ライフサイエンスコーパス: Fusobacteria

1 d the content of Bacteroidetes, TM7, SR1 and Fusobacteria.

2 is likely to play a role in the virulence of fusobacteria.

3 ria, Epsilonproteobacteria, Bacteroidia, and Fusobacteria.

4 be used as a marker to detect orally related fusobacteria.

5 roidetes (13.6%), Proteobacteria (3.6%), and Fusobacteria (2.5%).

6 rmicutes (62.9%), Proteobacteria (29.9%) and Fusobacteria (9.6%).

7 ide and fusobacterial lectin that explicates fusobacteria abundance in CRC.

8 e Bacteroidetes, Firmicutes, Proteobacteria, Fusobacteria and Actinobacteria, accounting for nearly 9

9 pared to adjacent normal mucosal tissue, and fusobacteria and beta-Proteobacteria levels increased wi

10 acterial taxa associated with Bacteroidetes, Fusobacteria and Proteobacteria and a reduced abundance

11 The abundances of Fusobacteria and Proteobacteria were also remarkably inc

12 o stool microbiome with more Actinobacteria, Fusobacteria and Proteobacteria, but fewer Bacteroidetes

13 wn, with examples throughout the Firmicutes, Fusobacteria and Proteobacteria.

14 ance, we explore the diversity and niches of fusobacteria and reconsider historic fusobacterial taxon

15 lostridium group and in the deeply branching Fusobacteria and Thermotogales lineages.

16 bacteria, Bacteroidetes, Proteobacteria, and Fusobacteria) and 6 genera (Veillonella, Streptococcus,

17 ing a greater abundance of Bacteroidetes and Fusobacteria, and AMH showing higher Firmicutes and Prot

18 wing an enrichment of the phyla Spirochetes, Fusobacteria, and Bacteroidetes associated with periodon

19 Bacteroides, Actinobacteria, Proteobacteria, Fusobacteria, and TM7, were represented.

20 However, fusobacteria are core members of the human oral microbio

21 Fusobacteria are found to be overrepresented in the colo

22 roteobacteria, Firmicutes, Bacteroidetes and Fusobacteria bacteria, which were also predominant in th

23 nce of dominant bacterial phyla (Firmicutes, Fusobacteria, Bacteriodetes, and Actinobacteria) and 24

24 A core alligator gut microbiome comprised of Fusobacteria, but depleted in Bacteroidetes and Proteoba

25 ancestral ADC, ODC, and LDC to include phyla Fusobacteria, Caldiserica, Nitrospirae, and Euryarchaeot

26 and ectopic fat occurred indirectly through Fusobacteria, Christensenellaceae R-7 group, Coprococcus

27 the relative abundances of Bacteroidetes and Fusobacteria decreased significantly, while those of Fir

28 sequencing revealed that the bacterial phyla Fusobacteria, Epsilonbacteraeota, Firmicutes, and Proteo

29 rs supported altered abundances in the phyla Fusobacteria, Firmicutes, Actinobacteria and Proteobacte

30 ruitment of tumor-infiltrating immune cells, fusobacteria generate a proinflammatory microenvironment

31 cer microbiota; however, the precise role of Fusobacteria in colorectal carcinoma pathogenesis requir

32 tively with the relative abundance of phylum Fusobacteria in the guts of tadpoles.

33 the healthy gut, raising questions about how fusobacteria localize to CRC.

34 ) describe a novel homing mechanism by which fusobacteria localize to tumors by recognizing a host po

35 cterial diversity and relative abundances of Fusobacteria might have lasting positive effects on amph

36 Fusobacteria (p < 0.007) and epsilon- Proteobacteria (p

37 in HOMIM scores of firmicutes (P </=0.001), fusobacteria (P = 0.003), proteobacteria (P </=0.001), s

38 rmicutes, Actinobacteria, Bacteroidetes, and Fusobacteria phyla.

39 Fusobacteria play a central role as physical bridges tha

40 In patients with AA, Fusobacteria populations proliferate and often persist d

41 pression signature that is shared with human fusobacteria-positive colorectal carcinomas.

42 ap2 or host epithelial Gal-GalNAc may reduce fusobacteria potentiation of CRC.

43 ral biofilm formation and pathogenesis, with fusobacteria proposed to serve as central 'bridging orga

44 in addition to the previously characterized fusobacteria, proteobacteria, firmicutes, and bacteroide

45 iae, Chloroflexi, Euryarchaeota, Firmicutes, Fusobacteria, Proteobacteria, Spirochaetes, SR1, Synergi

46 6, MMP-8) and bacteria (e.g., Bacteroidetes, Fusobacteria, Spirochaetes) discriminated the severity a

47 Clinical fusobacteria strains naturally lacking Fap2 or inactivat

48 normal human appendix harbors populations of Fusobacteria that are generally absent in fecal samples

49 yngeal microbiome composition showed a lower Fusobacteria to Actinobacteria ratio in OCD cases.

50 These capabilities allow Fusobacteria to survive in a mixed culture in the mouth.

51 in a Fap2-dependent manner, suggesting that fusobacteria use a hematogenous route to reach colon ade

52 esin, a system for transposon mutagenesis in fusobacteria was created.

53 Fusobacteria was only present 12 h post-infection.

54 Fusobacteria were also visualized within colorectal tumo

55 taxa from Cyanobacteria, Bacteroidetes, and Fusobacteria were more abundant with asthma, atopy, or h

56 icutes, Proteobacteria, Verrucomicrobia, and Fusobacteria were significantly increased, whereas Bacte

57 Faecalibacterium spp. and Fusobacteria were, however, decreased in the dogs with c

58 acteria, and a decrease of Bacteroidetes and Fusobacteria, when compared to weeks 5 and 9.

59 nterobacteriae, Neisseria, Streptococcus and Fusobacteria, whereas Prevotella, Treponema, Sphingomona

60 Clostridia and Fusobacteria, widely pathogenic to other vertebrates, do

61 We also undertake a critical reappraisal of fusobacteria with a focus on F. nucleatum as a mutualist

62 ive adhesin might mediate the interaction of fusobacteria with many partners and targets.

63 in Proteobacteria and a relative increase in Fusobacteria, with a rise in the beneficial genus Cetoba

64 ental plaque harbored a greater diversity of fusobacteria, with Fn. polymorphum dominating, whereas o

65 n. animalis typically outcompetes other oral fusobacteria within the inflammatory abscess environment