ライフサイエンスコーパス: endotoxin

1 al lipopolysaccharide (LPS) - also known as 'endotoxin'.

2 . administration of 2 ng/kg Escherichia coli endotoxin).

3 ntestinal tract is the dominant reservoir of endotoxin.

4 were negative for microbial contaminants and endotoxin.

5 flammatory and procoagulant host response to endotoxin.

6 he DVR did not change in the left lung after endotoxin.

7 m with lipopolysaccharide (LPS), a bacterial endotoxin.

8 rophages challenged with a super-low dose of endotoxin.

9 due to a marked decrease in its affinity for endotoxin.

10 development of IL-10-dependent tolerance to endotoxin.

11 nd injury induced in mice by a toxic dose of endotoxin.

12 ver, and increased serum levels of bacterial endotoxin.

13 H. zea susceptibility to Cry1Ac, a common Bt endotoxin.

14 nged with a shock-inducing dose of bacterial endotoxin.

15 ation along with an elevation of gut-derived endotoxin.

16 stantially protected from lethal exposure to endotoxin.

17 lammatory cytokine production in response to endotoxins.

18 d polymers (MIPs) with high affinity towards endotoxins.

19 to distension or stimulation with bacterial endotoxins.

20 elation between FEV1 % and concentrations of endotoxin, (1, 3)-beta-D-glucan, or any of the allergens

21 following microbiological markers: bacterial endotoxin, 3-hydroxy fatty acids, and muramic acid.

22 Endotoxin (4 ng/kg) was then instilled bronchoscopically

23 sis associated with monocyte deactivation by endotoxin, a process contributing to immunometabolic par

24 Results With endotoxin, a significantly increased contrast-to-noise r

25 return of spontaneous circulation using the endotoxin activity assay.

26 < 0.6 endotoxin activity), or high (>/= 0.6 endotoxin activity) according to manufacture guidelines.

27 Endotoxin level was classified as low (< 0.4 endotoxin activity), intermediate (0.4 to < 0.6 endotoxi

28 otoxin activity), intermediate (0.4 to < 0.6 endotoxin activity), or high (>/= 0.6 endotoxin activity

29 ed euglycemia and 2) insulin deprivation and endotoxin administration (KET).

30 ected against mortality following parenteral endotoxin administration.

31 diseases (burns, trauma, infection, sepsis, endotoxin and acute respiratory distress syndrome) and m

32 tion Examination Survey included measures of endotoxin and allergens in homes as well as specific IgE

33 rier function in CKD allows translocation of endotoxin and bacterial metabolites to the systemic circ

34 score, pulmonary oxygenation, and levels of endotoxin and humoral cytokines.

35 report of an association between house dust endotoxin and leukocyte count in a national survey.

36 aggerates inflammatory signaling to dsRNA or endotoxin and results in over production of type I IFN,

37 ractions between the preconditioning dose of endotoxin and the renal tubules.

38 and environmental exposures to allergens and endotoxin and to the development of allergic sensitizati

39 children, measuring levels of allergens and endotoxins and assessing the microbiome composition of i

40 Effective control of endotoxins and bacteria is crucial for normal wound heal

41 CLL and describes a cross-tolerance between endotoxins and tumors.

42 ness or dampness-related agents (in adults), endotoxin, and environmental tobacco smoke (in preschool

43 by (1, 3)-beta-D-glucan concentrations, for endotoxin, and for dust mite, cat, and dog allergen conc

44 inal barrier function, increased circulating endotoxin, and increased lymphocyte expression of ionize

45 ytic cells in response to varying dosages of endotoxin, and may shed light on our understanding of th

46 esponse patterns of human monocytes to MRP8, endotoxins, and various cytokines, we have developed a m

47 that DUSP3 deficiency confers resistance to endotoxin- and polymicrobial-induced septic shock.

48 llus fumigatus antigens, house dust mite and endotoxin antigens increase the risk of eczema, allergy

49 The affinity based-endotoxin assay can detect endotoxins in the concentrati

50 The early and prompt detection of endotoxin assumes prime importance in health care, pharm

51 We found that in vivo endotoxin at doses below 1.0 ng/kg triggers weak and var

52 eased Firmicutes-to-Bacteroidetes ratios and endotoxin-bearing Proteobacteria levels-but also maintai

53 The Bacillus thuringiensis delta-endotoxins (Bt toxins) are widely used insecticidal prot

54 malian hepatic defense response to bacterial endotoxin by modulating HDL.

55 able to respond to challenge with bacterial endotoxin by mounting an acute inflammatory response.

56 Bacterial endotoxin can induce inflammatory and metabolic changes

57 nd quantification of biocontaminants such as endotoxin can interfere with nanoparticles thus leading

58 P showed the potential of the technology for endotoxins capture, detection and risk management and al

59 /fl)) showed higher mortality in response to endotoxin challenge and bacterial infection.

60 nhanced inflammation and lethality following endotoxin challenge in vivo.

61 splenocytes on murine neonatal mortality to endotoxin challenge or polymicrobial sepsis and characte

62 es did not alter murine neonatal survival to endotoxin challenge or polymicrobial sepsis challenge.

63 o response of neutrophils evoked by systemic endotoxin challenge, the clonal response of leukocytes i

64 d mtDNA, reproduced a refractory state after endotoxin challenge.

65 nts, by multivariate linear regression, high endotoxin class (adjusted estimate -2.0; 95% CI, -3.90 t

66 Furthermore, high endotoxin class (adjusted estimate, 97.95; 95% CI, 20.5

67 stigated the relationship between house dust endotoxin concentration and peripheral leukocyte counts

68 ly significant, positive association between endotoxin concentration and total leukocyte number [esti

69 Log-transformed endotoxin concentrations were analyzed using logistic mo

70 such as the lactulose/mannitol ratio, plasma endotoxin concentrations, and serum levels of inflammati

71 Preconditioning with a low dose of endotoxin confers unparalleled protection against otherw

72 The OM outer leaflet is comprised of endotoxin containing lipid A, which can be modified to i

73 ses between rHuPH20 and BTH is likely due to endotoxin contaminants in BTH.

74 functionality and markedly reduced levels of endotoxin contamination.

75 dust and quality assurance samples for their endotoxin content using extreme quality assurance measur

76 s in an activation-dependent manner to which endotoxin contributes, associated with reduced frequency

77 ride-binding protein (LBP), immunoglobulin M endotoxin core antibodies to lipopolysaccharide (EndoCAb

78 inal fatty acid-binding protein [iFABP], and endotoxin core IgG antibody [EndoCAb]), acute-phase prot

79 There were negative correlations between endotoxin core IgM and IL-1beta levels.

80 vel (sCD14) was significantly higher and the endotoxin core immunoglobulin M (IgM) level lower in cas

81 Endotoxin-depleted BTH had much reduced proinflammatory

82 receive either a single infusion of low-dose endotoxin (derived from Escherichia coli; 0.8 ng/kg of b

83 There were no microbial contaminants or endotoxin detected in any of the samples.

84 d robust drug-assisted dot blot bioassay for endotoxin detection that can be used right by the critic

85 quency piezoelectric tuning forks (QTFs) for endotoxin detection.

86 However, scFv/TM injected after endotoxin did not reduce thrombin/antithrombin complexes

87 We tested whether bacterial endotoxin E. coli lipopolysaccharide (LPS) affected two

88 me cannot, affording a unique model to study endotoxin essentiality.

89 tile Worker Study is a longitudinal study of endotoxin-exposed cotton workers and endotoxin-unexposed

90 larities between the effects of occupational endotoxin exposure and those of tobacco smoke exposure o

91 The effects of occupational endotoxin exposure appear to persist even after the cess

92 ocyte count may be influenced by residential endotoxin exposure in diverse settings.

93 the relationship between these variants and endotoxin exposure in relation to the development of ast

94 ization, male sex, breast-feeding, and lower endotoxin exposure in year 1 but not with race/ethnicity

95 ion of the innate immune system to microbial endotoxin exposure through direct corticosterone-mediate

96 available, making this the largest study of endotoxin exposure to date.

97 ve contributions of smoking and occupational endotoxin exposure to parenchymal and airway remodeling

98 Occupational endotoxin exposure was associated with a decrease (-1.3%

99 .S. nationwide representative sample, higher endotoxin exposure was significantly associated with mea

100 Endotoxin exposure was significantly associated with whe

101 ory cytokines both at baseline and following endotoxin exposure when compared with infants with trans

102 Spirometry, occupational endotoxin exposure, and smoking habits were assessed at

103 ave increased IL10 production due to chronic endotoxin exposure.

104 Significant predictors of higher endotoxin exposures were lower family income; Hispanic e

105 s and copper, zinc, phosphorus, silicon, and endotoxin found in PM10-2.5.

106 hat allow the expression and purification of endotoxin-free antibody reagents suitable for testing in

107 d sensitizes cells to lipopolysaccharide, an endotoxin from bacteria.

108 to detection, quantification and removal of endotoxin from nanoformulations, and practical considera

109 d using solid-phase photopolymerisation with endotoxins from Escherichia coli 0111:B4 as the template

110 ially detoxify and eliminate xenobiotics and endotoxins from the body.

111 Stimulation with inflammatory cytokines and endotoxin immediately induced release of shedding type E

112 0.54 +/- 0.12, and the mean HUs by 11% after endotoxin in 6 volunteers who had positive iNOS staining

113 we demonstrate detection and distribution of endotoxin in a lethal murine F. novicida infection model

114 Tests exist to detect endotoxin in bodily fluids, but are expensive, not neces

115 Circulating levels of endotoxin in plasma from patients with AAH caused over e

116 Mattress endotoxin in the first year of life was inversely associ

117 ase identified increased levels of bacterial endotoxin in the portal circulation, suggesting a role f

118 s show that murine HSPCs directly respond to endotoxin in vivo and that persistent LPS, a feature of

119 he affinity based-endotoxin assay can detect endotoxins in the concentration range of 15.6-500 ng mL(

120 ia coli lipopolysaccharide (LPS; also called endotoxin) in humans with the positron emission tomograp

121 biologic exposures, including allergens and endotoxin, in urban homes stimulate the development of c

122 tivation of the immune system via peripheral endotoxin increases neuronal aromatase; a mechanism that

123 to human physiology, we show that persistent endotoxin increases the frequency of Ki-67(+) HSCs and s

124 ther exposure to fungi, house dust mites and endotoxin increases the risk of eczema, allergy and asth

125 eproduced by combined insulin deficiency and endotoxin-induced acute inflammation.

126 lves in inflammatory injuries, such as after endotoxin-induced acute lung injury.

127 efect in vitro, and significantly attenuated endotoxin-induced biliary damage and inflammation in viv

128 uced CNS neuroinflammation and morphine- and endotoxin-induced changes in glutamate transport, effect

129 Sepsis eQTL were enriched in endotoxin-induced epigenetic marks and modulated the ind

130 mice are more sensitive than normal mice to endotoxin-induced inflammation and sepsis.

131 al host protection by limiting the extent of endotoxin-induced inflammation in an MPO-dependent manne

132 mal miR-146a inhibits while miR-155 promotes endotoxin-induced inflammation in mice.

133 TRPM2 protects lungs from endotoxin-induced injury by reducing reactive oxygen spe

134 18)F-NOS could quantify iNOS expression from endotoxin-induced lung inflammation in healthy volunteer

135 4 signaling, such as Gram-negative bacterial endotoxin-induced lung injury and HDM-triggered allergic

136 magenic agonists used and exhibited 60% less endotoxin-induced mortality.

137 mmended beta-adrenergic drugs for supporting endotoxin-induced myocardial dysfunction.

138 to bind to lipopolysaccharide to reduce the endotoxin-induced proinflammatory cytokine response in m

139 ein kinase 1/2 inhibitor trametinib prevents endotoxin-induced renal injury in mice.

140 vealed that increased survival of animals in endotoxin-induced sepsis is Nr4a2-dependent.

141 gh they displayed similar sensitivity toward endotoxin-induced septic shock when compared to control

142 /-)) mice showed increased susceptibility to endotoxin-induced septic shock, leading to more severe p

143 n damage in models of sickle-cell disease or endotoxin-induced septic shock.

144 le for the HPA pathway in host resistance to endotoxin-induced septic shock.

145 rial infection and were largely resistant to endotoxin-induced septic shock.

146 ock caused by cecal ligation and puncture or endotoxin-induced shock.

147 Importantly, by using a mouse model of endotoxin-induced systemic inflammation, we show that th

148 Thus, endotoxin-induced transmigration of PMNs was secondary t

149 nder inflammation conditions such as EAE and endotoxin-induced uveitis.

150 Inhaled endotoxin induces airway inflammation and is an establis

151 Lipopolysaccharide (LPS), a bacterial endotoxin, induces inflammation in macrophages via activ

152 ple donors was transiently activated with an endotoxin injection [lipopolysaccharide (LPS)].

153 In mice, endotoxin injection to induce AKI also induced early and

154 igh-fiber diet also increased survival after endotoxin injection.

155 to sepsis by cecal ligation and puncture or endotoxin injection.

156 volumes of interest placed over the area of endotoxin instillation and in an equivalent lung region

157 was performed again approximately 16 h after endotoxin instillation.

158 ver tissues in a rat model of major burn and endotoxin insults are ameliorated by resolvin D2.

159 a variety of inflammatory stimuli, including endotoxin, interleukin-1beta (IL-1beta), and IL-6.

160 Gut-derived bacterial endotoxin is an important cofactor in the pathogenesis o

161 periments, we demonstrate that resistance to endotoxin is macrophage dependent and transferable, and

162 e GLP-1 was currently found to be induced by endotoxin, leading to insulin secretion and glucose lowe

163 receptor]-by-environment interaction in the endotoxin-leukocyte relationship using regression models

164 The endotoxin-leukocyte relationship was evaluated by linear

165 Endotoxin level was classified as low (< 0.4 endotoxin a

166 ifferent HDM extracts, differing in at least endotoxin levels [Lotox (LT) and HiTox (HT)].

167 urs after trauma, was associated with higher endotoxin levels and predicted subsequent maximal endoto

168 6 times as low in the Amish, whereas median endotoxin levels in Amish house dust was 6.8 times as hi

169 Concomitantly, endotoxin levels in portal serum and inflammatory macrop

170 Nonsurviving patients had higher endotoxin levels than survivors on day 1 (endotoxemia, 0

171 l translocation, significantly reduced serum endotoxin levels, and fully reversed all markers of syst

172 Microbial culture growth, endotoxin levels, and quantity and binding affinity of p

173 y, we found that GAP43 can be induced by the endotoxin lipopolysaccharide (LPS) in rat brain astrocyt

174 Gram-negative bacterial endotoxin lipopolysaccharide (LPS) is implicated in acut

175 The endotoxin lipopolysaccharide (LPS) promotes sepsis, but

176 Studies using the endotoxin lipopolysaccharide (LPS), a potent inflammogen

177 t the liver from injuries upon the bacterial endotoxin lipopolysaccharide (LPS).

178 roglia display less inflammatory response to endotoxin lipopolysaccharide (LPS).

179 first show that intrainsular infusion of the endotoxin lipopolysaccharide induces a local inflammatio

180 rat brain astrocytes by the proinflammatory endotoxin lipopolysaccharide via both nuclear factor-kap

181 ibocytidilic acid [Poly(I:C)], the bacterial endotoxin lipopolysaccharide, the locally acting inflamm

182 d three MPO knockout mice were injected with endotoxin (lipopolysaccharide) or fed a methionine and c

183 xidase inhibitor diphenyleneiodonium in both endotoxin (lipopolysaccharide)- and 1-methyl-4-phenyl-1,

184 regulated after stimulation with a bacterial endotoxin (lipopolysaccharide).

185 sure, 30 cm H2O) while receiving intravenous endotoxin (lipopolysaccharide-positive [LPS+] group; n =

186 re we show that in the presence of bacterial endotoxin, lipopolysaccharide (LPS), alpha-synuclein gen

187 Bacterial endotoxin, lipopolysaccharide, is a prototypic microbe-d

188 and subsequently translocation of bacterial endotoxin-lipopolysaccharide into the blood.

189 The bacterial endotoxins lipopolysaccharides (LPS) are important immun

190 e identified that subclinical super-low-dose endotoxin LPS can potently inhibit the process of endoso

191 Subclinical super-low-dose endotoxin LPS is a risk factor for the establishment of

192 ChQ prevents mouse PTBs induced by bacterial endotoxin LPS or progesterone receptor antagonist mifepr

193 This study used inhaled endotoxin (LPS) challenge as a model of innate immune ac

194 maT supplementation reduces eosinophilic and endotoxin (LPS)-induced neutrophilic airway inflammation

195 Endotoxin may be an appropriate therapeutic target in pa

196 Endotoxin measurement was performed in the 12 hours foll

197 tis and markedly reduced lethality following endotoxin-mediated fulminant hepatitis in mice.

198 t, both of which were further exacerbated by endotoxin-mediated injury.

199 xpected protective effect of RV infection on endotoxin-mediated shock in suckling mice.IMPORTANCE Ant

200 us to test protection of suckling mice from endotoxin-mediated shock, an outcome that is dependent o

201 n vivo relevance was established in a murine endotoxin model, in which we found that SGK1 inhibition

202 sults provide insights into the mechanism of endotoxin modification and will aid a structure-guided r

203 The developed SPR sensor with the novel endotoxins nanoMIP showed the potential of the technolog

204 been shown to possess anti-inflammatory and endotoxin neutralizing activity by interacting with LPS

205 Endotoxin or lipopolysaccharide (LPS) is a major constit

206 Cumulative concentrations of endotoxin over time in phage-treated conditions were low

207 .070, 0.301x10(3)/muL) per 10-fold change in endotoxin; p=0.004) in the NHANES.

208 , the innate immunity receptor for bacterial endotoxins, plays a pivotal role in the induction of inf

209 Following intra-peritoneal injection of endotoxin, pre-pubertal mice showed greater survival tha

210 that macrophages are essential mediators of endotoxin preconditioning and required for renal tissue

211 Endotoxin preconditioning can thus be used as a discover

212 Here, we show that endotoxin preconditioning confers renal epithelial prote

213 In immune cells, endotoxin preconditioning downregulates the inflammatory

214 Compared with preadministration of vehicle, endotoxin preconditioning in the cecal ligation and punc

215 Furthermore, endotoxin preconditioning reduced serum levels of proinf

216 ercoagulable TEG profile and platelet count, endotoxin, Protein C and fibrinogen were independent pre

217 e [Toll-like Receptor 4 (TLR4), encoding the endotoxin receptor]-by-environment interaction in the en

218 Imaging phenotype of occupational endotoxin-related lung function decline.

219 Endotoxin-related predicted functions were significantly

220 ial cells within <10 minutes, the associated endotoxin release (ER) in severe infections caused by gr

221 rapeutically relevant phages, with their low endotoxin release profile and fast bactericidal effect,

222 orming unit count, the concentration of free endotoxin released, and the cell morphology under light

223 At the present time, endotoxin removal through cartridge hemoperfusion is one

224 attern molecules (PAMPs) including bacterial endotoxin, respiratory viruses, and microbial DNA.

225 bone marrow-derived macrophages (BMMs) with endotoxin resulted in increased DJ-1 mRNA and protein ex

226 Injected concomitantly with or before endotoxin, scFv/TM provided more potent protection again

227 ansgenic mice exhibited significantly higher endotoxin sensitivity, as measured by enhanced cytokine

228 Tet2-deficient mice were more susceptible to endotoxin shock and dextran-sulfate-sodium-induced colit

229 cy in mice promotes tolerance to LPS-induced endotoxin shock and to polymicrobial septic shock after

230 uman monocytes and mast cells (MCs), a mouse endotoxin shock model (ESM), and mouse bone marrow (BM)-

231 Finally, studies of an experimental model of endotoxin shock show that iNOS deficiency results in mor

232 is likely to contribute to the pathology of endotoxin shock, signalling pathways regulating this mec

233 IL-15 SA treatment amplified endotoxin shock, which was prevented by NK cell or IFN-g

234 respectively, FAMIN determined resilience to endotoxin shock.

235 tial targets for therapeutic intervention in endotoxin shock.

236 es experimental colitis in mice and prevents endotoxin shock.

237 eficient neutrophil migration and associated endotoxin shock.

238 Females exposed to endotoxin showed greater increases in depressed mood and

239 ingle nucleotide polymorphisms (SNPs) in the endotoxin signaling pathway that may influence in vitro

240 This technique also allowed the endotoxin template to be reused successfully.

241 Humans and chimpanzees are more sensitive to endotoxin than are mice or monkeys, but any underlying d

242 LPS is an endotoxin that elicits a strong immune response from hum

243 oys, these nanoparticles bind and neutralize endotoxins that would otherwise trigger immune activatio

244 n, the situation for safe and effective anti-endotoxin therapy is problematical.

245 Serum endotoxin, TLR-4 levels, and inflammatory markers were h

246 y with lipopolysaccharide (LPS), a bacterial endotoxin, to induce an inflammatory episode.

247 led that immune cells and lipopolysaccharide endotoxin together stimulate epithelial cells to produce

248 Immune cells develop endotoxin tolerance (ET) after prolonged stimulation.

249 lays an important role in the development of endotoxin tolerance and targeted manipulation of this pr

250 role of the E3 ubiquitin ligase Pellino-1 in endotoxin tolerance and TLR signaling.

251 both miRNAs is coordinately regulated during endotoxin tolerance by a complex mechanism that involves

252 in shaping DCs phenotype and function under endotoxin tolerance conditions.

253 ent data further extend our understanding of endotoxin tolerance implications in AIS.

254 cesses in health and disease but its role in endotoxin tolerance in human DCs is still controversial.

255 es can be induced by UT12, 1Z105, and during endotoxin tolerance in the absence of CD14.

256 ibution of GILZ expression in macrophages to endotoxin tolerance in vivo, we treated GILZ KO mice wit

257 Regulation of endotoxin tolerance occurs at multiple levels of cell re

258 Endotoxin tolerance occurs to protect the organism from

259 se results reveal a novel mechanism by which endotoxin tolerance re-programs TLR4 signaling via suppr

260 Endotoxin tolerance reprograms Toll-like receptor (TLR)

261 Endotoxin tolerance requires tight regulation of genes o

262 portant microRNAs involved in development of endotoxin tolerance via (toll-like receptors) TLRs/ NF-k

263 of refractoriness to further LPS challenge (endotoxin tolerance).

264 ablation of Akt1, which is known to abrogate endotoxin tolerance, abolished induction of loci colocal

265 However, at the stage of endotoxin tolerance, both miR gene loci were occupied by

266 ding kinase (TBK) 1 as critical hallmarks of endotoxin tolerance, but mechanisms remain unclear.

267 tion, they exhibited the primary features of endotoxin tolerance, including low cytokine production,

268 A suppressed response, known as endotoxin tolerance, is associated with worse outcomes,

269 cluding HIF1alpha and mTOR, and mediators of endotoxin tolerance, T-cell activation, and viral defenc

270 ppressed phenotype that included features of endotoxin tolerance, T-cell exhaustion, and downregulati

271 During endotoxin tolerance, transcription of TNF mRNA is repres

272 icited proinflammatory cytokines, reflecting endotoxin tolerance, whereas CpG-ODN-primed mice showed

273 R-155 and miR-146a gene loci at the stage of endotoxin tolerance, whereas RNA-DNA-fluorescence in sit

274 ance, is associated with worse outcomes, yet endotoxin tolerance-inducing TLR4 ligands are known to p

275 nized as an immunosuppressive state known as endotoxin tolerance.

276 l proliferation and activation and exhibited endotoxin tolerance.

277 yk to control the production of TGF-beta1 in endotoxin tolerance.

278 g that this mechanism occurs specifically in endotoxin tolerance.

279 rophages with low-dose LPS, an effect termed endotoxin tolerance.

280 profile, contributing to the development of endotoxin tolerance.

281 regulation of the inflammatory response and endotoxin tolerance.

282 lunted response to bacterial LPS, resembling endotoxin tolerance.

283 TLR-mediated responses and is a hallmark of endotoxin tolerance.

284 ients with AIS exhibit a refractory state or endotoxin tolerance.

285 LPS and inhibits innate immune signaling and endotoxin tolerance; furthermore, unlike LPS from E. col

286 ll surface) was specifically up-regulated in endotoxin tolerant cells and the induction of Siglec-1 s

287 -dependent mega-dalton repressome in primary endotoxin-tolerant macrophages.

288 nocytes, THP-1, and MonoMac-6 cells, whereas endotoxin tolerization abrogated LPS inducibility of Pel

289 s on the basis of our previous findings that endotoxin toxicity to nonpreconditioned renal tubules wa

290 tudy of endotoxin-exposed cotton workers and endotoxin-unexposed silk workers that was initiated in 1

291 rial immune responses to lipopolysaccharide (endotoxin) using ELISpot assays, and used flow cytometry

292 mass, copper, zinc, phosphorus, silicon, and endotoxin, using land-use regression models.

293 ings demonstrate that flies detect bacterial endotoxins via a gustatory pathway through TRPA1 activat

294 Results showed that endotoxin (vs placebo) led to increases in proinflammato

295 Endobronchial endotoxin was followed by progressive alveolar neutrocyt

296 Endotoxin was the PM10-2.5 component most strongly assoc

297 rganism, a bacterial lipid virulence factor (endotoxin) was imaged and identified along with host pho

298 and can reprogramme the cellular response to endotoxin, where exosome-delivered miR-155 enhances whil

299 v/TM provided protection when injected after endotoxin, whereas sTM did not, and augmented APC produc

300 r scratches, has a lipopolysaccharide (LPS) (endotoxin) with low-inflammatory lipid A.