ライフサイエンスコーパス: ileitis

1 , TCR-delta-/- mice rapidly developed severe ileitis.

2 blocked LTB4-induced substance P action and ileitis.

3 or alpha4 integrins) was required to improve ileitis.

4 d the SAMP1/YitFc mouse model of spontaneous ileitis.

5 TB4 levels and toxin A- but not LTB4-induced ileitis.

6 contribute to the development of SAMP1/YitFc ileitis.

7 d with Deltasag1 parasites failed to develop ileitis.

8 n this experimental model of pathogen-driven ileitis.

9 treatment in the SAMP1/YitFc mouse model of ileitis.

10 orption of bile salts is observed in Crohn's ileitis.

11 le body hyperthermia and production of acute ileitis.

12 and decreased DC migration before developing ileitis.

13 ease in a mouse model of progressive CD-like ileitis.

14 in a spontaneous model of Crohn Disease-like ileitis.

15 P) mice that spontaneously develop a CD-like ileitis.

16 be elevated in a spontaneous mouse model of ileitis.

17 itiating molecular events underlying CD-like ileitis.

18 e in the mouse model of Crohn's disease-like ileitis.

19 xperienced disseminated infection and lethal ileitis.

20 ficient Teff cell homeostasis and attenuated ileitis.

21 es in a murine model of chronic eosinophilic ileitis.

22 rohn's disease patients and murine models of ileitis.

23 o assess the role of CD44 for development of ileitis.

24 population had no effect on the severity of ileitis.

25 moting inflammation in models of colitis and ileitis.

26 because GF SAMP1/YitFc mice develop chronic ileitis.

27 asma gondii surface protein stimulates acute ileitis.

28 SR140333 prevented AP-induced ileitis.

29 1/YitFc murine model of Crohn's disease-like ileitis.

30 zymes (trypsin I/II, trypsin IV, p23) caused ileitis.

31 teristic of the chronic phase of SAMP1/YitFc ileitis.

32 volved in the pathogenesis of chronic murine ileitis.

33 y T cells there, and reduced the severity of ileitis.

34 le during the early stages of chronic murine ileitis.

35 ile acid malabsorption is present in Crohn's ileitis.

36 ule results in attenuation of chronic murine ileitis, a disease previously resistant to antiadhesion

37 mice are resistant to the development of the ileitis after T. gondii infection.

38 dium sulfate (DSS) and developed spontaneous ileitis and colitis after 16 mo of age in specific patho

39 asmic reticulum (ER) stress, severe terminal ileitis and colitis.

40 wever, these mice later (>14 days) developed ileitis and colitis.

41 tosis and the TNF-independent development of ileitis and colitis.

42 Ccr2(-/-) mice suffered from acute ileitis and inflammation in the spleen that was associat

43 Ileitis and remodeling increased over the 40 weeks, as d

44 Histological and molecular features of ileitis and remodeling were assessed using immunohistoch

45 th TH1 and TH2 pathways mediate Crohn's-like ileitis and suggest that combined TH1/TH2 manipulation m

46 by 4 weeks of age and preceded the onset of ileitis, and (6) a subgroup of mice (approximately 5%) d

47 inct roles during the development of chronic ileitis, and influence the balance of effector and regul

48 ccharomyces cerevisiae can induce arthritis, ileitis, and interstitial pneumonitis in BALB/c ZAP70 (W

49 : (1) SAMP1/YitFc mice displayed established ileitis as early as 10 weeks of age, (2) the incidence o

50 The resulting ileitis bears a remarkable resemblance to human Crohn's

51 rapy significantly decreased the severity of ileitis both in the prevention (40% reduction, p < 0.05)

52 -inflammatory molecule capable of preventing ileitis by activating the transforming growth factor bet

53 and for their ability to detect and quantify ileitis by intravital microscopy and transabdominal US.

54 leum-specific effects of reducing CLR on TxA ileitis by local preinjection of double-stranded RNAs.

55 After induction of ileitis by means of 2, 4, 6-trinitrobenzene sulfonic aci

56 Acute and lethal ileitis can be elicited in certain strains of inbred mic

57 Toxoplasma gondii results in an acute lethal ileitis characterized by increased interferon gamma, tum

58 nt mice exposed to cigarette smoke developed ileitis, characterized by increased expression of interf

59 In contrast, the establishment of chronic ileitis coincided with significant increases in IL-5 (35

60 In Crohn's ileitis, COX-2 was present in the villus epithelial cell

61 been linked to a human chronic granulomatous ileitis (Crohn's disease).

62 proliferation in vitro, they cannot prevent ileitis development in SCID mice adoptively transferred

63 CDDO acid prevented ileitis development through the global down-regulation o

64 stress, autophagy induction and spontaneous ileitis emerge from Paneth-cell-specific deletion of Xbp

65 barrier function and developed a transmural ileitis following NSAID exposure.

66 resistant mice (BALB/c) that fail to develop ileitis following oral infection with T. gondii were ren

67 dysfunction and induced Crohn's disease-like ileitis following transfer into Rag1(-/-) hosts.

68 Using a TNF-driven model of chronic ileitis (i.e., B6.129P-Tnf(Delta)(ARE) mice) that recapi

69 Using novel models of Crohn's disease-like ileitis (i.e., SAMP1/YitFc and CD4+ T cell transfer mode

70 intestine in a spontaneous model of chronic ileitis (i.e., SAMP1/YitFc mice).

71 ecrosis factor (TNF)-driven model of chronic ileitis (ie, B6.129P-TNF(DeltaAU-rich element [ARE])) th

72 spontaneous Crohn's-disease-like transmural ileitis if both mechanisms are compromised.

73 Consistent with persistent mild ileitis in (B6 x SAMP1/Fc)F(1) mice, this locus appears

74 isease in specific pathogen-free (SPF) mice, ileitis in GF mice is significantly attenuated, and is a

75 Indomethacin-induced ileitis in Lewis rats leads to specific reductions in il

76 evidence that the primary defect conferring ileitis in SAMP mice originates from a nonhematopoietic

77 sion of periodontal disease and the onset of ileitis in SAMP mice was studied.

78 DC migration is required for development of ileitis in SAMP mice.

79 fects on migration of DCs and development of ileitis in SAMP mice.

80 at RELMbeta is involved in the initiation of ileitis in SAMP1/Fc mice and may act through the inducti

81 One of the earliest features of ileitis in SAMP1/Fc mice is an increase in the number of

82 sive imaging modality to detect and evaluate ileitis in SAMP1/YitFc (SAMP) mice.

83 py significantly ameliorates the severity of ileitis in SAMP1/YitFc mice by a mechanism involving dow

84 Initiation of ileitis in SAMP1/YitFc mice was T H 1-mediated because u

85 In this study, we examined whether ileitis in SAMP1/YitFc mice, a recombinant-inbred line t

86 mice, and ameliorated adoptively transferred ileitis in severe combined immunodeficient mice injected

87 AMP) mice, which develop spontaneous CD-like ileitis in the absence of NOD2 genetic mutations, fail t

88 tions may play a role in the pathogenesis of ileitis in this murine model of Crohn's disease.

89 e to the development of Crohn's disease-like ileitis in TNF(DeltaARE/+) mice.

90 e resulted in attenuation of the severity of ileitis in TNFDeltaARE mice.

91 lay an essential role in spontaneous chronic ileitis in vivo by promoting homing of disease-exacerbat

92 against CCR9 to TNFDeltaARE mice exacerbated ileitis in vivo, confirming the regulatory role of CD8(+

93 vitro, and attenuated adoptively transferred ileitis in vivo, most likely counteracting the proinflam

94 tis strongly correlated with the severity of ileitis, independent of age, suggesting that common path

95 1 (Th1) cell-associated immunity exacerbates ileitis induced by oral Toxoplasma gondii infection.

96 n producers of TNF-alpha and the predominant ileitis-inducing subpopulation.

97 hat the bacterial flora is not essential for ileitis induction, because GF SAMP1/YitFc mice develop c

98 oprotection against subsequent ricin-induced ileitis (Injury grade [from 0 = normal to 5 = severe]: 0

99 We show that ileitis is blocked in SAMP1/Fc mice by inheritance of AK

100 Ileitis is dependent on commensal microbiota and derives

101 Indomethacin-induced acute ileitis led to repression of ASBT in wild-type mice and

102 nism of heat stress protection against acute ileitis may involve local intestinal inhibition of leuko

103 ssed by CD4(+) and CD8(+) for development of ileitis mediated by TNF overproduction.

104 at histologic examination in a porcine acute ileitis model as a next step toward clinical translation

105 beta signaling pathway in a pathogen-driven ileitis model.

106 We show here that attenuated ileitis observed in interleukin-22 (IL-22)-deficient mic

107 at least 7 (>/=4 for patients with isolated ileitis) on ileocolonoscopy scored by a masked central r

108 normal appendix, and there may be associated ileitis or ileocolitis noted.

109 sease of the colon, ileal disease ("backwash ileitis"), or both appear to be at greater risk for the

110 ntly ameliorated the severity of established ileitis (P <.05) by decreasing the histologic indices fo

111 and metronidazole before the development of ileitis (prevention protocol) or after ileitis was fully

112 kuSlc, we demonstrate an association between ileitis progression and remodeling over the course of 40

113 pts of the small intestine, and treatment of ileitis-prone mice with a Ppargamma agonist decreased di

114 In ileitis-prone SAMP1/YitFc mice, Paneth cell levels of CR

115 fies intestinal inflammation in experimental ileitis, providing the potential for a reliable, noninva

116 PAR(2) deletion decreased TxA-induced ileitis, reduced luminal fluid secretion by 20%, decreas

117 mice spontaneously develop chronic terminal ileitis, reminiscent of the human disease described by C

118 nant-inbred line that spontaneously develops ileitis resembling human Crohn's disease, was associated

119 ), and administration of MBSelectin in acute ileitis resulted in a significantly higher (P < .001) im

120 ed bone marrow chimeras to determine if SAMP ileitis results from a primary immunological defect or f

121 ion in a spontaneous murine model of chronic ileitis (SAMP1/YitFc) using flow cytometry, real-time re

122 trong positive correlation was found between ileitis severity and ABL in SAMP mice, independent of ag

123 MLN B cell numbers correlate with ileitis severity in SAMP1/YitFc mice, and cotransfer of

124 B cells along with CD4(+) T cells increases ileitis severity in SCID mice compared with transfer of

125 with CD4(+) T cells resulted in exacerbated ileitis severity in SCID mice.

126 SAMP1/YitFc (SAMP) mice develop chronic ileitis similar to human CD.

127 LTB4 caused ileitis similar to that caused by toxin A and antagonism

128 thin two distinct mouse lines of spontaneous ileitis, suggesting that host genetics drive unique and

129 ium may represent the primary source of SAMP ileitis susceptibility.

130 essential for the generation of the chronic ileitis that is characteristic of these mice.

131 -expression of IRGM1 resulted in spontaneous ileitis that resembled human CD in symptoms and histolog

132 P) mice, which spontaneously develop chronic ileitis that resembles Crohn's disease, and that DC migr

133 SAMP1/Fc mice develop spontaneous ileitis that shares many features with human Crohn's dis

134 f lymphocyte populations during induction of ileitis through adoptive transfer studies, and generated

135 RA supplementation attenuates ileitis through its effects on CD103+ DCs, Tregs, and Th

136 d) mice develop a Th1-dependent acute lethal ileitis; TLR9(-/-) mice have higher parasite burdens tha

137 or necrosis factor (TNF) and develop chronic ileitis (TNF_ARE mice).

138 tly, CD4(+) but not CD8(+) T cells conferred ileitis to RAG(-/-) recipients and deficiency of one or

139 were sufficient for adoptively transferring ileitis to SCID recipients.

140 vere ileitis, whereas SAMP BM did not confer ileitis to WT recipients.

141 gh IL-18 exerted pathogenic functions during ileitis triggered by T. gondii, it was required for host

142 ing a mouse model that develops Crohn's-like ileitis (tumor necrosis factor Deltaadenosine uracyl-ric

143 effect of RA supplementation on TNF-induced ileitis using histologic, coculture, and suppression ass

144 hether stratification of children with CD as ileitis versus colitis results in different correlation

145 uced CLR plays a proinflammatory role in TxA ileitis via MAPK signaling and TNF-alpha.

146 Acute terminal ileitis was established in 19 pigs; four pigs served as

147 nt of ileitis (prevention protocol) or after ileitis was fully established (treatment protocol).

148 Ileitis was observed in germfree SAMP1/Fc mice, although

149 old (20-50 wk) SAMP1/YitFc Itgb7(-/-) mice, ileitis was reduced by 30-50% compared with SAMP1/YitFc

150 mph nodes (MLNs) and their ability to induce ileitis was tested after transfer to SCID recipients.

151 ess the role of beta(7) integrins in chronic ileitis, we generated SAMP1/YitFc lacking beta(7) integr

152 n vessels in the bowel wall of segments with ileitis were higher than in control ileum (5.1% +/- 3.7

153 ell adhesion molecule 1 failed to ameliorate ileitis, whereas P-selectin glycoprotein ligand 1 (PSGL-

154 eceiving wild-type (AKR) BM developed severe ileitis, whereas SAMP BM did not confer ileitis to WT re

155 SAMP1/Yit mouse strain develops spontaneous ileitis with histologic features of Crohn's disease.

156 ory cells became more pronounced at sites of ileitis with increasing age and inflammation.

157 y develop chronic, discontinuous, transmural ileitis with many features similar to Crohn's disease.

158 tFc mice that spontaneously develop terminal ileitis with perianal manifestations.

159 tinal inflammation, (3) mice develop chronic ileitis with prominent muscular hypertrophy and focal co

160 SAMP1/YitFc mice develop a spontaneous ileitis with similarities to human CD in regard to histo

161 e in SAMP1/YitFc mice, which develop chronic ileitis with similarity to human Crohn's disease.

162 e with Toxoplasma gondii results in a lethal ileitis within 7-9 days postinfection.