ライフサイエンスコーパス: C. sordellii

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1 C. sordellii and C. difficile form spores that are belie

2 C. sordellii spores germinated only in a narrow pH range

3 n the uterus impair immune responses against C. sordellii.

4 structure can affect the germination of both C. sordellii and C. difficile spores.

5 used by human and mouse macrophages to clear C. sordellii from the infected uterus.

6 Clinical C. sordellii infections were associated with intravagina

7 In contrast, C. sordellii spore germination was significantly less se

8 , we postulated a mechanism for differential C. sordellii spore activation in the female reproductive

9 TNF-alpha and chemokine generation following C. sordellii or peptidoglycan challenge, impaired leukoc

10 infections, we analyzed the requirements for C. sordellii spore germination in vitro.

11 ull mice were more susceptible to death from C. sordellii uterine infection than wild-type mice and e

12 rostol significantly worsened mortality from C. sordellii uterine infection, and impaired bacterial c

13 e isolated a 42-kDa extractable protein from C. sordellii culture supernatant that stimulates prolife

14 ceptor AI/II-deficient mice, showed impaired C. sordellii phagocytosis.

15 n important role in the characteristic LR in C. sordellii infection.

16 fate) revealed a role for these receptors in C. sordellii phagocytosis.

17 d TcsR as the toxin gene (tcsL) regulator in C. sordellii.

18 hormones and bile salts are able to increase C. sordellii spore germination rates.

19 We modeled C. sordellii endometritis in rats to test this hypothesi

20 Although the incidence of C. sordellii infection is low, it is fatal in most cases

21 Recently, an increased incidence of C. sordellii infections has been reported in women under

22 The analysis of the kinetics of C. sordellii spore germination showed strong allosteric

23 in our understanding of the pathogenesis of C. sordellii infections present major challenges to the

24 al virulence factor for the pathogenicity of C. sordellii.

25 hallenge, impaired leukocyte phagocytosis of C. sordellii, and inhibited uterine epithelial cell huma

26 Pathogenic strains of C. sordellii produce numerous virulence factors, includi

27 we tested the effect of sterane compounds on C. sordellii and C. difficile spore germination.

28 Bacilli species, d-alanine had no effect on C. sordellii spore germination.

29 o germinate, the occurrence of postpregnancy C. sordellii infections suggests that steroidal sex horm

30 agenous structure (MARCO) receptor prevented C. sordellii internalization, suggesting that MARCO is a

31 We also report that C. sordellii lethal toxin inhibited GR function in an ex

32 Our data showed that C. sordellii spores require three structurally different

33 etry, we have identified this protein as the C. sordellii neuraminidase, NanS.

34 r tcdR also restored toxin production to the C. sordellii tcsR mutant, showing that these sigma facto

35 Thus, even though C. sordellii and C. difficile are phylogenetically relat

36 High-throughput sequencing of two C. sordellii strains revealed that tcsR lies within a ge

37 avenger receptors to internalize unopsonized C. sordellii.

38 While C. sordellii spores require three structurally distinct

39 tis and toxic shock syndrome associated with C. sordellii that occurred within one week after medical

40 ticoid antagonist RU-486 in combination with C. sordellii lethal toxin additively prevented glucocort

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