistant M. tuberculosis Beijing strain (BJN) during autophagy induction by the starvation of host macrophages, while such increase was not observed in the H37Rv. KatG depletion using the CRISPR-dCas9 interference system in the BJN resulted in increased lysosomal delivery to its phagosome and decreased its survival upon autophagy induction by starvation. As KatG functions by catabolizing ROS, we determined the source of ROS contributing to the starvation-induced autophagic elimination of mycobacteria. Using siRNA-mediated knockdown, we found that Superoxide dismutase 2, which generates mitochondrial ROS but not NADPH oxidase 2, is important for the starvation-induced lysosomal delivery to mycobacterial phagosomes. Taken together, these findings showed that KatG is vital for the BJN to evade starvation-induced autophagic restriction.
MeSH term(s)	Autophagy/genetics ; Beijing ; Lysosomes/microbiology ; Mycobacterium tuberculosis/genetics ; Phagosomes/metabolism
Language	English
Publishing date	2022-01-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2049-632X
ISSN (online)	2049-632X
DOI	10.1093/femspd/ftac004
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Article ; Online: Host cell transcriptomic response to the multidrug-resistant <i>Mycobacterium tuberculosis</i> clonal outbreak Beijing strain reveals its pathogenic features.

Prombutara, Pinidphon / Adriansyah Putra Siregar, Tegar / Laopanupong, Thanida / Kanjanasirirat, Phongthon / Khumpanied, Tanawadee / Borwornpinyo, Suparerk / Rai, Awantika / Chaiprasert, Angkana / Palittapongarnpim, Prasit / Ponpuak, Marisa

Virulence

2022 Volume 13, Issue 1, Page(s) 1810–1826

Abstract: The upsurge of multidrug-resistant infections has rendered tuberculosis the principal cause of death among infectious diseases. A clonal outbreak multidrug-resistant triggering strain of ... Mycobacterium tuberculosis ... was identified in Kanchanaburi ... ...

Abstract	The upsurge of multidrug-resistant infections has rendered tuberculosis the principal cause of death among infectious diseases. A clonal outbreak multidrug-resistant triggering strain of Mycobacterium tuberculosis was identified in Kanchanaburi Province, labelled "MKR superspreader," which was found to subsequently spread to other regions, as revealed by prior epidemiological reports in Thailand. Herein, we showed that the MKR displayed a higher growth rate upon infection into host macrophages in comparison with the H37Rv reference strain. To further elucidate MKR's biology, we utilized RNA-Seq and differential gene expression analyses to identify host factors involved in the intracellular viability of the MKR. A set of host genes function in the cellular response to lipid pathway was found to be uniquely up-regulated in host macrophages infected with the MKR, but not those infected with H37Rv. Within this set of genes, the IL-36 cytokines which regulate host cell cholesterol metabolism and resistance against mycobacteria attracted our interest, as our previous study revealed that the MKR elevated genes associated with cholesterol breakdown during its growth inside host macrophages. Indeed, when comparing macrophages infected with the MKR to H37Rv-infected cells, our RNA-Seq data showed that the expression ratio of IL-36RN, the negative regulator of the IL-36 pathway, to that of IL-36G was greater in macrophages infected with the MKR. Furthermore, the MKR's intracellular survival and increased intracellular cholesterol level in the MKR-infected macrophages were diminished with decreased IL-36RN expression. Overall, our results indicated that IL-36RN could serve as a new target against this emerging multidrug-resistant M. tuberculosis strain.
MeSH term(s)	Beijing ; Cholesterol ; Cytokines/genetics ; Disease Outbreaks ; Humans ; Lipids ; Mycobacterium tuberculosis/genetics ; Thailand ; Transcriptome ; Tuberculosis/microbiology ; Tuberculosis, Multidrug-Resistant/epidemiology
Chemical Substances	Cytokines ; Lipids ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2022-10-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2657572-3
ISSN	2150-5608 ; 2150-5594
ISSN (online)	2150-5608
ISSN	2150-5594
DOI	10.1080/21505594.2022.2135268
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