ライフサイエンスコーパス: gastric inflammation

1 pepsinogen (PG) I and II levels (measures of gastric inflammation).

2 Coro1A(-/-) mice, resulting in an attenuated gastric inflammation.

3 on of host defense against the bacterium and gastric inflammation.

4 ls is important to regulatory suppression of gastric inflammation.

5 to H. felis-induced gastritis, with enhanced gastric inflammation.

6 t in individuals with non-H. pylori -induced gastric inflammation.

7 f the -511T/T genotype was related to severe gastric inflammation.

8 ction of IL-8, and induction of neutrophilic gastric inflammation.

9 igated whether BMP signaling pathways affect gastric inflammation after bacterial infection of mice.

10 s, H. pylori colonization of gerbils induced gastric inflammation and a systemic antibody response to

11 ich a high-salt diet leads to high levels of gastric inflammation and associated oxidative stress in

12 mucosal IL-1beta levels and were related to gastric inflammation and atrophy, factors thought to be

13 genicity island is associated with increased gastric inflammation and decreased epithelial repair.

14 ith the cagA mutant strain had low levels of gastric inflammation and did not develop hypochlorhydria

15 es that Th1-independent mechanisms can cause gastric inflammation and disease due to H. pylori.

16 7BL/10J and BALB/c mice also did not develop gastric inflammation and displayed a mixed Th1/Th2 splen

17 ins by Helicobacter pylori may contribute to gastric inflammation and epithelial damage.

18 se chain reaction and colony hybridization), gastric inflammation and epithelial injury (assessed his

19 .01), whereas IFN-gamma-/- mice exhibited no gastric inflammation and higher levels of IL-4 productio

20 pylori infection elevates IFN-gamma-mediated gastric inflammation and may suppress IFN-gamma signalin

21 l mucous gland cells to protect animals from gastric inflammation and resulting hyperplasia.

22 The intensity of gastric inflammation and the extent of Helicobacter colo

23 n was fully recapitulated in mouse models of gastric inflammation and tumorigenesis.

24 h factors influence mucosal IL-1beta levels, gastric inflammation, and atrophy, multiple regression a

25 e were evaluated for cellular proliferation, gastric inflammation, and cytokine and Ab production at

26 iated with bacterial virulence determinants, gastric inflammation, and duodenal ulceration, suggestin

27 itis, as indicated by anti-parietal cell Ab, gastric inflammation, and the presence of cells capable

28 licobacter pylori infection not only induces gastric inflammation but also increases the risk of gast

29 Helicobacter pylori infection induces gastric inflammation but the host fails to generate prot

30 GAS mice exhibited a significant increase in gastric inflammation compared with either uninfected or

31 L/6 mice exhibited a significant increase in gastric inflammation compared with uninfected or infecte

32 sa were well correlated with the severity of gastric inflammation, confirming that H. pylori-induced

33 Infected C57BL/6J SCID mice did not develop gastric inflammation despite colonization by many bacter

34 gastrin release could be related to chronic gastric inflammation, elevated luminal ammonia level, or

35 e protein oipA to promote IL-8 secretion and gastric inflammation have also been explored.

36 , those fed a high-salt diet had more severe gastric inflammation, higher gastric pH, increased parie

37 The mice were scored for severity of gastric inflammation, hyperplasia, glandular atrophy, an

38 roliferation correlated with the severity of gastric inflammation in both immunized/challenged (prote

39 1 cytokine IFN-gamma in H. pylori-associated gastric inflammation in C57BL/6J mice.

40 gamma resulted in a significant reduction of gastric inflammation in H. felis-infected, as well as im

41 ked whether Muc1 might also counter-regulate gastric inflammation in response to H. pylori infection.

42 lori in piglets but does induce neutrophilic gastric inflammation in some infected piglets.

43 at 18 weeks postinoculation revealed minimal gastric inflammation in the animals that received the mu

44 ase reactions can occur during IgE-dependent gastric inflammation in the mouse and that the infiltrat

45 eutrophils during immunoglobulin E-dependent gastric inflammation in the mouse.

46 as well as TH1 or TH2 cell lines exacerbated gastric inflammation in the recipients.

47 of IL-8 in vitro and significantly decreased gastric inflammation in vivo.

48 The gastric inflammation in wt and IL-10(-/-) mice contained

49 gated the role of IL-17 signaling in chronic gastric inflammation induced by Helicobacter pylori, a G

50 Immunoglobulin E-dependent gastric inflammation is characterized by neutrophil infi

51 of epithelial injury, and we have shown that gastric inflammation is increased in H. pylori-infected

52 diated injury, our experiments now show that gastric inflammation is increased within the context of

53 H. pylori infection and gastric inflammation may enhance humoral immunity to ora

54 D/+);gp130(F/F) mice promoted more extensive gastric inflammation, metaplastic transformation, and tu

55 onization density was higher and mononuclear gastric inflammation more severe in infected IL-17RA(-/-

56 ld-type mice did not affect the intensity of gastric inflammation or the extent of Helicobacter colon

57 acterial colonization density, the degree of gastric inflammation, or the presence of lymphoid follic

58 ction which can result in various degrees of gastric inflammation, peptic ulcer disease, and a predis

59 elicobacter pylori infection induces chronic gastric inflammation that can progress to cancer.

60 known to be responsible for inducing chronic gastric inflammation that progresses to atrophy, metapla

61 IgE-dependent gastric inflammation was elicited in genetically mast ce

62 Gastric inflammation was induced by infection of mice wi

63 Gastric inflammation was mild or was absent for all cats

64 Severe gastric inflammation was only observed in d3Tx mice.

65 on, two rodent models of chronic lymphocytic gastric inflammation were examined.

66 rences in bacterial colonization density and gastric inflammation were not apparent at 1 mo postinfec

67 Two rat models of mild gastric inflammation were studied.

68 Colonization induces chronic gastric inflammation which can progress to a variety of

69 gree of association of chronic intestinal or gastric inflammation with the development of cancer, has

70 ck a gastric microbiota, C. albicans induced gastric inflammation within 1 week of inoculation.