ライフサイエンスコーパス: S. agalactiae

1 S. agalactiae (Group B streptococci, GBS), E. faecalis,

2 S. agalactiae CovR promotes bladder infection and inflam

3 sequenced serotype V strain 2603 V/R and 19 S. agalactiae strains from several serotypes using whole

4 rapid detection of Streptococcus agalactiae (S. agalactiae).

5 Genome comparisons among S. agalactiae, Streptococcus pneumoniae, Streptococcus p

6 ys, revealed the genetic heterogeneity among S. agalactiae strains, even of the same serotype, and pr

7 r, secondary immunization with conjugate and S. agalactiae, although not S. pneumoniae, results in a

8 bladder uroepithelial cell models of UTI and S. agalactiae mutants in covR and related factors, inclu

9 inct populations; (ii) human host-associated S. agalactiae subtypes may occasionally be transmitted t

10 ic characteristics of 52 human and 83 bovine S. agalactiae isolates.

11 We conclude that (i) human and bovine S. agalactiae isolates represent distinct populations; (

12 lactiae; (ii) most human invasive and bovine S. agalactiae isolates represent distinct subtypes, sugg

13 rowth in human urine observed in ABU-causing S. agalactiae (ABSA) that was not seen among uropathogen

14 s improved with inocula of 100 and 1,000 CFU S. agalactiae, with the majority of these aliquots demon

15 broth-enhanced PCR nominally detected 10 CFU S. agalactiae after 4 h of carrot broth incubation with

16 Mice infected with covR-deficient S. agalactiae produced less proinflammatory cytokines th

17 For S. agalactiae, there was a single false-positive and fal

18 The putative gene for S. agalactiae gamma-GCS was identified and cloned, and t

19 ; an additional 26 (12.8%) were positive for S. agalactiae upon subculture.

20 ame homologous to the CAMP factor genes from S. agalactiae and Streptococcus uberis.

21 Furthermore, the Gap1 homologues from S. agalactiae and Streptococcus sanguinis rescued the Fa

22 with a putative peptidoglycan hydrolase from S. agalactiae and S. pneumoniae, indicative of a role in

23 Srr2, an SRRP from S. agalactiae strain COH1, has been implicated in bacter

24 ae that an unannotated homodimeric TetR from S. agalactiae (PDB 3KKC) is the bona fide zinc efflux re

25 cies which appear to synthesize glutathione (S. agalactiae ATCC 12927, S. pyogenes ATCC 8668, and Ent

26 We found that covR-deficient serotype III S. agalactiae 874391 was significantly attenuated for co

27 capsular polysaccharide (PPS14) and type III S. agalactiae containing a PPS14 core capsule identical

28 y altered the expression of several genes in S. agalactiae 874391 that encode key virulence factors,

29 he genomic region including the pur genes in S. agalactiae.

30 The results suggest a role for SkzL in S. agalactiae pathogenesis through fibrinolytic enhancem

31 suspected of being S. pseudoporcinus and not S. agalactiae.

32 rovides a discriminatory subtype analysis of S. agalactiae; (ii) most human invasive and bovine S. ag

33 ia (ABU); however, growth characteristics of S. agalactiae in human urine have not previously been re

34 ible loop region in GSH binding, chimeras of S. agalactiae gamma-GCS-GS were made containing gamma-GC

35 ase activity and other cellular functions of S. agalactiae.

36 The pathogenesis of S. agalactiae UTI is complex, multifactorial, and influe

37 may affect the persistence or progression of S. agalactiae ABU.

38 ctive and highly sensitive quantification of S. agalactiae cells in a concentration range of 10(1)-10

39 bles a rapid detection and quantification of S. agalactiae in environmental samples but also opens up

40 will promote comparative genomic studies of S. agalactiae recovered from diverse sources.

41 covered from the bottles with S. pneumoniae, S. agalactiae, E. coli, N. meningitidis, or H. influenza

42 treptococcal species, including S. pyogenes, S. agalactiae, S. dysgalactiae, S. equi, S. mutans, S. p

43 mouth, as well as in Streptococcus pyogenes, S. agalactiae and S. suis.

44 nium SALSA, bound to Streptococcus pyogenes, S. agalactiae, S. gordonii, and Escherichia coli.

45 eptococci, including Streptococcus pyogenes, S. agalactiae, S. pneumoniae, and S. equi.

46 Inhibition remained S. agalactiae-like (i.e., very weak).

47 d (iv) dissemination of antibiotic-resistant S. agalactiae appears to include both clonal spread of r

48 We conclude that some S. agalactiae strains can grow in human urine, and this

49 A] mutant of SCP from group B Streptococcus (S. agalactiae, SCPB) revealed SCPB is composed of five d

50 The S. agalactiae detection rate by early-aliquot carrot bro

51 ene reservoir available for inclusion in the S. agalactiae pan-genome is vast and that unique genes w

52 erence between the crystal structures of the S. agalactiae and the S. pneumoniae hyaluronate lyases.

53 d by comparing the crystal structures of the S. agalactiae and the Streptococcus pneumoniae enzymes,

54 sIII sequences were compared to those of the S. agalactiae cpsIa locus, and the primary difference be

55 The role of the S. agalactiae global virulence regulator, CovR, in UTI p

56 those available in databases showed that the S. agalactiae species can be described by a pan-genome c

57 f hexasaccharide hyaluronan complex with the S. agalactiae hyaluronate lyase was determined at 2.2 A

58 ed genes specific to the streptococci and to S. agalactiae.

59 (ABSA) that was not seen among uropathogenic S. agalactiae (UPSA) strains isolated from patients with