scholarly journals Interactions Between Streptococcus gordonii and Fusobacterium nucleatum Altered Bacterial Transcriptional Profiling and Attenuated the Immune Responses of Macrophages

2022 ◽  
Vol 11 ◽  
Author(s):  
Tingjun Liu ◽  
Ruiqi Yang ◽  
Jiani Zhou ◽  
Xianjun Lu ◽  
Zijian Yuan ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Transcriptional Profiling ◽  
Fusobacterium Nucleatum ◽  
Oral Bacteria ◽  
Streptococcus Gordonii ◽  
Rna Seq ◽  
Peptidoglycan Biosynthesis ◽  
Bacterial Pathogenicity ◽  
Transcriptional Changes ◽  
Physical Interactions

Interspecies coaggregation promotes transcriptional changes in oral bacteria, affecting bacterial pathogenicity. Streptococcus gordonii (S. gordonii) and Fusobacterium nucleatum (F. nucleatum) are common oral inhabitants. The present study investigated the transcriptional profiling of S. gordonii and F. nucleatum subsp. polymorphum in response to the dual-species coaggregation using RNA-seq. Macrophages were infected with both species to explore the influence of bacterial coaggregation on both species’ abilities to survive within macrophages and induce inflammatory responses. Results indicated that, after the 30-min dual-species coaggregation, 116 genes were significantly up-regulated, and 151 genes were significantly down-regulated in S. gordonii; 97 genes were significantly down-regulated, and 114 genes were significantly up-regulated in F. nucleatum subsp. polymorphum. Multiple S. gordonii genes were involved in the biosynthesis and export of cell-wall proteins and carbohydrate metabolism. F. nucleatum subsp. polymorphum genes were mostly associated with translation and protein export. The coaggregation led to decreased expression levels of genes associated with lipopolysaccharide and peptidoglycan biosynthesis. Coaggregation between S. gordonii and F. nucleatum subsp. polymorphum significantly promoted both species’ intracellular survival within macrophages and attenuated the production of pro-inflammatory cytokines IL-6 and IL-1β. Physical interactions between these two species promoted a symbiotic lifestyle and repressed macrophage’s killing and pro-inflammatory responses.

scholarly journals R213G polymorphism in SOD3 protects against bleomycin-induced inflammation and attenuates induction of proinflammatory pathways

2018 ◽  
Vol 50 (9) ◽  
pp. 807-816 ◽  
Author(s):  
Anastacia M. Garcia ◽  
Ayed Allawzi ◽  
Philip Tatman ◽  
Laura Hernandez-Lagunas ◽  
Kalin Swain ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Rna Seq ◽  
Single Nucleotide ◽  
Enhanced Resolution ◽  
The Matrix ◽  
Pathways Analysis ◽  
Transcriptional Changes ◽  
Differential Gene ◽  
Glycine Substitution ◽  
Downstream Processes

Extracellular superoxide dismutase (EC-SOD), one of three mammalian SOD isoforms, is the sole extracellular enzymatic defense against superoxide. A known human single nucleotide polymorphism (SNP) in the matrix-binding domain of EC-SOD characterized by an arginine-to-glycine substitution at position 213 (R213G) redistributes EC-SOD from the matrix into extracellular fluids. We previously reported that knock-in mice harboring the human R213G SNP (R213G mice) exhibited enhanced resolution of inflammation with subsequent protection against fibrosis following bleomycin treatment compared with wild-type (WT) littermates. Herein we set out to determine the underlying pathways with RNA-Seq analysis of WT and R213G lungs 7 days post-PBS and bleomycin. RNA-Seq analysis uncovered significant differential gene expression changes induced in WT and R213G strains in response to bleomycin. Ingenuity Pathways Analysis was used to predict differentially regulated up- and downstream processes based on transcriptional changes. Most prominent was the induction of inflammatory and immune responses in WT mice, which were suppressed in the R213G mice. Specifically, PKC signaling in T lymphocytes, IL-6, and NFΚB signaling were opposed in WT mice when compared with R213G. Several upstream regulators such as IFNγ, IRF3, and IKBKG were implicated in the divergent responses between WT and R213G mice. Our data suggest that the redistributed EC-SOD due to the R213G SNP attenuates the dysregulated inflammatory responses observed in WT mice. We speculate that redistributed EC-SOD protects against dysregulated alveolar inflammation via reprogramming of recruited immune cells toward a proresolving state.

scholarly journals Transcriptional profiling of coaggregation interactions between Streptococcus gordonii and Veillonella parvula by Dual RNA-Seq

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Naresh V. R. Mutha ◽  
Waleed K. Mohammed ◽  
Natalio Krasnogor ◽  
Geok Y. A. Tan ◽  
Wei Yee Wee ◽  
...  
Keyword(s):  
Transcriptional Profiling ◽  
Streptococcus Gordonii ◽  
Rna Seq

scholarly journals Efficacy of the De Novo-Derived Antimicrobial Peptide WLBU2 against Oral Bacteria

2007 ◽  
Vol 51 (5) ◽  
pp. 1837-1839 ◽  
Author(s):  
Karen F. Novak ◽  
William J. Diamond ◽  
Sreenatha Kirakodu ◽  
Rebecca Peyyala ◽  
Kimberly W. Anderson ◽  
...  
Keyword(s):  
Antimicrobial Peptide ◽  
De Novo ◽  
Fusobacterium Nucleatum ◽  
Oral Bacteria ◽  
Streptococcus Gordonii ◽  
Bacterial Burden ◽  
Oral Microorganisms

ABSTRACT The efficacy of a novel synthetic antimicrobial peptide (WLBU2) was evaluated against three oral microorganisms (grown planktonically): Streptococcus gordonii, Fusobacterium nucleatum, and Porphyromonas gingivalis. WLBU2 killed all three species, with F. nucleatum being the most susceptible. WLBU2 also reduced the bacterial burden of S. gordonii and F. nucleatum biofilms.

scholarly journals Distinct regulation of hippocampal neuroplasticity and ciliary genes by corticosteroid receptors

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Karen R. Mifsud ◽  
Clare L. M. Kennedy ◽  
Silvia Salatino ◽  
Eshita Sharma ◽  
Emily M. Price ◽  
...  
Keyword(s):  
Dna Sequences ◽  
Glucocorticoid Receptors ◽  
Acute Stress ◽  
Circadian Variation ◽  
Rna Seq ◽  
Physiological Regulation ◽  
Behavioural Adaptation ◽  
Neuronal Progenitor ◽  
Genome Wide ◽  
Transcriptional Changes

AbstractGlucocorticoid hormones (GCs) — acting through hippocampal mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs) — are critical to physiological regulation and behavioural adaptation. We conducted genome-wide MR and GR ChIP-seq and Ribo-Zero RNA-seq studies on rat hippocampus to elucidate MR- and GR-regulated genes under circadian variation or acute stress. In a subset of genes, these physiological conditions resulted in enhanced MR and/or GR binding to DNA sequences and associated transcriptional changes. Binding of MR at a substantial number of sites however remained unchanged. MR and GR binding occur at overlapping as well as distinct loci. Moreover, although the GC response element (GRE) was the predominant motif, the transcription factor recognition site composition within MR and GR binding peaks show marked differences. Pathway analysis uncovered that MR and GR regulate a substantial number of genes involved in synaptic/neuro-plasticity, cell morphology and development, behavior, and neuropsychiatric disorders. We find that MR, not GR, is the predominant receptor binding to >50 ciliary genes; and that MR function is linked to neuronal differentiation and ciliogenesis in human fetal neuronal progenitor cells. These results show that hippocampal MRs and GRs constitutively and dynamically regulate genomic activities underpinning neuronal plasticity and behavioral adaptation to changing environments.

scholarly journals Transcriptomic Analysis of Inbred Chicken Lines Reveals Infectious Bursal Disease Severity Is Associated with Greater Bursal Inflammation In Vivo and More Rapid Induction of Pro-Inflammatory Responses in Primary Bursal Cells Stimulated Ex Vivo

Viruses ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 933
Author(s):  
Amin S. Asfor ◽  
Salik Nazki ◽  
Vishwanatha R.A.P. Reddy ◽  
Elle Campbell ◽  
Katherine L. Dulwich ◽  
...  
Keyword(s):  
Rho Gtpases ◽  
Inflammatory Responses ◽  
Ex Vivo ◽  
Severe Disease ◽  
Infectious Bursal Disease ◽  
Rna Seq ◽  
Rapid Induction ◽  
Cytoskeletal Regulation ◽  
Bursal Disease

In order to better understand differences in the outcome of infectious bursal disease virus (IBDV) infection, we inoculated a very virulent (vv) strain into White Leghorn chickens of inbred line W that was previously reported to experience over 24% flock mortality, and three inbred lines (15I, C.B4 and 0) that were previously reported to display no mortality. Within each experimental group, some individuals experienced more severe disease than others but line 15I birds experienced milder disease based on average clinical scores, percentage of birds with gross pathology, average bursal lesion scores and average peak bursal virus titre. RNA-Seq analysis revealed that more severe disease in line W was associated with significant up-regulation of pathways involved in inflammation, cytoskeletal regulation by Rho GTPases, nicotinic acetylcholine receptor signaling, and Wnt signaling in the bursa compared to line 15I. Primary bursal cell populations isolated from uninfected line W birds contained a significantly greater percentage of KUL01+ macrophages than cells isolated from line 15I birds (p < 0.01) and, when stimulated ex vivo with LPS, showed more rapid up-regulation of pro-inflammatory gene expression than those from line 15I birds. We hypothesize that a more rapid induction of pro-inflammatory cytokine responses in bursal cells following IBDV infection leads to more severe disease in line W birds than in line 15I.

Fretibacterium fastidiosum gen. nov., sp. nov., isolated from the human oral cavity

2013 ◽  
Vol 63 (Pt_2) ◽  
pp. 458-463 ◽  
Author(s):  
Sonia R. Vartoukian ◽  
Julia Downes ◽  
Richard M. Palmer ◽  
William G. Wade
Keyword(s):  
New Genus ◽  
Novel Species ◽  
Fusobacterium Nucleatum ◽  
Oral Bacteria ◽  
Rrna Gene ◽  
Good Growth ◽  
Content Type ◽  
Cellular Fatty Acids ◽  
Link Type ◽  
Peptone Yeast Extract Glucose

SGP1T, a strain belonging to a lineage of the phylum Synergistetes with no previously cultivated representatives was subjected to a comprehensive range of phenotypic and genotypic tests. For good growth the strain was dependent on co-culture with, or extracts from, selected other oral bacteria. Cells of strain SGP1T were asaccharolytic and major amounts of acetic acid and moderate amounts of propionic acid were produced as end products of metabolism in peptone-yeast extract-glucose broth supplemented with a filtered cell sonicate of Fusobacterium nucleatum subsp. nucleatum ATCC 25586T (25 %, v/v). Hydrogen sulphide was produced and gelatin was weakly hydrolysed. The major cellular fatty acids were C14 : 0, C18 : 0 and C16 : 0. The DNA G+C content of strain SGP1T was 63 mol%. Phylogenetic analysis of the full-length 16S rRNA gene showed that strain SGP1T represented a novel group within the phylum Synergistetes . A novel species in a new genus, Fretibacterium fastidiosum gen. nov., sp. nov., is proposed. The type strain of Fretibacterium fastidiosum is SGP1T ( = DSM 25557T = JCM 16858T).

scholarly journals Effect of S-PRG Eluate on Biofilm Formation and Enzyme Activity of Oral Bacteria

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Masahiro Yoneda ◽  
Nao Suzuki ◽  
Yosuke Masuo ◽  
Akie Fujimoto ◽  
Kosaku Iha ◽  
...  
Keyword(s):  
Biofilm Formation ◽  
Composite Resin ◽  
Fusobacterium Nucleatum ◽  
Microtiter Plate ◽  
Oral Bacteria ◽  
Gelatin Film ◽  
Glass Ionomer ◽  
Microtiter Plate Assay ◽  
Substrate Hydrolysis ◽  
Adherence Ability

Recently, the antibacterial activity of a composite resin containing prereacted glass ionomer (S-PRG) filler was revealed. We examined the effect of an S-PRG eluate on various biologic activities ofStreptococcus mutansandPorphyromonas gingivalis. Adherence ability ofS. mutanswas evaluated by microtiter plate assay; protease and gelatinase activities ofP. gingivaliswere examined by synthetic substrate hydrolysis and gelatin film spot assay, respectively. Coaggregation ofP. gingivaliswithFusobacterium nucleatumwas also examined. S-PRG eluate was found to suppress streptococcal adherence. S-PRG eluate inhibited the protease and gelatinase activities ofP. gingivalisand the coaggregation betweenP. gingivalisandF. nucleatum. These results indicate that S-PRG eluate suppresses streptococcal adherence and inhibits the protease and coaggregation activities ofP. gingivalis. These findings may prompt research into novel strategies for preventing caries and periodontitis.

scholarly journals AB0056 TNFR2 PROMOTES INFLAMMATORY PROGRAMS IN FIBROBLAST-LIKE SYNOVIOCYTES

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1060.2-1060
Author(s):  
T. Suto ◽  
K. Von Dalwigk ◽  
A. Platzer ◽  
B. Niederreiter ◽  
T. M. Karonitsch
Keyword(s):  
Joint Destruction ◽  
Joint Inflammation ◽  
Rna Seq ◽  
Synovial Joint ◽  
Interferon Stimulated Genes ◽  
Transcriptional Changes ◽  
Proinflammatory Gene ◽  
Proinflammatory Gene Expression ◽  
Fibroblast Like Synoviocytes

Background:TNF-mediated fibroblast-like synoviocyte (FLS) activation is important for inflammation and joint destruction in rheumatoid arthritis (RA). The role of TNF-receptor 1 (TNFR1) in FLS activation has thoroughly been characterized. The functions of TNFR2 are, however, largely unknown.Objectives:To investigate the contribution of TNFR2 to the TNF-mediated activation of FLS.Methods:RA-FLS were transfected with TNFR2-targeting siRNA pools and transcriptional changes were determined by RNA-seq. QPCR, ELISA and immunoblotting were used to confirm the RNA-seq results and to gain insights into the pathways that regulate TNFR2-mediated changes in FLS.Results:TNF stimulation of FLS resulted in a strong upregulation of proinflammatory cytokines, chemokines, tissue-degrading enzymes and other genes that are associated with synovial inflammation in RA. Silencing of TNFR2 markedly diminished the TNF-response of RA-FLS. Especially, “interferon”-stimulated-genes (ISGs) including putative master regulators of joint inflammation, such as the CXCR3 chemokines CXCL9, CXCL10 and CXCL11 were affected by the knockdown of TNFR2. Consistently, immunoblots showed that TNFR2 was required for the TNF-induced phosphorylation of the transcription factor STAT1, which is known to mediate the transcription of ISGs, such as CXCR3 chemokines.Conclusion:TNFR2 regulates proinflammatory gene expression in RA-FLS via STAT1 and thereby contributes to the detrimental effects of TNF in synovial joint inflammation.Disclosure of Interests:None declared

scholarly journals Transcriptome Analyses of In Vitro Exercise Models by Clenbuterol Supplementation or Electrical Pulse Stimulation

2021 ◽  
Vol 11 (21) ◽  
pp. 10436
Author(s):  
Taku Fukushima ◽  
Miho Takata ◽  
Ayano Kato ◽  
Takayuki Uchida ◽  
Takeshi Nikawa ◽  
...  
Keyword(s):  
Gene Ontology ◽  
Electrical Pulse ◽  
C2c12 Myotubes ◽  
Rna Seq ◽  
Gene Expressions ◽  
Beneficial Effects ◽  
Electrical Pulse Stimulation ◽  
Transcriptional Changes ◽  
Pulse Stimulation

Exercise has beneficial effects on human health and is affected by two different pathways; motoneuron and endocrine. For the advancement of exercise research, in vitro exercise models are essential. We established two in vitro exercise models using C2C12 myotubes; EPS (electrical pulse stimulation) for a motoneuron model and clenbuterol, a specific β2 adrenergic receptor agonist, treatment for an endocrine model. For clenbuterol treatment, we found that Ppargc1a was induced only in low glucose media (1 mg/mL) using a 1-h treatment of 30 ng/mL clenbuterol. Global transcriptional changes of clenbuterol treatment were analyzed by RNA-seq and gene ontology analyses and indicated that mitogenesis and the PI3K-Akt pathway were enhanced, which is consistent with the effects of exercise. Cxcl1 and Cxcl5 were identified as candidate myokines induced by adrenaline. As for the EPS model, we compared 1 Hz of 1-pulse EPS and 1 Hz of 10-pulse EPS for 24 h and determined Myh gene expressions. Ten-pulse EPS induced higher Myh2 and Myh7 expression. Global transcriptional changes of 10-pulse EPS were also analyzed using RNA-seq, and gene ontology analyses indicated that CaMK signaling and hypertrophy pathways were enhanced, which is also consistent with the effects of exercise. In this paper, we provided two transcriptome results of in vitro exercise models and these databases will contribute to advances in exercise research.

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