ライフサイエンスコーパス: N. brasiliensis

1 N. brasiliensis infection and HDM challenge induced an i

2 N. brasiliensis infection-induced upregulation of IL-25

3 N. brasiliensis was expelled by mice that expressed IL-4

4 N. brasiliensis-induced changes in PAR-1 function and ex

5 es obtained from lungs as late as 45 d after N. brasiliensis inoculation were able to transfer accele

6 n the draining lymph node was examined after N. brasiliensis inoculation.

7 ns in Th2 cytokines and worm expulsion after N. brasiliensis inoculation.

8 uency of lung Th2 cells, but not ILC2, after N. brasiliensis infection and HDM challenge.

9 cy of Th2 cells and ILC2s in the lungs after N. brasiliensis infection.

10 hoid type 2 cells (ILC2s) in the lungs after N. brasiliensis infection.

11 ignificantly decreased in CCL2-/- mice after N. brasiliensis inoculation.

12 exited the draining lymph node shortly after N. brasiliensis inoculation.

13 o restore the impaired host immunity against N. brasiliensis infection in IL-13(-/-) mice.

14 ling is required for host protection against N. brasiliensis and T. spiralis but contributes to expul

15 opacification of Middlebrook 7H11 agar, and N. brasiliensis and N. pseudobrasiliensis were the only

16 IL-13, H. polygyrus, and N. brasiliensis, but not IL-4, also increased contractil

17 es to nerve stimulation in H. polygyrus- and N. brasiliensis-infected mice were dependent in part on

18 ated that the cellular infiltrates caused by N. brasiliensis transit through the lungs were quickly r

19 he cellular and molecular changes induced by N. brasiliensis infection, there was a significant reduc

20 - mice, the IL-13-/- animals failed to clear N. brasiliensis infections efficiently, despite developi

21 Following Gr-1+ cell depletion, N. brasiliensis infection resulted in transient, but sig

22 he development of a Th2-type response during N. brasiliensis infection, in vivo.

23 ent, which are two mechanisms that eliminate N. brasiliensis parasites from infected hosts.

24 mice and Stat6-deficient mice fail to expel N. brasiliensis, and a specific antagonist for IL-13, an

25 polygyrus infection or in the lung following N. brasiliensis infection, was unaltered by depletion of

26 impaired Th2 response was observed following N. brasiliensis infection.

27 on use of the TLR4-dependent adjuvant G3D6A, N. brasiliensis infection impaired selectively the induc

28 la(-/-) Retnlb(-/-) mice negatively impacted N. brasiliensis fitness, as demonstrated by significantl

29 responses, 3) the roles of IL-13 and IL-4 in N. brasiliensis infection-induced alterations in PAR-1 r

30 s the sole predictor of genetic variation in N. brasiliensis, and that slope, rivers, and historical

31 Furthermore, although IL-4 induces N. brasiliensis expulsion in the absence of B cells, T c

32 L-4-induced expulsion of T. spiralis but not N. brasiliensis.

33 MDSCs surprisingly enhanced the clearance of N. brasiliensis infection.

34 e mice, this did not impact the expulsion of N. brasiliensis after primary and secondary infection, o

35 pecific cell types in the small intestine of N. brasiliensis-infected mice.

36 e exploited the transient pulmonary phase of N. brasiliensis development to study the innate immune r

37 e responses induced during the lung phase of N. brasiliensis infection were similar in complexity and

38 All strains of N. brasiliensis, N. otitidiscavarium, and N. farcinica w

39 ccumulation after injection of C. elegans or N. brasiliensis.

40 le to correctly identify the human pathogens N. brasiliensis, N. cyriacigeorgica, N. farcinica, N. no

41 27-treated gammadelta T cells during primary N. brasiliensis lung infection conferred protection in m

42 In addition, the N. brasiliensis-altered pulmonary environment showed dra

43 Thus, N. brasiliensis expulsion requires signaling via IL-4Ral

44 inct effects on immunity and inflammation to N. brasiliensis To test the importance of both proteins,

45 al smooth muscle and epithelial responses to N. brasiliensis infection that were associated with an i

46 tinal nematode, Trichinella spiralis, unlike N. brasiliensis expulsion, is mast cell dependent, these

47 e the only species positive for PYR, whereas N. brasiliensis was the only species that hydrolyzed MNP

48 proteins driven by tRNA(Sec) (Trsp), whereas N. brasiliensis-infected Trsp(fl/fl)Cre(LysM) selenium-s

49 While N. brasiliensis did not induce alternate activation of l

50 t recipient mice following immunization with N. brasiliensis plus OVA.

51 ent Th1/Th17 responses in mice infected with N. brasiliensis was dependent on IL-4/IL-13.

52 Concurrent infection with N. brasiliensis or with Schistosoma mansoni promoted T c

53 ls in recipient IL-4-/- mice inoculated with N. brasiliensis plus OVA.

54 Infection of Gr-1+ cell-depleted mice with N. brasiliensis larvae that were pretreated with antibio

55 We therefore infected Nlrp3 (-/-) mice with N. brasiliensis Unexpectedly, compared with wild-type (W

56 ion was not evident early postinfection with N. brasiliensis, and in contrast to Nlrp3 (-/-) mice, an

57 cigeorgica and N. wallacei, tigecycline with N. brasiliensis and N. cyriacigeorgica, and sulfonamides