ライフサイエンスコーパス: B. dermatitidis

1 B. dermatitidis incubated with BALF and washed, plus BAM

2 B. dermatitidis possesses a remarkable ability to resist

3 nts commonly mediate antimicrobial activity, B. dermatitidis may utilize BALF constituents, such as S

4 Thus, although advanced B. dermatitidis infection may exhibit extracellular resi

5 of its promoter was transferred into African B. dermatitidis lacking a native BAD1 locus, and phase-s

6 arium spp., and P. boydii as well as against B. dermatitidis and H. capsulatum.

7 e showed impaired vaccine resistance against B. dermatitidis infection compared to that of wild-type

8 ls confer vaccine-induced resistance against B. dermatitidis, H. capsulatum, and C. posadasii.

9 - BALF inhibited TNF-alpha production by BAM-B. dermatitidis (P < 0.01).

10 th SP-D-/- BALF, TNF-alpha production by BAM-B. dermatitidis was inhibited (P < 0.01).

11 BAM plus B. dermatitidis (BAM-B. dermatitidis) TNF-alpha production was inhibited > or

12 BS contained MBL-C, which bound B. dermatitidis, as shown by IFA assay.

13 gulatory effects on complement activation by B. dermatitidis.

14 activation, binding, and processing of C3 by B. dermatitidis.

15 tial for the acquisition of pathogenicity by B. dermatitidis.

16 tion 94% when macrophages were stimulated by B. dermatitidis, whereas mouse immunoglobulin G (IgG) di

17 of TNF-alpha production by BAM stimulated by B. dermatitidis.

18 oxide as a potential target of subversion by B. dermatitidis yeast cells.

19 robe hybridized with DNA from H. capsulatum, B. dermatitidis, C. immitis, P. brasiliensis, and P. mar

20 Specific probes for H. capsulatum, B. dermatitidis, C. immitis, P. brasiliensis, P. marneff

21 l-time PCR assay to detect and differentiate B. dermatitidis and H. capsulatum from culture isolates

22 icities and sensitivities of 99% and 86% for B. dermatitidis and 100% and 73% for H. capsulatum compa

23 ed 100% specificity and 100% sensitivity for B. dermatitidis and 100% specificity and 94% sensitivity

24 c studies of putative virulence factors from B. dermatitidis.

25 Fungal cultures grew B. dermatitidis.

26 HK B. dermatitidis incubated with serum and then washed als

27 When serum was absorbed with HK B. dermatitidis or live B. dermatitidis, absorbed serum

28 atient's serum were negative for C. immitis, B. dermatitidis, and Histoplasma capsulatum antibodies.

29 a-galactosidase reporter fusions analysed in B. dermatitidis and H. capsulatum confirmed that BAD1 is

30 The role of BAD1 in B. dermatitidis yeast-complement interaction was also as

31 th types of animals showed no differences in B. dermatitidis killing.

32 ations of the genetic basis for virulence in B. dermatitidis.

33 Analbuminemic rat serum did not inhibit B. dermatitidis growth in vivo; however, the addition of

34 Instead, B. dermatitidis yeast cells appear to inhibit iNOS enzym

35 ressed capacity of their neutrophils to kill B. dermatitidis.

36 blood neutrophils from mature animals killed B. dermatitidis (41%) more than did those from immature

37 PM stimulated with heat-killed (HK) or live B. dermatitidis yeast cells.

38 was absorbed with HK B. dermatitidis or live B. dermatitidis, absorbed serum failed to significantly

39 If serum was absorbed with live B. dermatitidis, unbound serum was eluted, and bound ser

40 t anti-BAD1 antibody enhanced the ability of B. dermatitidis yeast to interact with the host compleme

41 ll clones against immunodominant antigens of B. dermatitidis is biased by a combination of the TCR re

42 BAD1 of B. dermatitidis thus co-opts normal host cell physiology

43 Yeast cells of B. dermatitidis display an adhesion promoting protein te

44 The BALF depleted by a coating of B. dermatitidis lost the ability to inhibit TNF-alpha pr

45 provides a rapid method for the detection of B. dermatitidis and H. capsulatum from culture isolates

46 ntranasal administration of a lethal dose of B. dermatitidis yeasts (Kaplan-Meier survival curve P va

47 mAbs to WI-1 enhanced binding and entry of B. dermatitidis yeasts into J774.16 cells but did not en

48 the mold form and 2 CFU of the yeast form of B. dermatitidis.

49 raldehyde-3-phosphate dehydrogenase genes of B. dermatitidis and H. capsulatum, respectively.

50 ype of human infection and genetic groups of B. dermatitidis and provides a framework for further inv

51 The assay identified all haplotypes of B. dermatitidis and five of six positive paraffin-embedd

52 assay allowed rapid (5-h) identification of B. dermatitidis from culture and from clinical specimens

53 ellites to genotype 227 clinical isolates of B. dermatitidis from Wisconsin patients.

54 licited cells were more impaired; killing of B. dermatitidis was insignificant, and killing of C. alb

55 Molecular genetic manipulation of B. dermatitidis represents a major advance in our abilit

56 es not appear to impair the pathogenicity of B. dermatitidis.

57 orescence, yet serum blocked IFA staining of B. dermatitidis by anti-1,3-beta-glucan IgG antibody.

58 ic sequences from three different strains of B. dermatitidis and the development of RNA interference

59 Strains of B. dermatitidis are a sister species of E. parva.

60 We investigated African strains of B. dermatitidis for expression of the surface protein ad

61 Herein, strains of B. dermatitidis with silenced expression of BYS1 were en

62 not in mycelia of North American strains of B. dermatitidis, and this expression pattern was confirm

63 how the protein localizes to the surface of B. dermatitidis.

64 Treatment of B. dermatitidis with anti-1,3-beta-glucan antibody inhib

65 l role of WI-1 in adherence and virulence of B. dermatitidis yeasts.

66 for TNF-alpha production and was detected on B. dermatitidis by IFA.

67 ggest that SP-D in BALF binds beta-glucan on B. dermatitidis, blocking BAM access to beta-glucan, the

68 BAM plus B. dermatitidis (BAM-B. dermatitidis) TNF-alpha producti

69 hibit TNF-alpha production by RAW cells plus B. dermatitidis, and immunoblotting showed that absorbed

70 BS inhibited TNF-alpha production by PM plus B. dermatitidis in a concentration-dependent manner.

71 glucan antibody, we showed by IFA assay that B. dermatitidis contained 1,3-beta-glucan.

72 We report that B. dermatitidis yeast cells reduce nitric oxide levels i

73 We show that B. dermatitidis yeast cells do not block upregulation of

74 by either a 375-bp promoter fragment of the B. dermatitidis WI-1 gene encoding adhesin or an Aspergi

75 ructure and function of BAD-1, as well as to B. dermatitidis acquisition of calcium from the environm

76 ALF inhibited the binding of SP-D in BALF to B. dermatitidis as demonstrated by IFA.

77 atitidis is mediated by serum MBL binding to B. dermatitidis at 1,3-beta-glucan sites or sterically m

78 icated that non-IgG serum factors binding to B. dermatitidis prevented access to 1,3-beta-glucan by a

79 -A or -C), we showed that serum MBL bound to B. dermatitidis.

80 g to new insights about adaptive immunity to B. dermatitidis.

81 ate proinflammatory immune response of PM to B. dermatitidis is mediated by serum MBL binding to B. d

82 otype toward Th1, and enhances resistance to B. dermatitidis infection.

83 n of optimal, protective T-cell responses to B. dermatitidis infection but may be dispensable for the

84 ss production of TNF-alpha than did unwashed B. dermatitidis (P < 0.05).

85 anti-SP-D antibody on BALF-treated unwashed B. dermatitidis in an immunofluorescence assay (IFA).

86 ung biopsy showed structures consistent with B. dermatitidis and S. stercoralis.

87 n lung alveolar fluids of mice infected with B. dermatitidis was severalfold higher for WI-1 knockout

88 tion against lethal pulmonary infection with B. dermatitidis in mice.

89 y against lethal experimental infection with B. dermatitidis.

90 resistance against pulmonary infection with B. dermatitidis.

91 BAM from CD-1 mice were stimulated with B. dermatitidis without or with normal BALF, surfactant

92 In an IFA study with B. dermatitidis, serum with an anti-mouse IgG conjugate