ライフサイエンスコーパス: mucosal inflammation

1 ed intestinal epithelial barrier and chronic mucosal inflammation.

2 to evaluate its potential therapeutic use in mucosal inflammation.

3 n and markedly reduced gastric dysplasia and mucosal inflammation.

4 CII from IECs reduces but does not eliminate mucosal inflammation.

5 plays a role as a master regulator of airway mucosal inflammation.

6 Apoptosis was induced in mouse models of mucosal inflammation.

7 (+) T regulatory cells to dampen exaggerated mucosal inflammation.

8 ith perturbed immune homeostasis and chronic mucosal inflammation.

9 protect against systemic metastases without mucosal inflammation.

10 cimens of CUC in mild or "refractory" severe mucosal inflammation.

11 ch was further elevated in those with severe mucosal inflammation.

12 This disruption may result from mucosal inflammation.

13 ective element of adenosine signaling during mucosal inflammation.

14 ransporter activity, has been used to detect mucosal inflammation.

15 ate and adaptive immune responses as well as mucosal inflammation.

16 le of prolonged colonization or induction of mucosal inflammation.

17 g immunoregulatory roles in animal models of mucosal inflammation.

18 intestine regulating both oral tolerance and mucosal inflammation.

19 m, resulting in loss of epithelial cells and mucosal inflammation.

20 ed sites, implicating LIGHT as a mediator of mucosal inflammation.

21 n and cecum and causes crypt hyperplasia and mucosal inflammation.

22 helia and lamina propria but failed to cause mucosal inflammation.

23 bers, as well as patients with other chronic mucosal inflammation.

24 serve as a barrier-protective element during mucosal inflammation.

25 prevents invasion by commensal bacteria and mucosal inflammation.

26 ne mechanisms in the condition of intestinal mucosal inflammation.

27 to the importance of SP and its receptor in mucosal inflammation.

28 omprehension for the role chemokines play in mucosal inflammation.

29 tion ability, H. pylori density, and gastric mucosal inflammation.

30 be therapeutic for diseases characterized by mucosal inflammation.

31 g physiologic and pathologic T cell-mediated mucosal inflammation.

32 levels of IFN-gamma may have down regulated mucosal inflammation.

33 pivotal role in promoting H. pylori-induced mucosal inflammation.

34 (PrMCs) and accumulate at sites of allergic mucosal inflammation.

35 internalized and by the underlying degree of mucosal inflammation.

36 in the pathogenesis of H. pylori-associated mucosal inflammation.

37 In each case, the pathology usually includes mucosal inflammation.

38 ory properties in the presence or absence of mucosal inflammation.

39 m, an event necessary for the development of mucosal inflammation.

40 nizes the human stomach and produces gastric mucosal inflammation.

41 en and nitrogen species, further alleviating mucosal inflammation.

42 lon shortening, epithelial crypt damage, and mucosal inflammation.

43 RS), is characterized by eosinophil-dominant mucosal inflammation.

44 ion of UTX downregulates T cell responses in mucosal inflammation.

45 creased susceptibility to microbiota-induced mucosal inflammation.

46 d by a relapsing and remitting course of gut mucosal inflammation.

47 laceae families, were associated with rectal mucosal inflammation.

48 helial barrier, which may be impaired during mucosal inflammation.

49 and potentially UC by driving resolution of mucosal inflammation.

50 indicate dynamic processes of long-standing mucosal inflammation.

51 These differences were independent of mucosal inflammation.

52 n contribute to innate IEL activation during mucosal inflammation.

53 mmensal Bacteroides ovatus ATCC 8384 reduces mucosal inflammation.

54 th IBD vs controls; some were independent of mucosal inflammation.

55 stable before and during the development of mucosal inflammation.

56 etic approach to test the effect of EhMIF on mucosal inflammation.

57 expression of multiple cytokines to promote mucosal inflammation.

58 lend insight into the complexity of treating mucosal inflammation.

59 uce regulatory T cells (T(regs)) to suppress mucosal inflammation.

60 y response, but may directly induce a type-2 mucosal inflammation.

61 not accompanied by a detectable increase in mucosal inflammation.

62 tentially serve as a biomarker of intestinal mucosal inflammation.

63 rimental models of systemic autoimmunity and mucosal inflammation.

64 intense search for the underlying drivers of mucosal inflammation.

65 site immunomodulator, which protects against mucosal inflammation.

66 tions for targeting neddylation in models of mucosal inflammation.

67 a can promote both immunity to pathogens and mucosal inflammation.

68 Disruption of Ts cell activities can lead to mucosal inflammation.

69 pulate the human intestine and contribute to mucosal inflammation.

70 +/- 1.5, independent of primary diagnosis or mucosal inflammation.

71 rohn's disease and appears to be involved in mucosal inflammation.

72 y response occurring at a site of persistent mucosal inflammation.

73 e panitumumab plus chemoradiotherapy group), mucosal inflammation (15 [24%] vs 48 [55%]), and radiati

74 most frequent grade 3-4 adverse events were mucosal inflammation (25 [40%] of 62 patients in the che

75 luded rash (22% v 8%), diarrhea (58% v 30%), mucosal inflammation (33% v 21%), neutropenia (13% v 4%)

76 0%, respectively; grade 3 or 4 stomatitis or mucosal inflammation, 5.6% and 0%; and grade 3 or 4 diar

77 [15%] of 344 patients in the placebo group), mucosal inflammation (50 [14%] vs 45 [13%]), dysphagia (

78 During mucosal inflammation, a complex array of proinflammatory

79 concentrations are associated with increased mucosal inflammation, a loss of epithelial junctional pr

80 tent pro-inflammatory cytokine in intestinal mucosal inflammation, activates CARD4/NOD1 mRNA transcri

81 lished also showed a significant decrease in mucosal inflammation after alpha E beta 7 mAb administra

82 vides a more nuanced understanding of rectal mucosal inflammation after injury, which can inform our

83 te that miR-223 is an important regulator of mucosal inflammation and acts to constrain the progressi

84 sophagitis (EoE) aim to eliminate esophageal mucosal inflammation and attenuate, stabilize, or revers

85 disease induction and expel NETs to trigger mucosal inflammation and bone destruction in vivo.

86 ntation in the colon, in suppressing colonic mucosal inflammation and carcinogenesis.

87 revealed upregulation of pathways related to mucosal inflammation and cell death in the patients with

88 rate signals important for the activation of mucosal inflammation and concurrently allows invading ba

89 mydia infection is associated with transient mucosal inflammation and cytokine recruitment.

90 ne responses in macrophages, contributing to mucosal inflammation and damage.

91 Increased mucosal inflammation and defective epithelial homeostasi

92 D concentration is inversely correlated with mucosal inflammation and disease activity.

93 nal epithelial barrier, commonly observed in mucosal inflammation and diseases such as inflammatory b

94 e my views on the major microbial drivers of mucosal inflammation and dysregulation of innate TH2-pro

95 xygenase (COX)-2 are important regulators of mucosal inflammation and epithelial cell growth.

96 ences of constitutive TL1A expression on gut mucosal inflammation and fibrostenosis using two murine

97 n play a role in the pathogenesis of gastric mucosal inflammation and gastroduodenal disease.

98 esis offer clues to the critical triggers of mucosal inflammation and guide the development of therap

99 of cytokines may be important in regulating mucosal inflammation and homeostasis.

100 nd Chlamydia trachomatis are associated with mucosal inflammation and human immunodeficiency virus 1

101 led to visceral hyperalgesia, accompanied by mucosal inflammation and impaired mucosal barrier functi

102 r to WD-fed knockout mice attenuated colonic mucosal inflammation and improved CEB.

103 in feces, even in the presence of low-grade mucosal inflammation and increased intestinal permeabili

104 tis because DR3(-/-) mice showed more severe mucosal inflammation and increased mortality.

105 r-activated receptor (PPAR) gamma suppresses mucosal inflammation and is regulated by GH through STAT

106 and immune cells, with a focus on pathologic mucosal inflammation and mechanisms of epithelial repair

107 +) T cell loss and inversely correlated with mucosal inflammation and microbial translocation.

108 cells and activated T cells are involved in mucosal inflammation and mucosal damage.

109 Both mucosal inflammation and psychologic dysfunction have be

110 ow that platelets can actively contribute to mucosal inflammation and represent a previously unrecogn

111 These findings suggest a synergy between mucosal inflammation and SIV infection, creating an immu

112 We characterised mucosal inflammation and systemic immune responses to C.

113 ssary for both induction and perpetuation of mucosal inflammation and T-cell activation in Tg(epsilon

114 to develop two novel scores of peri-implant mucosal inflammation and their clinical application to h

115 Chronic mucosal inflammation and tissue damage predisposes patie

116 ion of inflammatory cytokines and subsequent mucosal inflammation and tissue damage.

117 c immune cell circuits as crucial drivers of mucosal inflammation and tissue destruction in IBD.

118 n butyrate producing bacteria could regulate mucosal inflammation and tissue repair.

119 dy of CRS is to identify specific drivers of mucosal inflammation and translate these into more effec

120 t modulate HIV/SIV susceptibility (including mucosal inflammation), and interventions that may impact

121 A1 strains is associated with enhanced acute mucosal inflammation, and adherence to gastric epithelia

122 t common AEs were fatigue, nausea, diarrhea, mucosal inflammation, and anorexia.

123 g physiological development and pathological mucosal inflammation, and differential expression of the

124 l macromolecular damage, caspase activation, mucosal inflammation, and gastric mucosal injury.

125 olitis exhibited delayed ulcer healing, more mucosal inflammation, and impaired Wnt/beta-catenin sign

126 dex score of 220-450, endoscopic evidence of mucosal inflammation, and previous failure of standard t

127 of counter-regulation of Th1 T cell-mediated mucosal inflammation, and that IL-10 is necessary as a s

128 Children with enteropathy or intestinal mucosal inflammation are at greatest risk of growth fail

129 e identify aberrant T cell-dependent, type 1 mucosal inflammation as a critical tissue-specific patho

130 ion between serum 25(OH)D concentrations and mucosal inflammation as assessed by the Mayo endoscopy s

131 ia; and, 2) relationships between nausea and mucosal inflammation as defined by antral and duodenal e

132 , we hypothesized that CD73 is protective in mucosal inflammation as modeled by trinitrobenzene sulfo

133 were selectively reduced in areas of active mucosal inflammation associated with human IBD and IL-10

134 Patients with enteropathy or intestinal mucosal inflammation (associated with dysmotility or sho

135 epithelial hyperplasia with ulcerations and mucosal inflammation at 6 weeks.

136 ated with a delayed but markedly exacerbated mucosal inflammation at the later stages of infection as

137 only modulates the location and severity of mucosal inflammation, but also induces fibrostenosis.

138 idence has linked intestinal permeability to mucosal inflammation, but molecular studies are lacking.

139 BV is generally considered to induce mucosal inflammation, but the specific pathways and cell

140 study was to investigate the role of A 2A in mucosal inflammation by administering a selective A 2A a

141 tant modulator in the development of chronic mucosal inflammation by enhancing T(H)1 and T(H)17 effec

142 Angiotensin II appears to drive colonic mucosal inflammation by promoting intestinal epithelial

143 We propose that mucosal inflammation, by eliciting substantial and ongoi

144 commensal organisms, perhaps contributing to mucosal inflammation characteristic of disorders such as

145 ere diarrhea (cohort A, 74%; cohort B, 67%), mucosal inflammation (cohort A, 49%; cohort B, 60%), and

146 Chronic, low-grade, systemic, and mucosal inflammation correlates with increased morbidity

147 -NF-kappaB signaling pathway is required for mucosal inflammation-coupled airway remodeling and myofi

148 During Salmonella-induced gastroenteritis, mucosal inflammation creates a niche that favors the exp

149 of the cecum and colon and causes transient mucosal inflammation driven by Th17 and Th1 T helper cel

150 Allergic rhinitis (AR) is characterized by mucosal inflammation, driven by activated immune cells.

151 TREM-2 contributes to mucosal inflammation during development of colitis in mi

152 but failed to ameliorate C.albicans-mediated mucosal inflammation emphasizing the need to optimize th

153 a disease surrogate such as the severity of mucosal inflammation, epidemiologic consistency, and bio

154 r a specific parasite protein that increases mucosal inflammation, expands our knowledge of host-para

155 de 3 adverse events included abdominal pain, mucosal inflammation, fatigue, neutropenia, and hand-foo

156 Plasma fatty acid status, intestinal mucosal inflammation (fecal calprotectin), daily morbidi

157 determine the extent and nature of bronchial mucosal inflammation following experimental rhinovirus (

158 ited, activated, and retained in response to mucosal inflammation from persistent MCMV infection of t

159 iggers a pathway that contributes to chronic mucosal inflammation, GI barrier breakdown, and microbia

160 , genetics, and the immune system results in mucosal inflammation has increased knowledge of disease

161 What emerges is that murine models of mucosal inflammation have given us a road map that allow

162 products (proinflammatory mediators) amplify mucosal inflammation, ii) the capacity of necrotic cell

163 nces in the intestinal microbiota; low-grade mucosal inflammation, immune activation, and altered int

164 cies became the most abundant) and prevented mucosal inflammation, impairment to intestinal barrier f

165 ive method for monitoring colonic tumors and mucosal inflammation in a mouse model of colon cancer us

166 llin played a role in suppressing intestinal mucosal inflammation in a murine model of acute enteroco

167 llow a unified theory for how microbes cause mucosal inflammation in asthma.

168 the STAT5b transcription factor and reduces mucosal inflammation in colitis.

169 Mucosal inflammation in conditions ranging from infectiv

170 6 production potentially contributing to the mucosal inflammation in CRS patients.

171 gic examination results included nonspecific mucosal inflammation in four case patients, wall edema i

172 al bacteria that may initiate and perpetuate mucosal inflammation in genetically susceptible individu

173 enues for treatment of epithelial injury and mucosal inflammation in IBD patients.

174 stinal microorganisms is considered to drive mucosal inflammation in inflammatory bowel diseases.

175 Mucosal inflammation in later disease was dominated by i

176 lagella dramatically decreases the degree of mucosal inflammation in mice and the sole presence of to

177 matrix metalloproteinase 7 (MMP7) increases mucosal inflammation in mouse models of epithelial injur

178 might be a useful marker of gastrointestinal mucosal inflammation in neonates.

179 protein antibodies (ACPAs), implicating oral mucosal inflammation in RA pathogenesis.

180 Based on recent reports of low-grade mucosal inflammation in subpopulations of patients meeti

181 companied by transient crypt hyperplasia and mucosal inflammation in the colon and cecum at 2 but not

182 MPORTANCE There is low-level but significant mucosal inflammation in the gastrointestinal tract secon

183 propose that VacA augments H. pylori-induced mucosal inflammation in the human stomach by causing pro

184 role of prostaglandins in the regulation of mucosal inflammation in the IL-10(-/-) mouse model of IB

185 cytokine, is a potent negative regulator of mucosal inflammation in the intestine.

186 HIV and SIV) infections are characterized by mucosal inflammation in the presence of anti-inflammator

187 and adenomas and suggest a possible role for mucosal inflammation in this process.

188 with elevated levels seen in the setting of mucosal inflammation including inflammatory bowel diseas

189 edding was associated with the parameters of mucosal inflammation, including T cell activation, infla

190 s time) led to lower body weights, increased mucosal inflammation, increased colonic tumor numbers, e

191 These sensors also regulate mucosal inflammation independent of pathogen infections.

192 Here, we show that mucosal inflammation induced by Salmonella enterica sero

193 Inhibition of ICOS attenuates lung mucosal inflammation induced by Th2 but not Th1 effector

194 CD), and in contrast to most mouse models of mucosal inflammation, inflammatory lesions in the gastro

195 mechanisms of plasticity as key targets for mucosal inflammation intervention strategies.

196 he mechanisms by which M. genitalium elicits mucosal inflammation is an essential component to managi

197 Chronic mucosal inflammation is associated with a greater risk o

198 Mucosal inflammation is associated with iHsp down-regula

199 Regulation of mucosal inflammation is central to SMAD4 tumor suppresso

200 Whether the associated mucosal inflammation is important or redundant for effec

201 inflammatory condition in which Th17-driven mucosal inflammation leads to destruction of tooth-suppo

202 ere is epidemiological evidence that genital mucosal inflammation leads to enhanced HIV type 1 (HIV-1

203 l activation, which can result in intestinal mucosal inflammation, malabsorption, and numerous second

204 In conclusion, mucosal inflammation (mast cells and eosinophils) is ass

205 r study of the role of RNASET2 in regulating mucosal inflammation may lead to development of novel th

206 erate and consisted primarily of stomatitis, mucosal inflammation, mouth ulceration, rash, and fatigu

207 companied by a significant increase in acute mucosal inflammation, mucosal injury, luminal fluid secr

208 toxicities in > 1 patient (part A) included mucosal inflammation (n = 3) and hyponatremia (n = 2).

209 (grade 3 acne [n=1] and intolerable grade 2 mucosal inflammation [n=1]); hence, doses of 200 mg and

210 clear whether virus per se induces bronchial mucosal inflammation, nor whether this relates to exacer

211 The role of TNF-alpha in the mucosal inflammation of Crohn's disease has been demonst

212 ed with antibiotics results in self-limiting mucosal inflammation of the large intestine.

213 is characterized by persistent locoregional mucosal inflammation of the paranasal sinuses and upper

214 ells from patients with CD, independently of mucosal inflammation or disease-associated variants of A

215 intestinal microbiota affect development of mucosal inflammation or inflammatory bowel disease.

216 ivo correlate with disease such as increased mucosal inflammation, or both.

217 changes were associated with severe gastric mucosal inflammation, parietal cell loss, atrophy, and m

218 Despite smoking cessation, neutrophilic mucosal inflammation persistently damages the airways an

219 usceptibility to intestinal colonization and mucosal inflammation persists when mice are infected sev

220 ietary PUFAs as a trigger of GPX4-restricted mucosal inflammation phenocopying aspects of human CD.

221 Airway mucosal inflammation plays a critical role in the pathog

222 ting cells against stress and, in intestinal mucosal inflammation, potentially lessening the extent a

223 environment in pathological processes, like mucosal inflammation, preneoplasia, and neoplasia, altho

224 rovide insight into the relationship between mucosal inflammation, RA-related autoantibody generation

225 these mutants elicit markedly reduced early mucosal inflammation relative to their isogenic parent s

226 es, the tight junction protein occludin, and mucosal inflammation, respectively.

227 lammatory gene products necessary for airway mucosal inflammation seen in RSV disease.

228 Patients with ulcerative colitis have mucosal inflammation starting in the rectum that can ext

229 P < .001) with temsirolimus/bevacizumab were mucosal inflammation, stomatitis, hypophosphatemia, hype

230 nterobacteriaceae that exacerbated low-grade mucosal inflammation, suggesting that remediating dysbio

231 symptoms but no evidence of gastrointestinal mucosal inflammation (TD(IC-)).

232 wever, the mechanisms leading to the chronic mucosal inflammation that characterizes this disease rem

233 with Helicobacter induces a lymphocyte-rich mucosal inflammation that contains a minor population of

234 o provides a mechanistic explanation for the mucosal inflammation that is triggered during Salmonella

235 ity is a common and important consequence of mucosal inflammation that results in perturbed body home

236 ion of IL-9-producing iNKT cells involved in mucosal inflammation, their development remains unaddres

237 mechanistic role for chemokines and HBD2 in mucosal inflammation to include immunocyte trafficking a

238 However, mechanisms linking mucosal inflammation to the sequence of dysplasia are in

239 intestinal microbiotic dysbiosis and chronic mucosal inflammation.To assess phenotypic changes in pro

240 Furthermore, we demonstrate mucosal inflammation upon exposure of these constructs t

241 we examined global metabolic consequences of mucosal inflammation using both in vitro and in vivo mod

242 affected CD colon and contributes to chronic mucosal inflammation via down-regulation of local PPARga

243 Mechanistically, mucosal inflammation was increased in the LC-diet-fed mi

244 tance of epithelial cells to coordination of mucosal inflammation, we hypothesized that RvE1 elicits

245 may explain the abundance of MCs at sites of mucosal inflammation, where VCAM-1 and E-selectin are im

246 In addition, EAEC infections elicit mucosal inflammation, which can be observed in infected

247 patients with varying amounts of intestinal mucosal inflammation, which corresponded to increased le

248 ion resulted in mucositis, a destructive gut mucosal inflammation, which is a common complication of

249 increased oxygen and nitrate, suggestive of mucosal inflammation, which may have implications for re

250 raceable to the advent of multiple models of mucosal inflammation whose very existence is indicative

251 uals at-risk of RA have associated pulmonary mucosal inflammation with local production of ACPAs and