ライフサイエンスコーパス: N. brasiliensis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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