ライフサイエンスコーパス: macrophage cell

1 the oxidative burst of a zymosan-stimulated macrophage cell.

2 illumination microscopy (SIM) in J774 mouse macrophage cells.

3 ity index (SI) of 6.7 and no cytotoxicity to macrophage cells.

4 NA, protein, and promoter activity in murine macrophage cells.

5 evented LPS-mediated activation of Raw 264.7 macrophage cells.

6 owed for non-targeted, fluid-phase uptake by macrophage cells.

7 ent transcription from HIV-1 LTR in monocyte/macrophage cells.

8 mug/ml LPS exhibited no cytotoxic effects on macrophage cells.

9 mine the metabolic response of a 2D layer of macrophage cells.

10 e (LPS)-induced proinflammatory responses in macrophage cells.

11 ti-inflammatory activity on RAW 264.7 murine macrophage cells.

12 so demonstrated in the presence of RAW 264.7 macrophage cells.

13 osphate from small molecules present in host macrophage cells.

14 deacetylase-2 (HDAC2) in lung epithelial and macrophage cells.

15 shown to facilitate cAMP responses in murine macrophage cells.

16 to enucleate in vitro unless cocultured with macrophage cells.

17 pared with release in noncancerous RAW 264.7 macrophage cells.

18 correlating with TNFalpha secretion in mouse macrophage cells.

19 assessed in LPS-stimulated RAW 264.7 murine macrophage cells.

20 f ER- associated miRNPs observed in infected macrophage cells.

21 g intracellular MRSA present inside infected macrophage cells.

22 ) in lipopolysaccharide-stimulated RAW 264.7 macrophage cells.

23 uces the cytotoxicity of the chelator in the macrophage cells.

24 suppresses production of bactericidal NO in macrophage cells.

25 fect the viral replication in swine alveolar macrophage cells.

26 potted fever, able to activate dendritic and macrophage cells.

27 etion of mature IL-1beta (m-IL-1beta) in non-macrophage cells.

28 adhesive interactions between erythroid and macrophage cells.

29 gulation of necroptosis by cathepsins within macrophage cells.

30 Thus in these macrophage cells, all four major classes of G proteins c

31 Understanding the interaction between macrophage cells and Bacillus anthracis spores is of sig

32 binds the GM-CSF receptor on human monocyte/macrophage cells and bone marrow progenitors inducing di

33 the detection of nitric oxide released from macrophage cells and endothelial cells, demonstrating th

34 les (Ag-MBA@SiO(2)) were taken up by J774A.1 macrophage cells and measured a decrease in local pH dur

35 ging of HOCl fluctuations produced in living macrophage cells and peritonitis of living mice with hig

36 In this study, we show that in both RAW264.7 macrophage cells and primary bone marrow-derived macroph

37 diatom-biosilica is non-cytotoxic to J774.2 macrophage cells, and supports cell proliferation and gr

38 translocate the effector protein VgrG-1 into macrophage cells, and T6SS activation leads to fecal dia

39 expression level of IL-1beta in LPS induced macrophage cells, and to cause significant reduction of

40 ing LPS-induced proinflammatory responses in macrophage cells as well as in its interaction with LPS.

41 ble to inflict cellular damage in Caco-2 and macrophage cells, as assayed by LDH release, and escape

42 ld lower cytotoxicity toward RAW 264.7 mouse macrophage cells, as compared to the commercial transfec

43 -4 (IL-4) and IL-13 mediate their effects on macrophage cell biology, their biosynthesis, and respons

44 mulates C3 gene expression in human monocyte-macrophage cells but not in human hepatoma (HepG2) cells

45 ion of LPS-induced inflammatory responses in macrophage cells by melittin.

46 tigotes when transformed into amastigotes in macrophage cells cannot be cured by treatment of macroph

47 atory responses in RAW 264.7 murine monocyte/macrophage cells challenged with the TLR4 agonist LPS an

48 tected in the supernatants in VTRS1-infected macrophage cell culture.

49 F replicates as efficiently in primary swine macrophage cell cultures as the parental virus.

50 relation to atherosclerosis, using as model macrophage cell cultures enriched with LDL particles.

51 ory cytokine and chemokine programs in mouse macrophage cell cultures, along with depression of innat

52 49% of the mutant bank) that failed to cause macrophage cell death (release of 10% or less of the lac

53 as been well studied, processes that control macrophage cell death and HMGB1 release in animals are p

54 is essential for host defense, and leads to macrophage cell death and proinflammatory cytokine produ

55 were defective in Yop-mediated inhibition of macrophage cell death and ROS production in neutrophil-l

56 crosis as the dominant mechanism of alveolar macrophage cell death in pneumococcal pneumonia.

57 Mycobacterium tuberculosis modulation of macrophage cell death is a well-documented phenomenon, b

58 Macrophage cell death plays a role in many physiological

59 utant infection induces necrotic and oncotic macrophage cell death that requires bacterial protein sy

60 triggers in induction of Cer production and macrophage cell death through elevated expression of A-F

61 etwork analysis predicted that VTRS1-induced macrophage cell death was mediated by a proinflammatory

62 VTRS1-induced macrophage cell death was significantly inhibited by a c

63 TNF-alpha and IkappaB-alpha in VTRS1-induced macrophage cell death were further confirmed by individu

64 the role of A-FABP in promoting sFA-induced macrophage cell death with primary bone marrow-derived m

65 ent of the effects of IFN-beta on ST-induced macrophage cell death, but significantly dependent on IL

66 red for non-canonical inflammasome-triggered macrophage cell death, indicating that caspase-11 orches

67 r investigate the mechanism of VTRS1-induced macrophage cell death, microarrays were used to analyze

68 -8 and the RIP kinases are key regulators of macrophage cell death, NF-kappaB and inflammasome activa

69 ppressing IFN-gamma-mediated monocyte and/or macrophage cell death.

70 ted heme-induced oxidative burst and blocked macrophage cell death.

71 n VTRS1 (a vaccine candidate) induced strong macrophage cell death.

72 lammatory, caspase-2- and NF-kappaB-mediated macrophage cell death.

73 gy, which contributes to caspase-independent macrophage cell death.

74 olic event that controls caspase-independent macrophage cell death.

75 ted FAs (sFAs), are able to directly trigger macrophage cell death.

76 RC4 causes constitutive IL1FC production and macrophage cell death.

77 stimulation, NR4A receptor-depleted monocyte/macrophage cells display significantly altered expressio

78 aging, we found reduced numbers of alveolar macrophages, cells essential for lung homeostasis.

79 -4 signaling pathways that are important for macrophage cell fate choice.

80 of microenvironmental signals that determine macrophage cell fate decisions to establish appropriate

81 myelination, tumor suppression, and monocyte/macrophage cell fate determination.

82 test were conducted on J774A.1 cells murine macrophage cells for different glass concentrations.

83 phase binding assay, and it protected murine macrophage cells from intoxication with LT.

84 However, bone marrow macrophage cells from MAGP1Delta mice show a higher prop

85 how that TGF-beta-resistant RAW 264.7 murine macrophage cells have increased cytotoxic activity that

86 ts showed that in B10.S, SJL/J, and RAW264.7 macrophage cells, IL-6 expression was dependent on extra

87 of THP stimulated the proliferation of human macrophage cells in culture and partially restored the n

88 2 and IL-6) clustering with CD68(+) monocyte/macrophage cells in livers of subjects with dAIH, and is

89 was correlated with an increase in alveolar macrophage cells in the lungs and airways, early inducti

90 atory cytokines in RAW 264.7 and rat primary macrophage cells in the presence of LPS, MM-2 and Mel-SC

91 shapes, and (4) are efficiently taken up by macrophage cells in vitro.

92 lpha in mouse bone marrow cells and monocyte/macrophage cells, in the absence of receptor activator o

93 ell metabolomic profiling using rat alveolar macrophage cells incubated with different concentrations

94 that the inflammasome was not activated upon macrophage cell infection with murine gammaherpesvirus 6

95 fiber central nucleation and increased focal macrophage cell infiltration, indicating exacerbated dys

96 Phagocytosis is the central process by which macrophage cells internalize and eliminate infectious mi

97 eoclasts derived from MAGP1Delta bone marrow macrophage cells is increased relative to the wild type,

98 from a dendritic cell line (JAWS II), from a macrophage cell line (C2.3), and from murine primary bon

99 thout affecting potassium efflux, in a mouse macrophage cell line (J774), mouse bone marrow-derived d

100 A mouse macrophage cell line (RAW 264.7) was stimulated with var

101 the sequenced strain, PAO1, toward a murine macrophage cell line (RAW 264.7).

102 f cell migration response, particularly in a macrophage cell line (RAW/LR5) and only modestly in the

103 d monocyte chemotactic protein-1 in a murine macrophage cell line and human primary macrophages.

104 by DNA affinity isolation from the RAW264.7 macrophage cell line and identified by mass spectrometry

105 tify genes overexpressed in the HD11 chicken macrophage cell line and in primary chicken oviduct epit

106 mediators induced autophagy in the RAW246.7 macrophage cell line and in primary monocytes.

107 ession of GAP domain mutant Abr and Bcr in a macrophage cell line and of constitutively active Rac in

108 propose that exposure of macrophages (both a macrophage cell line and primary human alveolar macropha

109 nt debris both in vitro (using a human THP-1 macrophage cell line and primary human monocytes/macroph

110 induced IL-27 mRNA and protein levels in the macrophage cell line and primary lung monocytes/macropha

111 nducing secretion of TNF-alpha by a monocyte/macrophage cell line and primary macrophages.

112 llular bacterial killing by a mouse alveolar macrophage cell line and primary mouse neutrophils.

113 norovirus (MNV) replicates in the RAW 264.7 macrophage cell line and thus provides a tractable model

114 ein activates cytokine production in a human macrophage cell line as well.

115 Chlamydia muridarum in the RAW 264.7 murine macrophage cell line at different MOIs.

116 ty similar to their mammalian orthologs in a macrophage cell line bioassay.

117 hepatic macrophages (HMacs) and in a murine macrophage cell line by coupling transcriptional upregul

118 wild-type cells by iron chelation, and in a macrophage cell line by overexpression of FPN.

119 e responses to lipopolysaccharide in a human macrophage cell line cultured in 86 mM ethanol, 1 mM ace

120 ed with this aberrant translation in MEFs, a macrophage cell line depleted of CPEB and treated with l

121 We also show that the J774.2 macrophage cell line exhibits unusual intracellular upta

122 A macrophage cell line expressing Dectin-1 was employed to

123 The fragments were cultured with RAW 264.7 macrophage cell line for 9 weeks.

124 modulate the immune response in the chicken macrophage cell line HD11 and in chicken primary monocyt

125 tively high in the thymus and in the chicken macrophage cell line HD11.

126 computed tomography imaging in the RAW 264.7 macrophage cell line identified the formulation that pro

127 We found that supernatants of a human macrophage cell line infected with either of the bacteri

128 Overexpression of SLAT in a macrophage cell line inhibits the IgG Fcgamma receptor-m

129 Hca2 expression in the RAW264.7 murine macrophage cell line is strongly induced by LPS treatmen

130 ROS production was measured in the murine macrophage cell line J774 and in primary phagocytes usin

131 otic stress and killing by the mouse-derived macrophage cell line J774.

132 r knockdown of Aim2 expression in the murine macrophage cell line J774.A1, IFN-beta treatment of cell

133 reduced cytokine production in the alveolar macrophage cell line MH-S.

134 Moreover, macrophage cell line models RAW264.7 and THP-1, as well

135 Knockdown of Nab1 in a macrophage cell line prevented downregulation of IFNGR1

136 from M-JAK2(-/-) mice and Jak2 knockdown in macrophage cell line RAW 264.7 also showed lower levels

137 We also observed MET formation by the mouse macrophage cell line RAW 264.7 and by human THP-1 cell-d

138 We used macrophage cell line RAW 264.7 and human embryonic kidne

139 induced tolerant cells; knockdown of Neu1 in macrophage cell line RAW 264.7 cells resulted in enhance

140 In vitro, stable knockdown of HuR in mouse macrophage cell line RAW 264.7 corroborated in vivo data

141 uce PGE(2) but no PGD(2), whereas the murine macrophage cell line RAW 264.7 produced PGD(2) and only

142 The mouse macrophage cell line Raw 264.7, mouse primary lung monoc

143 se colon carcinoma cell line MC38, the mouse macrophage cell line RAW 264.7, or mouse and human organ

144 te-derived macrophages (MDMs) and the murine macrophage cell line RAW 264.7.

145 s effect on pro-inflammatory activity in the macrophage cell line RAW 264.7.

146 IH 3T12 fibroblasts as well as in the murine macrophage cell line RAW 264.7.

147 y, p66Shc was knocked down with siRNA in the macrophage cell line RAW264, and a 30% defect in superox

148 Similar results were obtained in the mouse macrophage cell line RAW264.7 after LPS treatment.

149 t on the inflammatory response of the murine macrophage cell line RAW264.7 and human monocyte THP-1 t

150 rmined that exosome production by the murine macrophage cell line RAW264.7 requires the endosomal sor

151 lates the expression of the tlr1 gene in the macrophage cell line RAW264.7, as well as in primary CD1

152 alveolar and peritoneal macrophages and the macrophage cell line RAW264.7, but not in primary bone m

153 hibition of dysferlin expression in the J774 macrophage cell line resulted in significantly enhanced

154 Overexpression of gga-miR-429 in the HD11 macrophage cell line significantly inhibited TMEFF2 and

155 Similar results were obtained in a murine macrophage cell line stimulated with the TLR7 agonist co

156 less toxic (IC50 = 0.7-6 microg/mL) to mouse macrophage cell line than to parasite cell lines.

157 fering RNA to develop a stable NIK knockdown macrophage cell line that had an approximately 50% decre

158 (B6.Nba2-ABC) splenic cells and in a murine macrophage cell line that overexpressed p202 protein was

159 Stimulation of the human macrophage cell line THP-1 and epithelial cells with a T

160 This effect was also observed in the macrophage cell line THP-1.

161 ival in primary murine macrophages and human macrophage cell line THP-1.

162 Use of a macrophage cell line to evaluate cytotoxic and ROS produ

163 derived from CD44-deficient mice, in an MH-S macrophage cell line treated with antibodies to CD44, or

164 Conversely, the AM macrophage cell line was more responsive to P. gingivali

165 Specifically, using the RAW 264.7 mouse macrophage cell line we show that whole OSPW containing

166 r alpha (TNFalpha) expression in RAW (murine macrophage cell line) and Kupffer cells at the transcrip

167 34Delta cells after phagocytosis by a murine macrophage cell line, and Atg8 expression was exhibited

168 J2-C8 cell line (AM cells), a mouse alveolar macrophage cell line, and ESK-1 cells, a mouse gingival

169 restingly, sCD16 inhibited MDALDL binding to macrophage cell line, as well as soluble forms of recomb

170 genesis of RAW264.7 cells, a murine monocyte/macrophage cell line, by suppressing the induction of NF

171 of SCN8A from THP-1 cells, a human monocyte-macrophage cell line, confirmed the expression of a full

172 of IL-12p40 was investigated using a murine macrophage cell line, CRL2019, in an in vitro MW model.

173 Ocm), a Ca(2+)-binding protein secreted by a macrophage cell line, is a potent axon-promoting factor

174 cells in the presence of an irradiated mouse macrophage cell line, J774A.1.

175 Similarly, treatment of human PBMCs or mouse macrophage cell line, RAW 264.4, with TGF-beta, induced

176 he effect of TGF-beta resistance on a murine macrophage cell line, RAW 264.7, by overexpressing a dom

177 and blocks the binding of LPS to the murine macrophage cell line, RAW 264.7, via an interaction with

178 In mouse macrophage cell line, RAW264.7, while both BLP and LPS s

179 In a macrophage cell line, regulation of IL-10 by BAR501 was

180 In vitro in a human macrophage cell line, SLM (10(-8) mol/L) enhanced FP (10

181 sts, although 2 of those were expressed in a macrophage cell line, suggesting that potential gene pro

182 Using a mouse macrophage cell line, this report studied the impact of

183 e inhibits the ability of RAW cells, a mouse macrophage cell line, to differentiate into osteoclasts

184 Using a murine macrophage cell line, we showed that the F. nucleatum-in

185 aB production upon light exposure in a model macrophage cell line.

186 efflux, such as Abca1, Abcg1, and Apoe, in a macrophage cell line.

187 ability to grow in mouse serum and a J774.16 macrophage cell line.

188 A ablation of C/EBPbeta in a murine alveolar macrophage cell line.

189 lood, spleen, and bone marrow and from a rat macrophage cell line.

190 th IL-36alpha activated NF-kappaB in a mouse macrophage cell line.

191 m and efficiency of nanoparticle uptake by a macrophage cell line.

192 e 50 promoter represses activity in a murine macrophage cell line.

193 ow-density lipoprotein (oxLDL) by a monocyte/macrophage cell line.

194 or poly(I:C), a TLR3 agonist in the RAW264.7 macrophage cell line.

195 nfected PBMC and in the latently infected U1 macrophage cell line.

196 of phage-mediated gene transfer in a murine macrophage cell line.

197 ccumulation of intracellular cyclic AMP in a macrophage cell line.

198 phagocytosed Escherichia coli in a cultured macrophage cell line.

199 ts the LPS effect using a PMJ2-PC peritoneal macrophage cell line.

200 optimize uptake conditions in the RAW 264.7 macrophage cell line.

201 nd c-Maf expression in microglia and the RAW macrophage cell line.

202 targeting of FXIII-A in the THP-1 (monocyte/macrophage) cell line and in human monocyte-derived macr

203 cessfully detected at therapeutic dosages in macrophages (cell line: NR8383).

204 Furthermore, macrophages cell line RAW 264.7 cells were treated with

205 Overexpression of NNT in a macrophage cell-line resulted in decreased levels of rea

206 o be upregulated in M. leprae-infected human macrophage cell lineages, primary monocytes, and skin le

207 The ability of 2 macrophage cell lines (HL-60; RAW 264.7) to kill archety

208 ages (C57BL/6, BALB/c, and p47(phox-/-)) and macrophage cell lines (RAW 264.7 and IC21) to investigat

209 Two murine macrophage cell lines (RAW 264.7 and J774A.1) and mouse

210 Two transformed murine macrophage cell lines (RAW 264.7 ATCC TIB-71 and CRL-227

211 ndirectly promoted the uptake of bacteria by macrophage cell lines and directly killed bacteria at ac

212 In vitro studies were performed in macrophage cell lines and in isolated mouse macrophages

213 ependent manner in human and murine monocyte/macrophage cell lines and in primary macrophages.

214 ver, the mutant shows impaired growth within macrophage cell lines and is severely attenuated in zebr

215 er into both folate receptor beta-expressing macrophage cell lines and primary mouse macrophages.

216 ssion of ArgII is induced by LXR agonists in macrophage cell lines and primary murine macrophages in

217 e in survival/growth within human and murine macrophage cell lines and was 100% defective in virulenc

218 for survival/growth within human and murine macrophage cell lines and was unable to escape from phag

219 Inhibition or deficiency of A-FABP in macrophage cell lines decreased sFA-induced Cer producti

220 ated in a time- and dose-dependent manner in macrophage cell lines derived from AFABP/aP2-EFABP/mal1

221 Interestingly, not all mouse macrophage cell lines permit GP-F88A entry.

222 Studies with RAW264.7 and J774 macrophage cell lines reveal that Dragon negatively regu

223 Invasion assays using epithelial and macrophage cell lines revealed differences in the abilit

224 e we show, with global proteomic analysis of macrophage cell lines treated with either IFNgamma or IL

225 fect different primary cells and established macrophage cell lines with deletions in the Toll-like re

226 ilitate such virulence screens, we developed macrophage cell lines with which the number of intact ho

227 thogen to inhibit the phagocytic activity of macrophage cell lines, an event that can be correlated w

228 GILZ was inducible by curcumin in macrophage cell lines, primary human monocyte-derived ma

229 Immortalized bone marrow-derived macrophage cell lines, termed T4Cr and T4ko, were establ

230 ing to stably knock out and recover Rab8a in macrophage cell lines, we match Akt signaling profiles w

231 human mammary epithelial cells and monocyte/macrophage cell lines, we show that the chromatin bounda

232 on of the HSV-1 DNA genome in differentiated macrophage cell lines.

233 production of cytotoxic ceramides (Cers) in macrophage cell lines.

234 uman epithelial, mouse fibroblast, and mouse macrophage cell lines.

235 ibodies to oxLDL (oxLDL-IC) in monocytic and macrophage cell lines.

236 ndent intracellular growth of B. neotomae in macrophage cell lines.

237 n vitro by stimulating airway epithelial and macrophage cell lines.

238 ty for respiratory epithelial, synovial, and macrophage cell lines.

239 we used primary hepatocytes and hepatoma and macrophage cell lines.

240 2(-/-) and TLR4(-/-) than in wild type mouse macrophage cell lines.

241 shed in murine MS1 endothelial and RAW 264.7 macrophage cell lines.

242 T12 (mouse fibroblast), and RAW 264.7 (mouse macrophage) cell lines.

243 ngs, CCR7 gene expression in human and mouse macrophages cell lines is induced when LXRalpha at S198

244 An in vitro assay on macrophage cell lysates showed complete inhibition of SP

245 rong inhibition of SPSB2-iNOS interaction in macrophage cell lysates.

246 om the WT bacterium regarding the binding to macrophage cell membrane, analysis of macrophage protein

247 ased (P < 0.05) CD3(+), CD4(+) T helper, and macrophage cell numbers per colon as compared with wt mi

248 esulted in significant reduction in monocyte/macrophage cell numbers within PBMCs in a dose-dependent

249 g vertebrates, was downregulated in RAW264.7 macrophage cells of the M2 phenotype in conditoned mediu

250 Using RAW 264.7 macrophage cells or 3T3-L1 adipocytes, C/EBPbeta knockdo

251 NADPH fluctuations during the activation of macrophage cells or wound response in vivo.

252 21R system should consider that monocyte and macrophage cell physiology may be affected by this syste

253 ed increased levels of DPP4 expression in DC/macrophage cell populations from visceral adipose tissue

254 It selectively visualized monocyte and macrophage cell populations in vitro, by live-cell imagi

255 00-500 nm was demonstrated by stimulation of macrophage cell proliferation.

256 sed on interference with FcgammaR-stimulated macrophage cell proliferation.

257 popolysaccharide (LPS) stimulation of murine macrophage cells (RAW 264.7).

258 Peripheral macrophage cells responded to rod cell loss, as evidence

259 siRNA or functional TR4 cDNA in the RAW264.7 macrophage cells resulted in either decreased or increas

260 ng functional CD36 cDNA in the TR4 knockdown macrophage cells reversed the decreased foam cell format

261 pressures in either epithelial, neuronal, or macrophage cells reverted to WT sequence.

262 Using a micropatterning approach to control macrophage cell shape directly, we demonstrate here that

263 We also show that Mtb infection of macrophage cells significantly increases the expression,

264 eritoneal macrophages, we confirm a role for macrophage cell surface beta3 integrin in this dl922-947

265 Neutralization of RA synovial fluid macrophage cell surface gp96 inhibited the constitutive

266 erized by expression of both DC and monocyte/macrophage cell surface markers.

267 inding of adiponectin to calreticulin on the macrophage cell surface.

268 We demonstrate the utility of these macrophage cell systems for siRNA screening of pathogen

269 epresent one of the frequently used monocyte/macrophage cell systems to study immune responses.

270 s approach by imaging human monocyte-derived macrophage cells that have been exposed to fibrils from

271 we hypothesize that the removal of the liver macrophages, cells that have been reported to take up th

272 based on the study of blood monocyte-derived macrophages, cells that have never been exposed to the w

273 Macrophage cell therapy improves clinically relevant par

274 Nfatc1, and Ctsk, and it reprograms monocyte/macrophage cells to OC-like cells.

275 asma virulence, we employed these transgenic macrophage cells to screen a collection of individual tr

276 F-SIMS imaging has been used here to compare macrophage cells treated to contain elevated levels of c

277 gas phase and fluorescence imaging of NO2 in macrophage cells treated with a nitrogen dioxide donor.

278 crease in the optical force was also seen in macrophage cells treated with cytochalasin D, both with

279 ivation of the NDRG1 gene in murine RAW264.7 macrophage cells treated with hypoxia or deferoxamine, a

280 xpressed JunB is cleaved in murine RAW 264.7 macrophage cells treated with the NALP1b inflammasome ac

281 the stress pathways activated, depending on macrophage cell type, consistent with the nonspecific na

282 onfirmed in vivo in mice with hepatocyte and macrophage cell-type-specific conditional Ron deletions.

283 us NO cytotoxicity in two well characterized macrophage cell types (J774 and RAW 264.7).

284 that overexpress AOAH in dendritic cells and macrophages, cell types that normally produce it.

285 s, the aggregates are stable and nontoxic to macrophage cells up to 55 x 10(-3) m Au.

286 in the optical force experienced by RAW264.7 macrophage cells upon the uptake of both microparticles

287 ied particles remained resistant to cultured macrophage cell uptake, although they were still quickly

288 The infiltration of polymorphonuclear and macrophage cells was associated with increased ocular me

289 lipopolysaccharide (LPS)-stimulated J774A.1 macrophage cells was investigated.

290 e viability and ATP levels in epithelial and macrophage cells, we discovered for fumed silica an impo

291 of the first indicators of oxidative burst, macrophage cells were exposed within the microfluidic de

292 Dendritic and macrophage cells were found to be important for this cro

293 ession analysis of bacteria infecting murine macrophage cells were performed under four distinct cond

294 RAW264.7 mouse macrophage cells were pretreated with phenylmethimazole

295 Finally, macrophage cells were treated with two selected nanopart

296 e latter case by taking PSFC measurements of macrophage cells when inoculated with enhanced green flu

297 sc1), is required for fungal survival inside macrophage cells, which is consistent with the role of F

298 Further, transfection of RAW264.7 macrophage cells with the miR-19a-3p mimic decreased the

299 of HO-1 upon CXCL-10, we cultured RW 264.7 (macrophage) cells with exogenous rIFN-beta to stimulate

300 Microglia, the resident macrophage cells within the central nervous system (CNS)