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1 elial cells during amino acid starvation, or intestinal inflammation.
2 of the TNF superfamily are key regulators of intestinal inflammation.
3 aling can activate asymmetric division after intestinal inflammation.
4 ocytes from NEC mice into naive mice induced intestinal inflammation.
5 the role of ADF in limiting the severity of intestinal inflammation.
6 investigate the role of IL-33 during chronic intestinal inflammation.
7 of ATIs in various foods and their effect on intestinal inflammation.
8 (including pathogens and pathobionts) during intestinal inflammation.
9 orm complementary roles in the regulation of intestinal inflammation.
10 rial defenses, but at the cost of increasing intestinal inflammation.
11 for enhancing mucosal immunity and treating intestinal inflammation.
12 tion, mucosal injury but failed to attenuate intestinal inflammation.
13 t endothelial cells to promote resolution of intestinal inflammation.
14 -specific strategies for treating pathologic intestinal inflammation.
15 fe and effective therapeutic approach during intestinal inflammation.
16 rease intestinal barrier function and reduce intestinal inflammation.
17 M cells may be a useful correlate of chronic intestinal inflammation.
18 RA metabolism mediated by microbiota-induced intestinal inflammation.
19 intestines to amniotic fluid, with resultant intestinal inflammation.
20 ts profound therapeutic effects in models of intestinal inflammation.
21 regulating the innate immune response during intestinal inflammation.
22 is, whereas dysbiosis decreased with reduced intestinal inflammation.
23 ctivation in the development of Stx-mediated intestinal inflammation.
24 atory molecules, including TSG6, that reduce intestinal inflammation.
25 suggested that certain nutrients can reduce intestinal inflammation.
26 LCs in mice and in human beings with chronic intestinal inflammation.
27 effector function and are poor mediators of intestinal inflammation.
28 with active IBD and in preclinical models of intestinal inflammation.
29 w alterations in autophagy can contribute to intestinal inflammation.
30 ontaneous IFN production and immune-mediated intestinal inflammation.
31 nt factor contributing to the development of intestinal inflammation.
32 responses in vivo and preventing autoimmune intestinal inflammation.
33 RNA induction in THC-mediated suppression of intestinal inflammation.
34 kine IL-18, intestinal barrier function, and intestinal inflammation.
35 sorption) has been shown to be suppressed in intestinal inflammation.
36 etermined in a model of oral antigen-induced intestinal inflammation.
37 wed that GM-CSF exerts beneficial effects in intestinal inflammation.
38 flammatory cells that participate in chronic intestinal inflammation.
39 y toxin-induced epithelial injury and marked intestinal inflammation.
40 kt1 that suppresses IEC proliferation during intestinal inflammation.
41 robiota, preventing diseases associated with intestinal inflammation.
42 e gut is a strong yet localized indicator of intestinal inflammation.
43 ase) diseases that have been associated with intestinal inflammation.
44 obiome is also complex and can contribute to intestinal inflammation.
45 n and treatment with oral iron may aggravate intestinal inflammation.
46 ically involved in controlling CD1d-mediated intestinal inflammation.
47 uring antiinflammatory function during acute intestinal inflammation.
48 variations in SLC22A23 were associated with intestinal inflammation.
49 ed for development of pathogenic T cells and intestinal inflammation.
50 lera toxin (CT) immunization without causing intestinal inflammation.
51 ing existing IFN treatment for infection and intestinal inflammation.
52 gut during the development and resolution of intestinal inflammation.
53 wel disease--may contribute substantially to intestinal inflammation.
54 so produced by gut microbiota and suppresses intestinal inflammation.
55 ing both T cell expansion and T cell-induced intestinal inflammation.
56 V1 promoted colitogenic T cell responses and intestinal inflammation.
57 vestigate expression and functions of SPM in intestinal inflammation.
58 ing G9A as a therapeutic target for treating intestinal inflammation.
59 ein 2 (NOD2) in Campylobacter jejuni-induced intestinal inflammation.
60 a likely target for the treatment of chronic intestinal inflammation.
61 y, gut microbial density, and development of intestinal inflammation.
62 te immune response and mediate recovery from intestinal inflammation.
63 hanism by which chronic hypoxia can activate intestinal inflammation.
64 eritance pattern with complete penetrance of intestinal inflammation.
65 lial mitochondria could be targeted to treat intestinal inflammation.
66 50 genetic variants associated with IBD-like intestinal inflammation.
67 and likely contributes to C. jejuni-induced intestinal inflammation.
68 disease includes nutrient malabsorption and intestinal inflammation.
69 ol of bacterial replication, and exacerbated intestinal inflammation.
70 r risk for Crohn's disease, characterized by intestinal inflammation.
71 ng very clear, to go alongside their role in intestinal inflammation.
72 ents remain symptomatic and still have small intestinal inflammation.
73 nuated C. jejuni-induced crypt abscesses and intestinal inflammation.
74 important pathogenic factor contributing to intestinal inflammation.
75 iome shifts occurred in the absence of overt intestinal inflammation.
76 ion factor Foxp3 are critical for regulating intestinal inflammation.
77 an Il10-deficiency-induced chronic model of intestinal inflammation.
78 Defective IL-10 allele is a risk factor for intestinal inflammation.
79 cell recruitment, and contribute to chronic intestinal inflammation.
80 3), which confer protection against lung and intestinal inflammation.
81 ism provides new treatment opportunities for intestinal inflammation.
82 ts that caused immunoglobulin deficiency and intestinal inflammation.
83 ega 3 long-chain fatty acids protect against intestinal inflammation.
84 trated that CS may ameliorate stress-induced intestinal inflammation.
85 Mice were imaged using MSOT to detect intestinal inflammation.
86 y gluten-containing diet increased low-level intestinal inflammation.
87 to prevent development of severe spontaneous intestinal inflammation.
88 be-reactive T cells in patients with chronic intestinal inflammation.
89 gene networks contributing to the underlying intestinal inflammation.
90 sis and compensate for otherwise-detrimental intestinal inflammation.
91 nges in actin dynamics lead to IEC death and intestinal inflammation.
92 hages mediates bacterial internalization and intestinal inflammation.
93 ut-homing perturbing agents used in treating intestinal inflammation.
94 accompanied with a distinct amelioration of intestinal inflammation.
95 its known pathogenic function during chronic intestinal inflammation.
96 r how ILC3s could be manipulated to regulate intestinal inflammation.
97 le of the ECS also extends to the control of intestinal inflammation.
98 n Th2 effector responses that drive allergic intestinal inflammation.
99 the production of microbial metabolites and intestinal inflammation.
100 gs prevented the development of diarrhea and intestinal inflammation.
101 be a promising approach for the treatment of intestinal inflammation.
102 ory cytokines and enhanced susceptibility to intestinal inflammation.
104 s emerged as a critical event in controlling intestinal inflammation, acting to limit elevation of pr
105 ion was similarly critical for regulation of intestinal inflammation after chemically induced intesti
106 n leukocytes and endothelial cells to reduce intestinal inflammation and analyze the clinical studies
108 ining 12 (NLRP12) plays a protective role in intestinal inflammation and carcinogenesis, but the phys
111 ome activator, show significantly attenuated intestinal inflammation and colitis-associated cancer in
112 8, and several inflammasomes protect against intestinal inflammation and colitis-associated colon can
113 e report that protein ISGylation exacerbates intestinal inflammation and colitis-associated colon can
114 ight arrowNF-kappaB signaling contributes to intestinal inflammation and colon cancer progression.
115 mice, colitogenic Th1 and Th17 cells promote intestinal inflammation and colonic tissue damage but ha
116 bolite, histamine, in suppression of chronic intestinal inflammation and colorectal tumorigenesis.
117 a protective role during the acute stage of intestinal inflammation and contributes to the preventio
118 Administration of exogenous AREG limited intestinal inflammation and decreased disease severity i
119 y suppressed the development of diarrhea and intestinal inflammation and decreased the numbers of DCs
120 mice receiving control bone marrow cells had intestinal inflammation and dysplasia, and reduced expre
121 ithelial cells ameliorates ER stress-induced intestinal inflammation and eases NF-kappaB overactivati
122 D in mice increased susceptibility to severe intestinal inflammation and epithelial dysregulation, ac
123 obalt protoporphyrin-IX treatment eradicated intestinal inflammation and fully protected KO mice from
125 tion of commensal enteric bacteria mitigates intestinal inflammation and IL-17 production triggered b
126 has been shown to play an important role in intestinal inflammation and in the progression of estrog
127 e might lead to new therapeutics for chronic intestinal inflammation and inflammation-associated canc
128 r the first time the role of Muc4 in driving intestinal inflammation and inflammation-associated tumo
129 ptor (TNFR) families] help drive and control intestinal inflammation and injury/repair responses.
130 S administration, characterized by increased intestinal inflammation and intestinal barrier disruptio
131 ent mice during the first two weeks of life, intestinal inflammation and macrophage dysfunction begin
132 s the role of Toll-like receptor 4 (TLR4) in intestinal inflammation and microbiota recognition.
133 (-/-) mice were significantly protected from intestinal inflammation and mucosal damage compared with
134 ra-amniotic C.albicans infection would cause intestinal inflammation and mucosal injury in an ovine m
135 Persistent diarrhea in CDI correlates with intestinal inflammation and not fecal pathogen burden.
136 ble antibiotics restored eubiosis, decreased intestinal inflammation and permeability, and reduced AL
137 hat monitored daily illness, monthly growth, intestinal inflammation and permeability, pathogen burde
138 vided therapeutic benefit in mouse models of intestinal inflammation and reduced the frequency of TH1
140 (Delta9-THC) inhibited viral replication and intestinal inflammation and slowed disease progression.
141 HRF-IgE interactions in the amplification of intestinal inflammation and suggest HRF as a therapeutic
142 eceptor (IL-1R) signaling pathways, controls intestinal inflammation and suppresses colon tumorigenes
143 stinal epithelial cells resulted in enhanced intestinal inflammation and T helper 17 cell (TH17) resp
144 -27 may be a critical factor for controlling intestinal inflammation and Th17 and Th1 development by
145 ies describe their anti-inflammatory role in intestinal inflammation and the locus containing IFNAR,
146 e precise role of these cells in stimulating intestinal inflammation and the subsequent tissue damage
147 were remarkably unaffected by development of intestinal inflammation and there were no differences in
151 tion of orally given iron may be impaired by intestinal inflammation and treatment with oral iron may
152 sults demonstrate that Lcn2 protects against intestinal inflammation and tumorigenesis associated wit
153 4 has an important role in the regulation of intestinal inflammation and tumorigenesis, and could be
154 ion contributes to undernutrition by causing intestinal inflammation and/or by altering intestinal ba
155 l zinc supplementation could improve weight, intestinal inflammation, and diarrhea in undernourished
157 aximin altered the gut microbiota, prevented intestinal inflammation, and improved gut barrier functi
159 a protective role during the acute stages of intestinal inflammation, and its absence promotes the de
161 membership was associated independently with intestinal inflammation, antibiotic use, and therapy.
163 eficiency disorders might be associated with intestinal inflammation as one of their leading clinical
164 and sustained bacterial titers and profound intestinal inflammation associated with extensive necros
165 al cells (IECs) spontaneously develop severe intestinal inflammation associated with IEC apoptosis le
166 crobiota that is associated with exacerbated intestinal inflammation at steady-state and following DS
167 lated by AZA therapy, which may help resolve intestinal inflammation but could increase malignancy ri
168 00A knock-in mice do not develop spontaneous intestinal inflammation, but exhibit morphological defec
169 esistant to proteases and heat, and increase intestinal inflammation by activating gut and mesenteric
172 on p40 production in vivo and prevention of intestinal inflammation by LGG, mice were gavaged with L
173 Therefore, IRAK1 plays an important role in intestinal inflammation by mediating T cell activation,
174 n of SIRT1, we found this protein to prevent intestinal inflammation by regulating the gut microbiota
175 re we demonstrate in mice that GCN2 controls intestinal inflammation by suppressing inflammasome acti
176 ntial role for Tregs in selectively averting intestinal inflammation by Th17 CD4(+) T cells with comm
178 studies provide a simple means of preventing intestinal inflammation caused by enteric pathogens.
179 ed in the absence of B7 selectively mitigate intestinal inflammation caused by Th17 effector CD4(+) T
181 crosis factor (TNF)-alpha, a key mediator of intestinal inflammation, causes an increase in intestina
182 esponses, leading to exacerbation of chronic intestinal inflammation characteristic of SAMP mice.
183 /-) mice exhibited reduced infection-induced intestinal inflammation, characterized by decreased leuk
184 within the fetal gut with mucosal injury and intestinal inflammation, characterized by increased CD3(
185 in various disease settings, but its role in intestinal inflammation, commensal homeostasis, and muco
186 creasing body weight and reducing markers of intestinal inflammation, compared with control mice.
187 ed the ability of the endothelium to resolve intestinal inflammation, compared with mice with colitis
188 significant primary or contributing cause of intestinal inflammation, diarrhea, dehydration, and asso
189 erative colitis, is characterized by chronic intestinal inflammation due to a complex interaction of
190 rferon (IFN-gamma) is an important driver of intestinal inflammation during colitis caused by Salmone
191 but how miRNA circuits orchestrate aberrant intestinal inflammation during inflammatory bowel diseas
192 flammasome is activated in mice during acute intestinal inflammation elicited by dextran sodium sulfa
193 CD1d signals contribute to NKT-cell-mediated intestinal inflammation, engagement of epithelial CD1d e
194 and progression; these include regulation of intestinal inflammation, epithelial proliferation, stem
196 , Il10(-/-); Nod2(-/-) mice developed severe intestinal inflammation following C. jejuni infection, c
197 diarrhea, enteropathogens, and systemic and intestinal inflammation for their interrelation and thei
198 In an animal model of anti-TNF-resistant intestinal inflammation, genetic deletion or pharmacolog
199 ogy is fundamental to assess two-dimensional intestinal inflammation; however, inflammatory bowel dis
202 827-T was recently nominally associated with intestinal inflammation in a genome-wide association stu
203 sis that genetic deletion of G2A would limit intestinal inflammation in a mouse model of colitis indu
208 oduct, carbon monoxide (CO), protect against intestinal inflammation in experimental models of coliti
210 kers have all been explored as indicators of intestinal inflammation in IBD, and although none has be
214 minal E. coli increases proportionately with intestinal inflammation in KO mice and enhances the susc
216 cells, the degree of H. hepaticus-triggered intestinal inflammation in mice in which Tbx21 was excis
217 A and showed moderately higher pathology and intestinal inflammation in mice infected with S. Paratyp
218 that PPI exposure increases the severity of intestinal inflammation in mice with C. difficile-associ
220 tic triggering of Rho-A signaling suppressed intestinal inflammation in mice with GGTase-I-deficient
224 Cannabinoids including Delta9-THC attenuated intestinal inflammation in mouse colitis models and SIV-
228 of fecal EhMIF correlated with the level of intestinal inflammation in persons with intestinal amebi
231 ent mouse strain, which exhibits significant intestinal inflammation in response to intestinal C. jej
233 ntrast, GPBAR1 activation by BAR501 reversed intestinal inflammation in the trinitrobenzenesulfonic a
235 th no endoscopic or radiological evidence of intestinal inflammation) in patients with treatment-refr
236 on, IKKalpha(DeltaIEC) mice exhibited severe intestinal inflammation, increased bacterial disseminati
238 Blimp1CKO mice) spontaneously develop severe intestinal inflammation, indicating a crucial role for B
248 colitis, the role of acid ceramidase (AC) in intestinal inflammation is yet to be characterized.
249 long appreciated to be a key determinant of intestinal inflammation, is also playing a key role in c
250 few studies have examined their role during intestinal inflammation, it appears that iNKT cells prot
251 proved ileal barrier function by attenuating intestinal inflammation, leading to reduced BTL and thus
252 volved in bile acid homeostasis, hepatic and intestinal inflammation, liver fibrosis, and cardiovascu
253 ET, are being investigated to identify early intestinal inflammation, longitudinally monitor disease
256 he PPARalpha signaling pathway in regulating intestinal inflammation, mucosal immunity, and commensal
257 Given the key role of AIEC in the chronic intestinal inflammation of CD patients, these results su
260 and can harbour pathobionts that exacerbate intestinal inflammation or manifest systemic disease.
264 atase D (INPP5D, also known as SHIP) develop intestinal inflammation resembling that of patients with
265 P nick-end labeling assay was performed, and intestinal inflammation severity was evaluated histologi
267 These Th17 cells are considered important in intestinal inflammation, such as seen in Crohn's disease
268 ed replication plan of key experiments from 'Intestinal Inflammation Targets Cancer-Inducing Activity
269 urium and H. polygyrus developed more severe intestinal inflammation than animals infected with S. Ty
270 OXP3+ Tregs resulted in more severe Th2-type intestinal inflammation than that observed in mice with
271 tory bowel disease causes chronic, relapsing intestinal inflammation that can lead to the development
272 we show using Helicobacter hepaticus-induced intestinal inflammation that IL-17A(Cre)- or Rag1(Cre)-m
273 ia and activation of Th2 immunity in chronic intestinal inflammation that is dependent on the gut mic
274 Absence of MHCII on cDCs resulted in chronic intestinal inflammation that was alleviated by antibioti
275 1 in T cells in mice resulted in spontaneous intestinal inflammation that was characterized by aberra
276 imer in GITR-L(-/-) splenic monocytes during intestinal inflammation, the migratory capability of spl
277 fficile incites epithelial injury and marked intestinal inflammation, the primary determinant of dise
278 efv-/- mice reduced epithelial permeability, intestinal inflammation, the severity of colitis, and co
280 ve, CD4-negative, ILC3s in mice with chronic intestinal inflammation (TRUC mice) by increasing IL23-
281 ore set the threshold for the development of intestinal inflammation upon hypomorphic ATG16L1 functio
282 ore, colonization with P. mirabilis promoted intestinal inflammation upon intestinal injury via the p
285 ntly, acute amino acid starvation suppressed intestinal inflammation via a mechanism dependent on GCN
287 ether RELMalpha promoted Citrobacter-induced intestinal inflammation via IL-17A, infected WT and IL-1
288 suggest that G2A signaling serves to dampen intestinal inflammation via the production of IFN-gamma,
294 insight into how AC up-regulation can impact intestinal inflammation, we investigated the selective l
296 levels of S Typhimurium gut colonization and intestinal inflammation were not observed in Jackson Lab
297 LPS-induced increases in intestinal TJP and intestinal inflammation were regulated by TLR4-dependent
298 ost consistently colonized site and produced intestinal inflammation, where specific cytokines were i
299 Pggt1b, in IECs exhibit spontaneous chronic intestinal inflammation with accumulation of granulocyte
300 asive, accurate, and inexpensive measures of intestinal inflammation would allow clinicians to adopt
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