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1 n contribute to innate IEL activation during mucosal inflammation.
2 cimens of CUC in mild or "refractory" severe mucosal inflammation.
3 ch was further elevated in those with severe mucosal inflammation.
4 ective element of adenosine signaling during mucosal inflammation.
5 ransporter activity, has been used to detect mucosal inflammation.
6 ate and adaptive immune responses as well as mucosal inflammation.
7 le of prolonged colonization or induction of mucosal inflammation.
8 g immunoregulatory roles in animal models of mucosal inflammation.
9 intestine regulating both oral tolerance and mucosal inflammation.
10 m, resulting in loss of epithelial cells and mucosal inflammation.
11 etic approach to test the effect of EhMIF on mucosal inflammation.
12 ed sites, implicating LIGHT as a mediator of mucosal inflammation.
13 n and cecum and causes crypt hyperplasia and mucosal inflammation.
14 expression of multiple cytokines to promote mucosal inflammation.
15 helia and lamina propria but failed to cause mucosal inflammation.
16 bers, as well as patients with other chronic mucosal inflammation.
17 serve as a barrier-protective element during mucosal inflammation.
18 ne mechanisms in the condition of intestinal mucosal inflammation.
19 to the importance of SP and its receptor in mucosal inflammation.
20 omprehension for the role chemokines play in mucosal inflammation.
21 tion ability, H. pylori density, and gastric mucosal inflammation.
22 be therapeutic for diseases characterized by mucosal inflammation.
23 g physiologic and pathologic T cell-mediated mucosal inflammation.
24 levels of IFN-gamma may have down regulated mucosal inflammation.
25 pivotal role in promoting H. pylori-induced mucosal inflammation.
26 (PrMCs) and accumulate at sites of allergic mucosal inflammation.
27 internalized and by the underlying degree of mucosal inflammation.
28 in the pathogenesis of H. pylori-associated mucosal inflammation.
29 In each case, the pathology usually includes mucosal inflammation.
30 ory properties in the presence or absence of mucosal inflammation.
31 m, an event necessary for the development of mucosal inflammation.
32 nizes the human stomach and produces gastric mucosal inflammation.
33 lend insight into the complexity of treating mucosal inflammation.
34 uce regulatory T cells (T(regs)) to suppress mucosal inflammation.
35 y response, but may directly induce a type-2 mucosal inflammation.
36 not accompanied by a detectable increase in mucosal inflammation.
37 tentially serve as a biomarker of intestinal mucosal inflammation.
38 rimental models of systemic autoimmunity and mucosal inflammation.
39 intense search for the underlying drivers of mucosal inflammation.
40 site immunomodulator, which protects against mucosal inflammation.
41 th IBD vs controls; some were independent of mucosal inflammation.
42 tions for targeting neddylation in models of mucosal inflammation.
43 stable before and during the development of mucosal inflammation.
44 a can promote both immunity to pathogens and mucosal inflammation.
45 Disruption of Ts cell activities can lead to mucosal inflammation.
46 pulate the human intestine and contribute to mucosal inflammation.
47 +/- 1.5, independent of primary diagnosis or mucosal inflammation.
48 rohn's disease and appears to be involved in mucosal inflammation.
49 y response occurring at a site of persistent mucosal inflammation.
50 to evaluate its potential therapeutic use in mucosal inflammation.
51 n and markedly reduced gastric dysplasia and mucosal inflammation.
52 plays a role as a master regulator of airway mucosal inflammation.
53 Apoptosis was induced in mouse models of mucosal inflammation.
54 (+) T regulatory cells to dampen exaggerated mucosal inflammation.
55 ith perturbed immune homeostasis and chronic mucosal inflammation.
56 protect against systemic metastases without mucosal inflammation.
57 e panitumumab plus chemoradiotherapy group), mucosal inflammation (15 [24%] vs 48 [55%]), and radiati
58 most frequent grade 3-4 adverse events were mucosal inflammation (25 [40%] of 62 patients in the che
59 luded rash (22% v 8%), diarrhea (58% v 30%), mucosal inflammation (33% v 21%), neutropenia (13% v 4%)
61 concentrations are associated with increased mucosal inflammation, a loss of epithelial junctional pr
62 tent pro-inflammatory cytokine in intestinal mucosal inflammation, activates CARD4/NOD1 mRNA transcri
63 lished also showed a significant decrease in mucosal inflammation after alpha E beta 7 mAb administra
64 rate signals important for the activation of mucosal inflammation and concurrently allows invading ba
67 e my views on the major microbial drivers of mucosal inflammation and dysregulation of innate TH2-pro
69 ences of constitutive TL1A expression on gut mucosal inflammation and fibrostenosis using two murine
71 led to visceral hyperalgesia, accompanied by mucosal inflammation and impaired mucosal barrier functi
72 in feces, even in the presence of low-grade mucosal inflammation and increased intestinal permeabili
74 r-activated receptor (PPAR) gamma suppresses mucosal inflammation and is regulated by GH through STAT
75 and immune cells, with a focus on pathologic mucosal inflammation and mechanisms of epithelial repair
77 ow that platelets can actively contribute to mucosal inflammation and represent a previously unrecogn
78 These findings suggest a synergy between mucosal inflammation and SIV infection, creating an immu
79 ssary for both induction and perpetuation of mucosal inflammation and T-cell activation in Tg(epsilon
83 dy of CRS is to identify specific drivers of mucosal inflammation and translate these into more effec
84 t modulate HIV/SIV susceptibility (including mucosal inflammation), and interventions that may impact
85 A1 strains is associated with enhanced acute mucosal inflammation, and adherence to gastric epithelia
87 g physiological development and pathological mucosal inflammation, and differential expression of the
88 olitis exhibited delayed ulcer healing, more mucosal inflammation, and impaired Wnt/beta-catenin sign
89 of counter-regulation of Th1 T cell-mediated mucosal inflammation, and that IL-10 is necessary as a s
91 ion between serum 25(OH)D concentrations and mucosal inflammation as assessed by the Mayo endoscopy s
92 , we hypothesized that CD73 is protective in mucosal inflammation as modeled by trinitrobenzene sulfo
93 were selectively reduced in areas of active mucosal inflammation associated with human IBD and IL-10
96 ated with a delayed but markedly exacerbated mucosal inflammation at the later stages of infection as
97 only modulates the location and severity of mucosal inflammation, but also induces fibrostenosis.
98 idence has linked intestinal permeability to mucosal inflammation, but molecular studies are lacking.
99 study was to investigate the role of A 2A in mucosal inflammation by administering a selective A 2A a
100 tant modulator in the development of chronic mucosal inflammation by enhancing T(H)1 and T(H)17 effec
103 commensal organisms, perhaps contributing to mucosal inflammation characteristic of disorders such as
104 ere diarrhea (cohort A, 74%; cohort B, 67%), mucosal inflammation (cohort A, 49%; cohort B, 60%), and
105 During Salmonella-induced gastroenteritis, mucosal inflammation creates a niche that favors the exp
106 of the cecum and colon and causes transient mucosal inflammation driven by Th17 and Th1 T helper cel
107 Allergic rhinitis (AR) is characterized by mucosal inflammation, driven by activated immune cells.
109 but failed to ameliorate C.albicans-mediated mucosal inflammation emphasizing the need to optimize th
110 a disease surrogate such as the severity of mucosal inflammation, epidemiologic consistency, and bio
111 r a specific parasite protein that increases mucosal inflammation, expands our knowledge of host-para
112 de 3 adverse events included abdominal pain, mucosal inflammation, fatigue, neutropenia, and hand-foo
114 ited, activated, and retained in response to mucosal inflammation from persistent MCMV infection of t
115 , genetics, and the immune system results in mucosal inflammation has increased knowledge of disease
117 products (proinflammatory mediators) amplify mucosal inflammation, ii) the capacity of necrotic cell
118 nces in the intestinal microbiota; low-grade mucosal inflammation, immune activation, and altered int
119 cies became the most abundant) and prevented mucosal inflammation, impairment to intestinal barrier f
120 ive method for monitoring colonic tumors and mucosal inflammation in a mouse model of colon cancer us
121 llin played a role in suppressing intestinal mucosal inflammation in a murine model of acute enteroco
125 gic examination results included nonspecific mucosal inflammation in four case patients, wall edema i
126 al bacteria that may initiate and perpetuate mucosal inflammation in genetically susceptible individu
128 lagella dramatically decreases the degree of mucosal inflammation in mice and the sole presence of to
129 matrix metalloproteinase 7 (MMP7) increases mucosal inflammation in mouse models of epithelial injur
132 companied by transient crypt hyperplasia and mucosal inflammation in the colon and cecum at 2 but not
133 propose that VacA augments H. pylori-induced mucosal inflammation in the human stomach by causing pro
134 role of prostaglandins in the regulation of mucosal inflammation in the IL-10(-/-) mouse model of IB
136 HIV and SIV) infections are characterized by mucosal inflammation in the presence of anti-inflammator
138 with elevated levels seen in the setting of mucosal inflammation including inflammatory bowel diseas
141 CD), and in contrast to most mouse models of mucosal inflammation, inflammatory lesions in the gastro
143 he mechanisms by which M. genitalium elicits mucosal inflammation is an essential component to managi
146 ere is epidemiological evidence that genital mucosal inflammation leads to enhanced HIV type 1 (HIV-1
147 l activation, which can result in intestinal mucosal inflammation, malabsorption, and numerous second
148 r study of the role of RNASET2 in regulating mucosal inflammation may lead to development of novel th
149 erate and consisted primarily of stomatitis, mucosal inflammation, mouth ulceration, rash, and fatigu
150 companied by a significant increase in acute mucosal inflammation, mucosal injury, luminal fluid secr
151 (grade 3 acne [n=1] and intolerable grade 2 mucosal inflammation [n=1]); hence, doses of 200 mg and
154 ells from patients with CD, independently of mucosal inflammation or disease-associated variants of A
157 changes were associated with severe gastric mucosal inflammation, parietal cell loss, atrophy, and m
158 Despite smoking cessation, neutrophilic mucosal inflammation persistently damages the airways an
159 usceptibility to intestinal colonization and mucosal inflammation persists when mice are infected sev
161 ting cells against stress and, in intestinal mucosal inflammation, potentially lessening the extent a
162 environment in pathological processes, like mucosal inflammation, preneoplasia, and neoplasia, altho
163 rovide insight into the relationship between mucosal inflammation, RA-related autoantibody generation
164 these mutants elicit markedly reduced early mucosal inflammation relative to their isogenic parent s
168 P < .001) with temsirolimus/bevacizumab were mucosal inflammation, stomatitis, hypophosphatemia, hype
170 wever, the mechanisms leading to the chronic mucosal inflammation that characterizes this disease rem
171 with Helicobacter induces a lymphocyte-rich mucosal inflammation that contains a minor population of
172 o provides a mechanistic explanation for the mucosal inflammation that is triggered during Salmonella
173 ity is a common and important consequence of mucosal inflammation that results in perturbed body home
174 ion of IL-9-producing iNKT cells involved in mucosal inflammation, their development remains unaddres
175 mechanistic role for chemokines and HBD2 in mucosal inflammation to include immunocyte trafficking a
177 we examined global metabolic consequences of mucosal inflammation using both in vitro and in vivo mod
178 affected CD colon and contributes to chronic mucosal inflammation via down-regulation of local PPARga
179 tance of epithelial cells to coordination of mucosal inflammation, we hypothesized that RvE1 elicits
180 may explain the abundance of MCs at sites of mucosal inflammation, where VCAM-1 and E-selectin are im
182 patients with varying amounts of intestinal mucosal inflammation, which corresponded to increased le
183 ion resulted in mucositis, a destructive gut mucosal inflammation, which is a common complication of
184 raceable to the advent of multiple models of mucosal inflammation whose very existence is indicative
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