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 es emzantsi (n = 9, 26%), from South Africa; B. dermatitidis (n = 1, 3%), from the Democratic Republi

6 s; B. emzantsi (n=9, 26%) from South Africa; B. dermatitidis (n=1, 3%) from Democratic Republic of Co

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

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

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

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

11 om Africa deposited in global collections as B. dermatitidis; for 5, we sequenced the internal transc

12 om Africa deposited in global collections as B. dermatitidis; for 5, we sequenced the internal transc

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

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

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

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

17 gulatory effects on complement activation by B. dermatitidis.

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

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

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

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

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

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

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

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

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

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

28 It differs from B. dermatitidis in morphological presentation in culture

29 ere caused by species that are distinct from B. dermatitidis Increasing clinical awareness and access

30 ch were closely related to but distinct from B. dermatitidis, Blastomyces gilchristii, and Blastomyce

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

32 Fungal cultures grew B. dermatitidis.

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

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

35 We identified B. dermatitidis as the predominant pathogen in 38 cases

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 MiraVista quantitative EIAs for detection of B. dermatitidis GM in urine.

55 al-time PCR assay for the differentiation of B. dermatitidis and B. gilchristii The new assay permitt

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 Correlation between the quantitative B. dermatitidis antigen levels by the Gotham and MiraVis

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

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

84 Mechanistic studies reveal that B. dermatitidis infection, as well as B-glucan exposure,

85 Mechanistic studies reveal that B. dermatitidis infection, as well as beta-glucan exposu

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

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

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

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

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

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

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

93 ogy and epidemiology of blastomycosis due to B. dermatitidis and B. gilchristii.

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

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

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

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

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

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

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

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

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

103 y against lethal experimental infection with B. dermatitidis.

104 resistance against pulmonary infection with B. dermatitidis.

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

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