ライフサイエンスコーパス: ileitis

1 ltaARE)(/+) mice, which develop Crohn's-like ileitis.

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

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

4 volved in the pathogenesis of chronic murine ileitis.

5 a spontaneous model of Crohn's disease-like ileitis.

6 le during the early stages of chronic murine ileitis.

7 with extensive fibrostenosing Crohn's jejuno-ileitis.

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

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

10 blocked LTB4-induced substance P action and ileitis.

11 or alpha4 integrins) was required to improve ileitis.

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

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

14 contribute to the development of SAMP1/YitFc ileitis.

15 d with Deltasag1 parasites failed to develop ileitis.

16 n this experimental model of pathogen-driven ileitis.

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

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

19 le body hyperthermia and production of acute ileitis.

20 ths in a mouse model of Crohn's-disease-like ileitis.

21 1 did not develop obvious characteristics of ileitis.

22 associated acidosis in both murine and human ileitis.

23 acidification in the TNF ARE model of murine ileitis.

24 due to lymphatic disorders in the absence of ileitis.

25 1A/DR3 signaling drives experimental CD-like ileitis.

26 ce that spontaneously develop a Crohn's-like ileitis.

27 be elevated in a spontaneous mouse model of ileitis.

28 ficient Teff cell homeostasis and attenuated ileitis.

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

30 and decreased DC migration before developing ileitis.

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

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

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

34 itiating molecular events underlying CD-like ileitis.

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

36 xperienced disseminated infection and lethal ileitis.

37 es in a murine model of chronic eosinophilic ileitis.

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

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

40 population had no effect on the severity of ileitis.

41 moting inflammation in models of colitis and ileitis.

42 because GF SAMP1/YitFc mice develop chronic ileitis.

43 asma gondii surface protein stimulates acute ileitis.

44 SR140333 prevented AP-induced ileitis.

45 1/YitFc murine model of Crohn's disease-like ileitis.

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

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

48 icantly ameliorated the established, chronic ileitis and also protected mice from developing acute DS

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

50 nhibition of ADAR in mice causes spontaneous ileitis and colitis.

51 athogenic role for LND cells in both Crohn's ileitis and colitis.

52 l differentiation in mouse models of CD-like ileitis and colitis.

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

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

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

56 protected against Toxoplasma gondii-induced ileitis and dextran sulfate sodium-induced colitis.

57 ame expression patterns in both experimental ileitis and IBD patients.

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

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

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

61 l PAR-2 and CGRP levels by EA attenuates the ileitis and resultant VH.

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

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

64 0/153) had ITB, 6.5% (10/153) had infectious ileitis, and 9.15% (14/153) were indeterminate on histop

65 1a-overexpression in mice causes spontaneous ileitis, and exacerbates induced proximal colitis and fi

66 erichia coli (E2348/69) to induce infectious ileitis, and ileum contents were quantified by polymeras

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

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

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

70 nal cord (T(11)) were sampled for evaluating ileitis at days 7 and 22, and distribution and expressio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 The implication of microscopic ileitis finding in patients referred for ileocolonoscopy

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

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

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

90 Patients in the microscopic ileitis group were significantly associated with Crohn's

91 biopsy and were included in the microscopic ileitis group.

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

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

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

95 Using an established murine model of CD-like ileitis, i.e., the SAMP1/YitFc (SAMP) mouse strain, we s

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

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

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

99 The discovery of microscopic ileitis in clinically suspected IBD is associated with i

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

101 TLOs in this location are associated with ileitis in humans and mice.

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

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

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

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

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

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

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

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

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

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

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

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

114 ency in T cells exacerbated bile acid-driven ileitis in T cell-reconstituted Rag1(-/-) or Rag2(-)(/)(

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

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

117 rived LTalphabeta(2) would critically affect ileitis in TNF(DeltaARE+/-) mice.

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

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

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

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

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

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

124 1 (Th1) cell-associated immunity exacerbates ileitis induced by oral Toxoplasma gondii infection.

125 To assess the effects of EA on ileitis-induced VH and confirm whether EA attenuates VH

126 However, the mechanism by which EA treats ileitis-induced VH is not clearly known.

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

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

129 (normal or reactive changes) and microscopic ileitis (inflammation or ileitis of any severity).

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

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

132 Ileitis is dependent on commensal microbiota and derives

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

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

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

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

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

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

139 es) and microscopic ileitis (inflammation or ileitis of any severity).

140 Patients with granuloma or moderate-severe ileitis on biopsy were significantly associated with Cro

141 -ileitis on day 7, microscopically low-grade ileitis on day 22 and VH at days 7-22.

142 -treated-goats exhibited apparent transmural-ileitis on day 7, microscopically low-grade ileitis on d

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 lymph nodes from TNF( ARE) mice, a model of ileitis, revealed TLO formation at valves of CLVs.

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

159 m), short-chain fatty acids, microbiome, and ileitis severity (mean histopathology score decreases of

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

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

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

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

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

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

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

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

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

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

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

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

172 As with isolated ileitis the findings of nonspecific small bowel enteriti

173 Our mouse model of Crohn's disease-like ileitis, the SAMP1/YitFc (SAMP) mouse, was subjected to

174 our mouse model of Crohn's disease (CD)-like ileitis, the SAMP1/YitFc (SAMP1), does not exhibit basel

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

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

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

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

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

180 were sufficient for adoptively transferring ileitis to SCID recipients.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 d to evaluate the correlation of microscopic ileitis with long-term clinical outcome.

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

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

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

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

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

204 eta(2) and LTalpha(3) have distinct roles in ileitis, with the role of LTalpha(3) unexpectedly protec

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