ライフサイエンスコーパス: allergen exposure

1 in early life to induce persistent AHR after allergen exposure.

2 accumulation in AD skin following cutaneous allergen exposure.

3 te units for the assessment of environmental allergen exposure.

4 n Baltimore should prioritize reducing mouse allergen exposure.

5 -fat- or high-fructose-fed mice even without allergen exposure.

6 and inflammation following acute and chronic allergen exposure.

7 t is unknown whether pollen counts represent allergen exposure.

8 s were detectable in the lungs after chronic allergen exposure.

9 s to public health associated with increased allergen exposure.

10 velopment of eosinophilic inflammation after allergen exposure.

11 gic inflammation in the absence of exogenous allergen exposure.

12 s expressed on lung inflammatory cells after allergen exposure.

13 h to study effectively how AD is affected by allergen exposure.

14 lic inflammation, and IL-13 levels following allergen exposure.

15 e that later primes the esophagus on further allergen exposure.

16 ing the migration of Th2 cells into sites of allergen exposure.

17 tion, particularly in the setting of ongoing allergen exposure.

18 ay is involved in the Tfh response to peanut allergen exposure.

19 at are differentially expressed after airway allergen exposure.

20 development of lung pathology in response to allergen exposure.

21 d CXCL13) were increased only after a second allergen exposure.

22 ed airway inflammation and obstruction after allergen exposure.

23 the resolution of MCM following cessation of allergen exposure.

24 d asthma among children with a wide range of allergen exposure.

25 sthma are modified by the level of dust mite allergen exposure.

26 ss-switching of B-cells to produce IgE after allergen exposure.

27 hese cells substantially increase after oral allergen exposure.

28 lability for recruitment to the airway after allergen exposure.

29 ent of in vivo allergic responses to inhaled allergen exposure.

30 oth T cell and NK cell populations following allergen exposure.

31 production in NT4(-/-) mice after early life allergen exposure.

32 t data variability secondary to inconsistent allergen exposure.

33 eosinophilopoiesis in the bone marrow after allergen exposure.

34 ributing to epithelial wall damage following allergen exposure.

35 d in the airways of asthmatic patients after allergen exposure.

36 s led to exacerbated lung inflammation after allergen exposure.

37 ges in the airways following chronic inhaled allergen exposure.

38 es persisted for 6 months after cessation of allergen exposure.

39 odulating Th2 inflammation following mucosal allergen exposure.

40 exposure and poor antioxidant response after allergen exposure.

41 ed by Th2-cell-type cytokines in response to allergen exposure.

42 el spontaneously resolves after cessation of allergen exposure.

43 ional and environmental (indoor and outdoor) allergen exposure.

44 nophils recruited and activated by pulmonary allergen exposure.

45 egulatory cells, exaggerated with additional allergen exposure.

46 was increased in waved-2 mice skin following allergen exposure.

47 and no rise in serum IgE after multiple HDM-allergen exposures.

48 res and have often lacked well-characterized allergen exposures.

49 y changes at the small molecule level due to allergen exposure, (2) determine perturbed pathways due

50 esponse ratio was significantly higher after allergen exposure (57 mg/% FEV1 fall [27-121] to 147 mg/

51 veloped AHR and some lung eosinophilia after allergen exposure alone and when RSV infection preceded

52 Allergen exposure also induces acute extracellular accum

53 SPDEF was induced following intratracheal allergen exposure and after Th2 cytokine stimulation and

54 een the lungs and bone marrow, we used acute allergen exposure and airway inflammation models in mice

55 that the dose-response relationship between allergen exposure and allergic disease may differ betwee

56 increased quickly within several hours after allergen exposure and continued to rise throughout the c

57 showed reduced lung pathology after chronic allergen exposure and decreased type 2 cytokine producti

58 s induced by environmental challenge chamber allergen exposure and had a favorable safety profile.

59 igning costly and labor-intensive studies of allergen exposure and health outcomes, commonly used in

60 mucosal cytokine responses induced by nasal allergen exposure and humoral immune responses that incl

61 ned genes modulated in concomitance with the allergen exposure and inhibition of responses in non-all

62 ed with oxidative stress in the lungs before allergen exposure and poor antioxidant response after al

63 o in human subjects, oxidative stress before allergen exposure and poor antioxidant responses were as

64 from indoor environments in order to assess allergen exposure and possible relationships to health o

65 cells are rapidly recruited to the lung upon allergen exposure and release eotaxins that coordinately

66 In allergic rhinitis, initial allergen exposure and sensitization involves antigen-pre

67 The relationship between dose of allergen exposure and symptom severity is unclear.

68 ules is profoundly dependent on the route of allergen exposure and the child's IgE sensitization stat

69 Allergen exposure and the resulting symptoms vary, and t

70 Environmental assessments included allergen exposure and, in a nested case-control study of

71 Rationale: The relationships between allergen exposures and allergy and asthma are complex.

72 t underlie the synergistic interplay between allergen exposures and viral infections.

73 vironmental tobacco smoke exposure, obesity, allergen exposure, and availability of health care.

74 t eosinophils express CAR4 following IL-5 or allergen exposure, and that CAR4 is involved in regulati

75 thickness were increased following cutaneous allergen exposure, and these were further enhanced in th

76 Atopy, mite allergen exposure, and vitamin D levels were also measur

77 ze (maternal smoking, breast-feeding, indoor allergen exposures, and lower respiratory infections).

78 Although environmental factors such as allergen exposure are risk factors in the development of

79 Allergen exposure at lung and gut mucosae can lead to ab

80 d a temporary association between higher HDM allergen exposure at the age of 3 months and more asthma

81 impact of concurrent influenza infection and allergen exposure at the genomic level, using whole-geno

82 ity of predicting and determining individual allergen exposure because of many factors (eg, pollen se

83 ifferences were observed in MCM at 5 days of allergen exposure between +/+ and -/- mice, despite redu

84 ing and breast-feeding behaviors, as well as allergen exposure, birth weight, and lower respiratory i

85 rigger degranulation of mast cells following allergen exposure, but also to enhance their survival.

86 hat healthy individuals are not oblivious to allergen exposure, but rather react with an active modul

87 chronic allergic asthma, we mimicked natural allergen exposure by giving tiny doses of dust-mite extr

88 ole in mucus overproduction after early life allergen exposure by orchestrating PNEC innervation and

89 Following passive sensitization and allergen exposure, C57BL/6+/+ mice developed altered air

90 Long-term allergen exposure can attenuate inflammation and revert

91 Allergen exposure can confound the management of asthma.

92 Inflammatory responses induced by allergen exposure cause mucous cell metaplasia (MCM) by

93 Longitudinal evidence that indoor allergen exposure causes morbidity in sensitized individ

94 ing the efficacy of sublingual tablets in an allergen exposure chamber over a 4-month period.

95 Allergen exposure chambers (AECs) are clinical facilitie

96 levated in Bax -/- mice following 15 days of allergen exposure compared with +/+ mice, while the numb

97 Bedroom allergen exposures contribute to allergic disease morbid

98 leukotrienes phenocopied the WT response to allergen exposure; conversely, anti-PlGF Ab administrati

99 emic or mucosal administration of ISS before allergen exposure could provide a novel form of active i

100 ctivity, suppressed as a result of long-term allergen exposure, could be reestablished by depleting g

101 Subsequent allergen exposure cross-links mast cell-bound IgE, resul

102 Following allergen exposure, cytokines and other pro-inflammatory

103 evels to exogenous allergens were boosted by allergen exposure, declined thereafter, and seemed to be

104 uces IgE synthesis by B cells in response to allergen exposure, decreases the expression of IgE recep

105 Whereas OVA allergen exposure did not induce inflammation in WT cont

106 Dog allergen exposure did not show such interaction.

107 cepsilonRI complexes that prime cells before allergen exposure dissociate extremely slowly and cannot

108 cates that oxidative stress condition before allergen exposure due to an inadequate antioxidant respo

109 Indoor environmental allergen exposure during early life can also affect dise

110 lacebo-controlled field studies with natural allergen exposure during the allergen season.

111 We investigated the effect of maternal allergen exposures during pregnancy on allergen-induced

112 In our model, maternal allergen exposures during pregnancy prevented later alle

113 memory (CD62L(hi)) subsets, which vary with allergen exposure (e.g., during, or out with, pollen sea

114 Early life allergen exposure elevated the level of NT4 and caused P

115 climate change in the context of plants and allergen exposure, emphasizing direct effects on plant p

116 e the magnitude of effect in an uncontrolled allergen exposure environment.

117 After cessation of allergen exposure, eosinophils and T cells were cleared

118 After 5 days of allergen exposure, extensive MCM had developed but was r

119 ion as an appropriate alternative to natural allergen exposure for AIT product efficacy assessment.

120 Prenatal allergen exposure has been linked to both induction and

121 not single phenotypes, and it is likely that allergen exposure has different effect on distinct subgr

122 After allergen exposure, HDM-specific memory cells persisted a

123 ase in childhood food allergy (FA), the dual-allergen exposure hypothesis has been the most extensive

124 RNA-seq analysis following allergen exposure identified a network of pro-inflammato

125 CM levels were decreased 4-fold at 7 days of allergen exposure in -/- mice and at 15 days in +/+ mice

126 ive hypersensitivity responses to subsequent allergen exposure in an allergen-specific manner, effect

127 Pulmonary allergen exposure in C5aR-targeted mice resulted in incr

128 Standardized allergen exposure in challenge chamber settings might be

129 data define the importance of age at initial allergen exposure in dictating subsequent responses in t

130 l drawbacks, such as the high variability of allergen exposure in different trial sites or seasons an

131 It is unclear whether the initial route of allergen exposure in early life could influence the subs

132 lia, eosinophilic esophagitis was induced by allergen exposure in IL-5-deficient and wild-type mice.

133 a gene deficiency were studied in a model of allergen exposure in mice sensitised and challenged with

134 We found that allergen exposure in neonatal mice, but not in adult mic

135 unotherapy (AIT) mediates protection against allergen exposure in part due to allergen-specific antib

136 of eotaxin mRNA are known to increase after allergen exposure in sensitized animals.

137 RATIONALE: Allergen exposure in sensitized individuals with asthma

138 vivo role of IL-12 in the immune response to allergen exposure in susceptible (A/J) and resistant (C3

139 The role of allergen exposure in the development of allergic disease

140 arch to elucidate the role of chronic indoor allergen exposure in the development of glaucomatous opt

141 OSS) were assessed every 15 min during a 4-h allergen exposure in the Vienna Challenge Chamber.

142 enitors of goblet cells induced by pulmonary allergen exposure in vivo.

143 conducting airway epithelium after pulmonary allergen exposure in vivo.

144 nd climatic factors, associated with bedroom allergen exposures in a nationally representative sample

145 stic interplay between respiratory virus and allergen exposures in the onset and progression of asthm

146 or monitoring environmental and occupational allergen exposure including sampling strategies and meth

147 lung and draining lymph nodes revealed that allergen exposure increased TREM-2 expression on all DC

148 Our study supports the hypothesis that early allergen exposure increases tolerance and lowers risk of

149 Allergen exposure induced Serpinb3a expression in the sk

150 are present in allergic subjects and (2) cat allergen exposure induces an IgG4 response in a TH2 cell

151 We propose that allergen exposure induces elevation in SP-D protein leve

152 Allergen exposure induces the airway epithelium to produ

153 Thus, T-bet deficiency, in the absence of allergen exposure, induces a murine phenotype reminiscen

154 n 5 French regions according to the route of allergen exposure (inhaled vs food allergens).

155 Allergen exposure is associated with the development of

156 he time interval between viral infection and allergen exposure is critical in determining whether vir

157 vation through the alternative pathway after allergen exposure is critical to the development of AHR

158 This synergy between DEP and natural allergen exposure is suggested as a key feature in incre

159 These data suggest that repeated allergen exposure leads to progressive decreases in AHR

160 Our current observations suggest that allergen exposure may contribute to poor asthma control

161 t use of COX-inhibiting drugs during initial allergen exposure may increase the risk of developing al

162 tial period of bronchoconstriction following allergen exposure may involve neither mast cells nor IgE

163 uman epidemiologic studies suggest high-dose allergen exposure may paradoxically protect against sens

164 ence with CD28-mediated costimulation during allergen exposure might be an attractive therapeutic con

165 We have developed a novel chronic allergen exposure model using the clinically relevant an

166 in the healthy immune response to high-dose allergen exposure models in humans, T regulatory cells a

167 Dust mite allergen exposure modifies the estimated effect of rs117

168 In mixed models, allergen exposure modulated (q </= 0.2) miRNAs including

169 tly, marked airway hyperreactivity only when allergen exposure occurred during an acute influenza A i

170 h2 responses to allergens, particularly when allergen exposure occurs concomitantly with exposure to

171 -VLA-4 and anti-IL-5 in a model of secondary allergen exposure of previously sensitized and challenge

172 The effect(s) of allergen exposure on airway responsiveness to indirect-a

173 f this study was to determine the effects of allergen exposure on leukotriene generation and inflamma

174 the present study, we examined the effect of allergen exposure on TREM-2 expression in the airways an

175 tolerance has been observed after high-dose allergen exposure or after completed allergen immunother

176 It is currently unknown why allergen exposure or environmental triggers in patients

177 Other factors such as timing of allergen exposure or other environmental adjuvants may c

178 signaling was antagonized concomitantly with allergen exposure, or the development of allergic airway

179 ticosteroid use, but not atopic status, mite allergen exposure, or vitamin D levels, modified the ass

180 Susceptibility to allergen exposure, other environmental exposures and the

181 ays in regulating immunological tolerance to allergen exposure outside the GI tract and proposes the

182 Cumulative allergen exposure over the first 3 years was associated

183 be predictive of symptom severity upon grass allergen exposure (P = 0.029).

184 Eos recruited to the airways after allergen exposure produce and respond to IL-5 and GM-CSF

185 ate that elevated levels of IL-5 and mucosal allergen exposure promote eotaxin-dependent eosinophil t

186 (such as passive or active smoking, ongoing allergen exposure, psychosocial factors) have to be a pr

187 that leads to IgG4 induction during chronic allergen exposure remains poorly understood.

188 Allergen exposure resulted in airway recruitment of Gal-

189 vations in both mice and humans suggest that allergen exposure results in increased output of eosinop

190 After allergen exposure, rhinovirus-induced neutrophilic and e

191 ce in children in the presence or absence of allergen exposure/sensitization in the Cincinnati Childh

192 l models that closely mimic natural modes of allergen exposure should prove most informative.

193 esponsible for Th2 sensitization at sites of allergen exposure, such as airway and skin, is crucial f

194 Some aspects of work-related allergen exposure, such as route and frequency of exposu

195 recruitment to the lungs of asthmatics after allergen exposure suggests platelets participate in vari

196 ly inflammatory response following cutaneous allergen exposure, supporting a role for Serpinb3a (mice

197 rved in human subjects as the consequence of allergen exposures that recurrently activate memory B ce

198 Allergic airway inflammation is triggered by allergen exposure through several steps including releas

199 onse in peanut-tolerant groups suggests that allergen exposure through the GI tract induces tolerance

200 postnatal growth, thereby linking early-life allergen exposure to persistent airway dysfunction.

201 We sought to determine whether exposure to allergen, exposure to diesel exhaust (DE), or coexposure

202 a, prior to sensitization, challenge, or all allergen exposures, to assess the role of oxidative stre

203 im to operate with a stable and reproducible allergen exposure under highly standardized environmenta

204 Allergen exposure upregulated IL-25 and induced type 2 c

205 Allergen exposure was defined as dog or cat in the home

206 fer repeated relapses caused by intermittent allergen exposure, we hypothesized that allergen- specif

207 eosinophilia and AHR after RSV infection and allergen exposure were also markedly reduced.

208 ermore, early and late phases resulting from allergen exposure were shown to involve similar lung reg

209 ch measures to reduce prenatal and postnatal allergen exposure were undertaken (active HRA) (n=145) o

210 ed increased CCR5 expression after high-dose allergen exposure while CXCR4, CXCR5, CCR6, and CCR7 exp

211 xhibited increased airway inflammation after allergen exposure, with massive eosinophilic lung infilt