Suppression of cell division-associated genes by Helicobacter pylori attenuates proliferation of RAW264.7 monocytic macrophage cells

Tan, Guan Huat; Looi, Chung Yeng; Fernandez, Keith Conrad; Vadivelu, Jamuna; Loke, Mun Fai; Wong, Won Fen

doi:10.1038/srep11046

Cited by 23 publications

(20 citation statements)

References 92 publications

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“…RNA was isolated from cells as described previously (7). Briefly, 1 ml TRIzol Reagent (Invitrogen, Carlsbad, CA) and 200 μl chloroform were added to cells and vortexed vigorously for 15 sec.…”

Section: Methodsmentioning

confidence: 99%

“…Activated macrophage or other phagocytes are able to eliminate most of the engulfed pathogens via formation of phagolysosome, nitric oxide and reactive oxygen activities. As with other successful pathogens such as Helicobacter pylori, C. neoformans has evolved a number of elaborate strategies to evade immune destruction by macrophages (7) . The encapsulated C. neoformans can defend itself against the onslaught of macrophages through non-lytic expulsion (8, 9), a process that involves alteration of host cell Arp2/3 complex-mediated actin polymerization and phagosome pH (10, 11), thereby allowing the pathogen to survive and propagate within macrophages.…”

Section: Introductionmentioning

confidence: 99%

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Interleukin-17A Secreted from the Lung–infiltrating T Helper 17 Cells Renders Protective Immunity to PulmonaryCryptococcus neoformansInfection

Movahed

Tan

Cheong

et al. 2018

Preprint

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16IL-17A has emerged as a key player in the pathologies of inflammation, autoimmune disease, 17 and immunity to microbes since its discovery two decades ago. In this study, we aim to elucidate 18 the activity of IL-17A in the protection against Cryptococcus neoformans, an opportunistic 19 fungus that causes fatal meningoencephalitis among AIDS patients. For this purpose, we 20 examined if C. neoformans infection triggers IL-17A secretion in the in vitro setting using 21 RAW264.7 murine macrophage cells, and in vivo using wildtype C57BL/6 mice. In addition, an 22 enhanced green fluorescence protein (eGFP) reporter and a knockout (KO) mouse models were 23 used to track the source of IL-17A secretion and explore the protective function of IL-17A, 24 respectively. Our findings showed that both in vivo and in vitro models of C. neoformans 25 infection demonstrated induction of abundant IL-17A secretion. By examining the lung 26 bronchoalveolar lavage fluid (BALF), mediastinal lymph node (mLN) and spleen of the IL-17A-27 EGFP reporter mice, we showed that intranasal inoculation with C. neoformans promoted 28 leukocytes lung infiltration. A large proportion (~50%) of the infiltrated CD4 + helper T cell 29 population secreted EGFP, indicating vigorous T H 17 activity in the C. neoformans-infected lung.30

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Interleukin-17A Secreted from the Lung–infiltrating T Helper 17 Cells Renders Protective Immunity to PulmonaryCryptococcus neoformansInfection

Movahed

Tan

Cheong

et al. 2018

Preprint

Self Cite

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show abstract

“…Briefly, RNA and cDNA was prepared using TRIzol reagent and M‐MLV reverse transcriptase, respectively (Invitrogen, Carlsbard, CA), as previously described . PCR amplification was carried out using SsoAdvanced SYBR Green Supermix (Biorad, Hercules, CA) in a Real‐Time PCR 7500 (Applied Biosystems, Foster City, CA).…”

Section: Methodsmentioning

confidence: 99%

Temporal proteomic profiling of Chlamydia trachomatis–infected HeLa‐229 human cervical epithelial cells

et al. 2016

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Chlamydia trachomatis is the leading causative agent of bacterial sexually transmitted infections worldwide which can lead to female pelvic inflammatory disease and infertility. A greater understanding of host response during chlamydial infection is essential to design intervention technique to reduce the increasing incidence rate of genital chlamydial infection. In this study, we investigated proteome changes in epithelial cells during C. trachomatis infection by using an isobaric tags for relative and absolute quantitation (iTRAQ) labeling technique coupled with a liquid chromatography-tandem mass spectrometry (LC-MS(3) ) analysis. C. trachomatis (serovar D, MOI 1)-infected HeLa-229 human cervical carcinoma epithelial cells (at 2, 4 and 8 h) showed profound modifications of proteome profile which involved 606 host proteins. MGST1, SUGP2 and ATXN10 were among the top in the list of the differentially upregulated protein. Through pathway analysis, we suggested the involvement of eukaryotic initiation factor 2 (eIF2) and mammalian target of rapamycin (mTOR) in host cells upon C. trachomatis infection. Network analysis underscored the participation of DNA repair mechanism during C. trachomatis infection. In summary, intense modifications of proteome profile in C. trachomatis-infected HeLa-229 cells indicate complex host-pathogen interactions at early phase of chlamydial infection.

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“…For microarray assay, all samples were run in duplicate and were prepared as previously described [ 21 ]. Briefly, RNA isolated from yeast cells were first labeled using a Low Input Quick Amp Labeling Kit, One-Color (Agilent Technologies).…”

Section: Methodsmentioning

confidence: 99%

Genome-Wide Transcription Study of Cryptococcus neoformans H99 Clinical Strain versus Environmental Strains

et al. 2015

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The infection of Cryptococcus neoformans is acquired through the inhalation of desiccated yeast cells and basidiospores originated from the environment, particularly from bird’s droppings and decaying wood. Three environmental strains of C. neoformans originated from bird droppings (H4, S48B and S68B) and C. neoformans reference clinical strain (H99) were used for intranasal infection in C57BL/6 mice. We showed that the H99 strain demonstrated higher virulence compared to H4, S48B and S68B strains. To examine if gene expression contributed to the different degree of virulence among these strains, a genome-wide microarray study was performed to inspect the transcriptomic profiles of all four strains. Our results revealed that out of 7,419 genes (22,257 probes) examined, 65 genes were significantly up-or down-regulated in H99 versus H4, S48B and S68B strains. The up-regulated genes in H99 strain include Hydroxymethylglutaryl-CoA synthase (MVA1), Mitochondrial matrix factor 1 (MMF1), Bud-site-selection protein 8 (BUD8), High affinity glucose transporter 3 (SNF3) and Rho GTPase-activating protein 2 (RGA2). Pathway annotation using DAVID bioinformatics resource showed that metal ion binding and sugar transmembrane transporter activity pathways were highly expressed in the H99 strain. We suggest that the genes and pathways identified may possibly play crucial roles in the fungal pathogenesis.

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Suppression of cell division-associated genes by Helicobacter pylori attenuates proliferation of RAW264.7 monocytic macrophage cells

Cited by 23 publications

References 92 publications

Interleukin-17A Secreted from the Lung–infiltrating T Helper 17 Cells Renders Protective Immunity to PulmonaryCryptococcus neoformansInfection

Interleukin-17A Secreted from the Lung–infiltrating T Helper 17 Cells Renders Protective Immunity to PulmonaryCryptococcus neoformansInfection

Temporal proteomic profiling of Chlamydia trachomatis–infected HeLa‐229 human cervical epithelial cells

Genome-Wide Transcription Study of Cryptococcus neoformans H99 Clinical Strain versus Environmental Strains

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