ライフサイエンスコーパス: intestinal inflammation

1 iRNA profiling and SCFA level in response to intestinal inflammation.

2 ic treatment, dramatically reduces IL-18 and intestinal inflammation.

3 ed the severity of TcdA/B-induced damage and intestinal inflammation.

4 lation patterns observed in patients without intestinal inflammation.

5 in IL-10-deficient mice was associated with intestinal inflammation.

6 s in human IBD and in experimental models of intestinal inflammation.

7 anti-inflammatory signals and causes chronic intestinal inflammation.

8 cies and shifts in the microbiome that drive intestinal inflammation.

9 lonization and amelioration of fungal-driven intestinal inflammation.

10 gene networks contributing to the underlying intestinal inflammation.

11 r how ILC3s could be manipulated to regulate intestinal inflammation.

12 ism that inhibits the NLRP6-IL-18 pathway in intestinal inflammation.

13 of ATIs in various foods and their effect on intestinal inflammation.

14 t endothelial cells to promote resolution of intestinal inflammation.

15 regulating the innate immune response during intestinal inflammation.

16 with active IBD and in preclinical models of intestinal inflammation.

17 uring antiinflammatory function during acute intestinal inflammation.

18 lera toxin (CT) immunization without causing intestinal inflammation.

19 vestigate expression and functions of SPM in intestinal inflammation.

20 y, gut microbial density, and development of intestinal inflammation.

21 an Il10-deficiency-induced chronic model of intestinal inflammation.

22 ism provides new treatment opportunities for intestinal inflammation.

23 ts that caused immunoglobulin deficiency and intestinal inflammation.

24 ega 3 long-chain fatty acids protect against intestinal inflammation.

25 trated that CS may ameliorate stress-induced intestinal inflammation.

26 Mice were imaged using MSOT to detect intestinal inflammation.

27 y gluten-containing diet increased low-level intestinal inflammation.

28 to prevent development of severe spontaneous intestinal inflammation.

29 be-reactive T cells in patients with chronic intestinal inflammation.

30 sis and compensate for otherwise-detrimental intestinal inflammation.

31 nges in actin dynamics lead to IEC death and intestinal inflammation.

32 hages mediates bacterial internalization and intestinal inflammation.

33 ut-homing perturbing agents used in treating intestinal inflammation.

34 accompanied with a distinct amelioration of intestinal inflammation.

35 its known pathogenic function during chronic intestinal inflammation.

36 le of the ECS also extends to the control of intestinal inflammation.

37 n Th2 effector responses that drive allergic intestinal inflammation.

38 the production of microbial metabolites and intestinal inflammation.

39 gs prevented the development of diarrhea and intestinal inflammation.

40 be a promising approach for the treatment of intestinal inflammation.

41 ory cytokines and enhanced susceptibility to intestinal inflammation.

42 colitis models, SBA supplementation reduces intestinal inflammation.

43 elial cells during amino acid starvation, or intestinal inflammation.

44 of the TNF superfamily are key regulators of intestinal inflammation.

45 aling can activate asymmetric division after intestinal inflammation.

46 ocytes from NEC mice into naive mice induced intestinal inflammation.

47 the role of ADF in limiting the severity of intestinal inflammation.

48 investigate the role of IL-33 during chronic intestinal inflammation.

49 (including pathogens and pathobionts) during intestinal inflammation.

50 orm complementary roles in the regulation of intestinal inflammation.

51 rial defenses, but at the cost of increasing intestinal inflammation.

52 for enhancing mucosal immunity and treating intestinal inflammation.

53 tion, mucosal injury but failed to attenuate intestinal inflammation.

54 -specific strategies for treating pathologic intestinal inflammation.

55 fe and effective therapeutic approach during intestinal inflammation.

56 rease intestinal barrier function and reduce intestinal inflammation.

57 M cells may be a useful correlate of chronic intestinal inflammation.

58 RA metabolism mediated by microbiota-induced intestinal inflammation.

59 intestines to amniotic fluid, with resultant intestinal inflammation.

60 ts profound therapeutic effects in models of intestinal inflammation.

61 is, whereas dysbiosis decreased with reduced intestinal inflammation.

62 ctivation in the development of Stx-mediated intestinal inflammation.

63 atory molecules, including TSG6, that reduce intestinal inflammation.

64 suggested that certain nutrients can reduce intestinal inflammation.

65 LCs in mice and in human beings with chronic intestinal inflammation.

66 effector function and are poor mediators of intestinal inflammation.

67 w alterations in autophagy can contribute to intestinal inflammation.

68 ontaneous IFN production and immune-mediated intestinal inflammation.

69 nt factor contributing to the development of intestinal inflammation.

70 responses in vivo and preventing autoimmune intestinal inflammation.

71 RNA induction in THC-mediated suppression of intestinal inflammation.

72 iver Laboratories; and (3) mice subjected to intestinal inflammation.

73 ells in patients with CD and mouse models of intestinal inflammation.

74 ghts into treatments that quiet pathological intestinal inflammation.

75 ds worsened inflammation in the DSS model of intestinal inflammation.

76 interferon (IFN)-gamma-secreting T cells and intestinal inflammation.

77 activation, the latter being associated with intestinal inflammation.

78 evere diarrhea in the absence of substantial intestinal inflammation.

79 since DON ingestion may result in persistent intestinal inflammation.

80 host immune responses and the propagation of intestinal inflammation.

81 ired for mast cell expansion during allergic intestinal inflammation.

82 ed established fibrosis in mice with chronic intestinal inflammation.

83 senting with primary immunodeficiency and/or intestinal inflammation.

84 iting endosomal TLR signaling and consequent intestinal inflammation.

85 body weight, autoantibodies, and pronounced intestinal inflammation.

86 the gut lumen and induces the development of intestinal inflammation.

87 nization, limit fungal dysbiosis, and dampen intestinal inflammation.

88 ve been largely overlooked in the context of intestinal inflammation.

89 re associated with poor growth and increased intestinal inflammation.

90 enuated with luminal contents from mice with intestinal inflammation.

91 ack of adipose tissue, leptin deficiency and intestinal inflammation.

92 ed dramatic, female-specific exacerbation of intestinal inflammation accompanied by significant reduc

93 f bacteria in intestinal lymphoid organs and intestinal inflammation after induction of chronic colit

94 s have been associated with malnutrition and intestinal inflammation among children in low-resource s

95 Low-grade intestinal inflammation and alterations of gut barrier i

96 acteroides-derived sphingolipids resulted in intestinal inflammation and altered host ceramide pools

97 Moreover, we observed increased small intestinal inflammation and apoptosis after hepatic IR i

98 Also, ROS are produced at high levels during intestinal inflammation and cause tissue damage.

99 This dysregulation ultimately mediates intestinal inflammation and clinical symptoms typically

100 ome activator, show significantly attenuated intestinal inflammation and colitis-associated cancer in

101 8, and several inflammasomes protect against intestinal inflammation and colitis-associated colon can

102 microflora is inextricably linked to chronic intestinal inflammation and colitis-associated colorecta

103 ight arrowNF-kappaB signaling contributes to intestinal inflammation and colon cancer progression.

104 bolite, histamine, in suppression of chronic intestinal inflammation and colorectal tumorigenesis.

105 show how V. cholerae MARTX toxin suppresses intestinal inflammation and contributes to cholera being

106 a protective role during the acute stage of intestinal inflammation and contributes to the preventio

107 y suppressed the development of diarrhea and intestinal inflammation and decreased the numbers of DCs

108 ssing EZH2 activity ameliorates experimental intestinal inflammation and delayed the onset of colitis

109 mice receiving control bone marrow cells had intestinal inflammation and dysplasia, and reduced expre

110 D in mice increased susceptibility to severe intestinal inflammation and epithelial dysregulation, ac

111 ream events within Paneth cells that inhibit intestinal inflammation and establish host defense again

112 rich in TGF-beta2 could reduce TNBS-induced intestinal inflammation and fibrosis.

113 obalt protoporphyrin-IX treatment eradicated intestinal inflammation and fully protected KO mice from

114 ce of Streptococcus salivarius was linked to intestinal inflammation and gut barrier dysfunction, whe

115 ouse model of UC determined the magnitude of intestinal inflammation and IL-1beta-dependent type 17 i

116 wild-type (WT) mice evidenced by more severe intestinal inflammation and impaired bacterial clearance

117 fate sodium-induced colitis due to prolonged intestinal inflammation and impaired tissue repair.

118 has been shown to play an important role in intestinal inflammation and in the progression of estrog

119 r the first time the role of Muc4 in driving intestinal inflammation and inflammation-associated tumo

120 ptor (TNFR) families] help drive and control intestinal inflammation and injury/repair responses.

121 S administration, characterized by increased intestinal inflammation and intestinal barrier disruptio

122 NEC is characterized by intestinal inflammation and ischemia, as well derangemen

123 ent mice during the first two weeks of life, intestinal inflammation and macrophage dysfunction begin

124 s the role of Toll-like receptor 4 (TLR4) in intestinal inflammation and microbiota recognition.

125 (-/-) mice were significantly protected from intestinal inflammation and mucosal damage compared with

126 ra-amniotic C.albicans infection would cause intestinal inflammation and mucosal injury in an ovine m

127 Mice on HFD/ATI developed only mild signs of intestinal inflammation and myeloid cell activation but

128 ing disease affecting premature infants with intestinal inflammation and necrosis.

129 ations in gut microbiota are known to affect intestinal inflammation and obesity.

130 ble antibiotics restored eubiosis, decreased intestinal inflammation and permeability, and reduced AL

131 hway in intestinal APCs in resolving chronic intestinal inflammation and protecting against CAC in re

132 vided therapeutic benefit in mouse models of intestinal inflammation and reduced the frequency of TH1

133 tains IESCs at homeostasis and contribute to intestinal inflammation and repair after injury.

134 (Delta9-THC) inhibited viral replication and intestinal inflammation and slowed disease progression.

135 t reduction of RIPK1 expression, spontaneous intestinal inflammation and splenomegaly, which can be r

136 HRF-IgE interactions in the amplification of intestinal inflammation and suggest HRF as a therapeutic

137 r T(RM) cells in the pathogenesis of chronic intestinal inflammation and suggest that these cells cou

138 stinal epithelial cells resulted in enhanced intestinal inflammation and T helper 17 cell (TH17) resp

139 ency rendered mice more susceptible to acute intestinal inflammation and that a significantly higher

140 Change in faecal calprotectin as a marker of intestinal inflammation and the primary outcome was simi

141 e precise role of these cells in stimulating intestinal inflammation and the subsequent tissue damage

142 were remarkably unaffected by development of intestinal inflammation and there were no differences in

143 We found that intestinal inflammation and tissue damage were significa

144 Dysbiosis-induced intestinal inflammation and TNFRI signaling in intestina

145 te contributions of lymphatic obstruction to intestinal inflammation and to study profiles of SPMs, w

146 sults demonstrate that Lcn2 protects against intestinal inflammation and tumorigenesis associated wit

147 4 has an important role in the regulation of intestinal inflammation and tumorigenesis, and could be

148 Resolution of intestinal inflammation and wound repair are active proc

149 challenges significantly induced NE, severe intestinal inflammation, and body weight (BW) loss in br

150 assessed by clinical disease activity index, intestinal inflammation, and collagen deposition.

151 e T6SS to evade phagocytic eukaryotes, cause intestinal inflammation, and compete against other bacte

152 Indole modulates oxidative stress, intestinal inflammation, and hormone secretion in animal

153 between Coronavirus Disease 2019 (COVID-19), intestinal inflammation, and IBD treatment.

154 to play an integral role in both hepatic and intestinal inflammation, and in atherosclerosis.

155 sex, the intestinal innate immune response, intestinal inflammation, and intestinal microbiota have

156 a protective role during the acute stages of intestinal inflammation, and its absence promotes the de

157 Symptoms, intestinal inflammation, and mesenteric lymph node and i

158 microbiota are essential to prevent chronic intestinal inflammation, as observed in inflammatory bow

159 on (TJ) barrier contribute to development of intestinal inflammation associated with diseases.

160 and sustained bacterial titers and profound intestinal inflammation associated with extensive necros

161 crobiota that is associated with exacerbated intestinal inflammation at steady-state and following DS

162 addresses the role of microbiome in driving intestinal inflammation, barrier disruption and bacteria

163 lated by AZA therapy, which may help resolve intestinal inflammation but could increase malignancy ri

164 ) mice reduced markers of microbiota-induced intestinal inflammation but not tumor development.

165 esistant to proteases and heat, and increase intestinal inflammation by activating gut and mesenteric

166 Here, we report that miR-223 limits intestinal inflammation by constraining the nlrp3 inflam

167 Therefore, NEMO prevents intestinal inflammation by inhibiting RIPK1 kinase activ

168 on p40 production in vivo and prevention of intestinal inflammation by LGG, mice were gavaged with L

169 that presence of the PTPN22 variant affects intestinal inflammation by modulating the host's respons

170 a-3 fatty acids, has been reported to dampen intestinal inflammation by promoting anti-inflammatory r

171 ow that STAT1 enables CD4(+) T-cell-mediated intestinal inflammation by protecting them from natural

172 n of SIRT1, we found this protein to prevent intestinal inflammation by regulating the gut microbiota

173 re we demonstrate in mice that GCN2 controls intestinal inflammation by suppressing inflammasome acti

174 Intestinal inflammation can impair mucosal healing, ther

175 crosis factor (TNF)-alpha, a key mediator of intestinal inflammation, causes an increase in intestina

176 esponses, leading to exacerbation of chronic intestinal inflammation characteristic of SAMP mice.

177 within the fetal gut with mucosal injury and intestinal inflammation, characterized by increased CD3(

178 in various disease settings, but its role in intestinal inflammation, commensal homeostasis, and muco

179 with Cj-P1-DCA-Anaero showed attenuation of intestinal inflammation compared to Cj-P1.

180 creasing body weight and reducing markers of intestinal inflammation, compared with control mice.

181 ed the ability of the endothelium to resolve intestinal inflammation, compared with mice with colitis

182 Two mouse models of intestinal inflammation (dextran sodium sulphate treatme

183 significant primary or contributing cause of intestinal inflammation, diarrhea, dehydration, and asso

184 bidity and mortality that is associated with intestinal inflammation driven by the microbiota(1-3).

185 erative colitis, is characterized by chronic intestinal inflammation due to a complex interaction of

186 lial barrier integrity, further perpetuating intestinal inflammation during experimental colitis.

187 but how miRNA circuits orchestrate aberrant intestinal inflammation during inflammatory bowel diseas

188 flammasome is activated in mice during acute intestinal inflammation elicited by dextran sodium sulfa

189 and progression; these include regulation of intestinal inflammation, epithelial proliferation, stem

190 e (CTD) associated with a predisposition for intestinal inflammation, food allergy, and failure to th

191 diarrhea, enteropathogens, and systemic and intestinal inflammation for their interrelation and thei

192 In an animal model of anti-TNF-resistant intestinal inflammation, genetic deletion or pharmacolog

193 polysaccharides were assessed as markers for intestinal inflammation, gut permeability and bacterial

194 utoimmune diseases, but a role in idiopathic intestinal inflammation has not been described.

195 Because current treatments for intestinal inflammation have a high percentage of failur

196 colon that may have therapeutic potential in intestinal inflammation, IBD, and CAC.

197 Intestinal inflammation identified with MSOT was also co

198 sis that genetic deletion of G2A would limit intestinal inflammation in a mouse model of colitis indu

199 with fewer pathological lesions and reduced intestinal inflammation in Ccdc88b-deficient mice.

200 Intestinal inflammation in Crohn's disease (CD) is cause

201 se activity reduced PD1n-3 DPA and augmented intestinal inflammation in experimental colitis.

202 -monocyte progenitors (GMP) during joint and intestinal inflammation in experimental spondyloarthriti

203 a-specific signaling contributes to enhanced intestinal inflammation in female SAMP/YitFC mice, a spo

204 and that these genes are upregulated during intestinal inflammation in IBD.

205 We investigated mechanisms of intestinal inflammation in Inpp5d(-/-) mice (SHIP-null m

206 orescence to delineate pancreatic, liver, or intestinal inflammation in living mice.

207 DCs) contribute significantly to DSS-induced intestinal inflammation in LRBA-deficient mice.

208 cells, the degree of H. hepaticus-triggered intestinal inflammation in mice in which Tbx21 was excis

209 A and showed moderately higher pathology and intestinal inflammation in mice infected with S. Paratyp

210 that PPI exposure increases the severity of intestinal inflammation in mice with C. difficile-associ

211 Consumption of wheat or wheat ATIs increases intestinal inflammation in mice with colitis, via TLR4,

212 TSG6 is sufficient to reduce intestinal inflammation in mice with colitis.

213 tic triggering of Rho-A signaling suppressed intestinal inflammation in mice with GGTase-I-deficient

214 und that tuft cell expansion reduced chronic intestinal inflammation in mice.

215 ompounds as biomarkers of chemically induced intestinal inflammation in mice.

216 Leptin has been shown to modulate intestinal inflammation in mice.

217 ion in the epithelium at baseline and during intestinal inflammation in mice.

218 Cannabinoids including Delta9-THC attenuated intestinal inflammation in mouse colitis models and SIV-

219 ells from controls; this might contribute to intestinal inflammation in patients with CD.

220 senting cells and might promote and maintain intestinal inflammation in patients with celiac disease

221 This pathway might be induced to resolve intestinal inflammation in patients with colitis.

222 of fecal EhMIF correlated with the level of intestinal inflammation in persons with intestinal amebi

223 r host, a necessary step required to trigger intestinal inflammation in response to C. jejuni.

224 sensitized mice expressing HLA-DQ8 increased intestinal inflammation in response to gluten in the die

225 ent mouse strain, which exhibits significant intestinal inflammation in response to intestinal C. jej

226 Tg6F therapy was also effective in reducing intestinal inflammation in the Cox2 MKO/CCHF model.

227 Alcohol feeding for 8 weeks induced intestinal inflammation in the jejunum, which is charact

228 ntrast, GPBAR1 activation by BAR501 reversed intestinal inflammation in the trinitrobenzenesulfonic a

229 is and enhanced LGG-mediated amelioration of intestinal inflammation in this model.

230 nate to mice expanded tuft cells and reduced intestinal inflammation in TNF(DeltaARE/+) mice and anti

231 mice demonstrate the neonate isolate induces intestinal inflammation in vivo, with increased expressi

232 ontribute to the efficacy of GCs in treating intestinal inflammation in vivo.

233 th no endoscopic or radiological evidence of intestinal inflammation) in patients with treatment-refr

234 med that emulsifier exposure induced chronic intestinal inflammation, increased adiposity, and altere

235 on, IKKalpha(DeltaIEC) mice exhibited severe intestinal inflammation, increased bacterial disseminati

236 Chronic intestinal inflammation increases the risk for the devel

237 Blimp1CKO mice) spontaneously develop severe intestinal inflammation, indicating a crucial role for B

238 Chronic intestinal inflammation is a major risk factor for the d

239 Intestinal inflammation is associated with low levels of

240 Intestinal inflammation is attenuated after inoculation

241 Intestinal inflammation is frequently associated with an

242 c expansion of mesenteric tissue on sites of intestinal inflammation is known as creeping fat.

243 A predominant feature of intestinal inflammation is the accumulation of neutrophi

244 Intestinal inflammation is the central pathological feat

245 colitis, the role of acid ceramidase (AC) in intestinal inflammation is yet to be characterized.

246 few studies have examined their role during intestinal inflammation, it appears that iNKT cells prot

247 proved ileal barrier function by attenuating intestinal inflammation, leading to reduced BTL and thus

248 ET, are being investigated to identify early intestinal inflammation, longitudinally monitor disease

249 Diarrhea, high intestinal inflammation, low concentrations of fecal SCF

250 Furthermore, it appears that intestinal inflammation may reduce the antiepileptic eff

251 Therefore, we suggest that intestinal inflammation may represent a valid antiepilep

252 Using a pathobiont-induced intestinal inflammation model and a defined bacterial co

253 he PPARalpha signaling pathway in regulating intestinal inflammation, mucosal immunity, and commensal

254 We studied the effects of intestinal inflammation on pentylenetetrazole (PTZ)-indu

255 Analysis of intestinal inflammation on-chip revealed that immune cel

256 and while all treatments were able to reduce intestinal inflammation, only ALAC and NaB exhibited sig

257 Participants without intestinal inflammation or symptoms served as controls (

258 nces defenses against intestinal bacteria vs intestinal inflammation or what cells are responsible fo

259 uced neuronal loss, enteric glia activation, intestinal inflammation, oxidative stress and histologic

260 reat potential as therapeutic agents against intestinal inflammation, potential cytotoxicity, anti-in

261 However, Lcn2 function in chronic intestinal inflammation remains unclear.

262 Here, we report that intestinal inflammation reprograms the metabolic pathway

263 atase D (INPP5D, also known as SHIP) develop intestinal inflammation resembling that of patients with

264 P nick-end labeling assay was performed, and intestinal inflammation severity was evaluated histologi

265 Biomarkers of intestinal inflammation, such as faecal calprotectin and

266 ease of IL-1beta sEVs in the pathogenesis of intestinal inflammation, such as that observed in IBD.

267 ed replication plan of key experiments from 'Intestinal Inflammation Targets Cancer-Inducing Activity

268 OXP3+ Tregs resulted in more severe Th2-type intestinal inflammation than that observed in mice with

269 tory bowel disease causes chronic, relapsing intestinal inflammation that can lead to the development

270 we show using Helicobacter hepaticus-induced intestinal inflammation that IL-17A(Cre)- or Rag1(Cre)-m

271 ia and activation of Th2 immunity in chronic intestinal inflammation that is dependent on the gut mic

272 Absence of MHCII on cDCs resulted in chronic intestinal inflammation that was alleviated by antibioti

273 1 in T cells in mice resulted in spontaneous intestinal inflammation that was characterized by aberra

274 veral IEC death regulating factors result in intestinal inflammation, the loss of the anti-apoptotic

275 efv-/- mice reduced epithelial permeability, intestinal inflammation, the severity of colitis, and co

276 Our study demonstrates that reducing intestinal inflammation through ALAC or NaB administrati

277 first evidence that GITR negatively controls intestinal inflammation through NK cell functions.

278 ss and consequences of DR3 signaling-induced intestinal inflammation through regulation of ILC3s.

279 expression to inhibit enteric infection and intestinal inflammation, thus, maintaining the intestina

280 or neutralizing IL-1alpha uniformly reduces intestinal inflammation, tissue damage, donor T cell exp

281 Celiac disease is characterized by intestinal inflammation triggered by gliadin, a componen

282 ore, colonization with P. mirabilis promoted intestinal inflammation upon intestinal injury via the p

283 ntly, acute amino acid starvation suppressed intestinal inflammation via a mechanism dependent on GCN

284 t couples amino acid sensing with control of intestinal inflammation via GCN2.

285 suggest that G2A signaling serves to dampen intestinal inflammation via the production of IFN-gamma,

286 Intestinal inflammation was assessed by quantitative PCR

287 Chronic intestinal inflammation was characterized by increased b

288 Additionally, high-dose LPS-induced intestinal inflammation was dependent on the TLR4/FAK/My

289 Intestinal inflammation was induced by dextran sulfate s

290 Chronic intestinal inflammation was induced in male rabbits with

291 insight into how AC up-regulation can impact intestinal inflammation, we investigated the selective l

292 To evaluate the role of BAs in intestinal inflammation, we performed metabolomic, micro

293 Effects of oral ATIs on intestinal inflammation were determined in healthy C57BL

294 levels of S Typhimurium gut colonization and intestinal inflammation were not observed in Jackson Lab

295 Levels of calprotectin, a marker of intestinal inflammation, were measured in intestinal tis

296 oid knockout (MKO) mice develop Crohn's-like intestinal inflammation when fed cholate-containing high

297 ost consistently colonized site and produced intestinal inflammation, where specific cytokines were i

298 sets (Callithrix jacchus) are susceptible to intestinal inflammation which leads to chronic diarrhea,

299 rg1fl/fl mice into WT recipients ameliorated intestinal inflammation, while transfers from WT litterm

300 Pggt1b, in IECs exhibit spontaneous chronic intestinal inflammation with accumulation of granulocyte