ライフサイエンスコーパス: S. mitis

1 for both platelet binding and aggregation by S. mitis.

2 wed a protective function for the capsule in S. mitis.

3 ed the mitilysin gene from seven isolates of S. mitis.

4 levels of bacteremia caused predominantly by S. mitis.

5 owever, hybridized to DNA from S. oralis and S. mitis.

6 ern China was caused by a toxigenic clone of S. mitis.

7 ic regions contribute to platelet binding by S. mitis.

8 ine Streptococcus spp. were found, including S. mitis (25 strains, 50.0% of 50); currently unnamed St

9 ion mutant showed that the capsule protected S. mitis against phagocytosis by RAW 264.7 macrophages.

10 groups demonstrated increased proportions of S. mitis and S. oralis by day 1.

11 pneumococci and the closely related species S. mitis and S. oralis, showing up to 10.4% nucleotide d

12 e than to most CSPs previously reported from S. mitis and S. oralis, suggesting that these particular

13 oniae, isolates phenotypically identified as S. mitis and S. oralis, which included isolates previous

14 ovel CSPs from disease-associated strains of S. mitis and S. oralis.

15 s genetic exchange is known to occur between S. mitis and Streptococcus pneumoniae, this finding may

16 rains of S. gordonii, S. sanguis, S. mutans, S. mitis, and S. oralis but only weakly by S. salivarius

17 sly characterized isolates of S. pneumoniae, S. mitis, and S. oralis.

18 S. mitis appear to release mitilysin extracellularly.

19 and genetically are most closely related to S. mitis but which harbor genes encoding the virulence d

20 s, we hypothesize that P. gingivalis induces S. mitis cell death by an unknown mechanism, shaping the

21 In a multivariate analysis, S. aureus, S. mitis, Corynebacterium accolens, and bacilli were sig

22 lts demonstrating that P. gingivalis induces S. mitis death and DNA fragmentation in an in vitro biof

23 common among the strains of S. gordonii and S. mitis examined.

24 ked the toxic effect of E. corrodens extract S. mitis extracts contained a single, strongly reactive

25 treptococcus pneumoniae from nonpneumococcal S. mitis group species.

26 oval from the chamber compared to cells from S. mitis-infected chambers.

27 These results suggest that S. mitis is the most common cause of viridans streptococ

28 but one other mitis group streptococci (one S. mitis isolate generated an OD-value above 2.1).

29 olates did fall into a well-separated group, S. mitis isolates did not cluster into a well-separated

30 We show that while the polysaccharide from S. mitis J22 is flexible, requiring multiple conformatio

31 the oral streptococci, including isolates of S. mitis known to possess pneumolysin and autolysin.

32 neutralization assay results, one isolate of S. mitis may produce a further hemolytic toxin in additi

33 S. mitis/oralis endophthalmitis is a devastating complic

34 lecular testing confirmed a common strain of S. mitis/oralis.

35 the affected patients also were positive for S. mitis/oralis.

36 tients, and 13 of those cases were caused by S. mitis (P = 0.007).

37 Under such conditions, S. mitis resistance to clearance could be enhanced by ca

38 d against challenge by the oral streptococci S. mitis, S. mutans, and S. salivarius.

39 cation observed for other species, including S. mitis, S. oralis, and S. pseudopneumoniae.

40 We found that S. mitis, S. oralis, and S. sanguis, as well as oral act

41 be SSA-3 hybridized to DNA from S. gordonii, S. mitis, S. oralis, S. parasanguinis, and S. vestibular

42 The LLY gene was identified in strains of S. mitis, S. pneumoniae, and Streptococcus pseudopneumon

43 This effect was enhanced in the S. mitis strain expressing the S. pneumoniae capsule, wh

44 ened a Tn916deltaE-derived mutant library of S. mitis strain SF100 for reduced binding to human plate

45 g S. mitis strains (28.0%, 7/25) and not non-S. mitis strains (0/25) (P = 0.004).

46 n (MIC, 4 to 12 mug/ml) was noted only among S. mitis strains (28.0%, 7/25) and not non-S. mitis stra

47 When the direct binding of S. mitis strains SF100 and PS344 to immobilized ganglios

48 Significantly more S. mitis strains than non-S. mitis strains were resistan

49 Significantly more S. mitis strains than non-S. mitis strains were resistant to fluoroquinolones and

50 S. mitis survival in horse blood or in a mouse model of

51 Since SM1 is the first prophage of S. mitis that has been identified and because of the pos

52 -198) also inhibited the binding in vitro of S. mitis to human fibrinogen and platelets.

53 ge life cycle, lysin mediates the binding of S. mitis to human platelets via its interaction with fib

54 pblA and pblB mediate the attachment of S. mitis to platelets and play a significant role in S.

55 GR4 showed higher rates of survival than the S. mitis type strain or the capsule-switching mutant, ex

56 In this study, the S. mitis type strain switched capsule by acquisition of

57 to platelets and play a significant role in S. mitis virulence in the endocardium, but have never pr

58 c to HL60 cells, whereas similar extracts of S. mitis were nontoxic.

59 le cells in chambers from mice infected with S. mitis were PI positive (apoptotic) or negative (live)