ライフサイエンスコーパス: peritoneal macrophage

1 gulate MEK-1/2 and ERK-1/2 in BALB/c-derived peritoneal macrophages.

2 urvived significantly less in BALB/c-derived peritoneal macrophages.

3 osis factor-alpha from RAW 264.7 and primary peritoneal macrophages.

4 , Gata6 is expressed selectively in resident peritoneal macrophages.

5 stantial alterations in the transcriptome of peritoneal macrophages.

6 d a significant reduction in survival within peritoneal macrophages.

7 KO was required for stimulation of elicited peritoneal macrophages.

8 rophage-dense atherosclerotic lesions and in peritoneal macrophages.

9 ve microenvironment via paracrine effects on peritoneal macrophages.

10 iation, metabolism, and survival of resident peritoneal macrophages.

11 by spleen and an 85% reduction in uptake by peritoneal macrophages.

12 8.5 mug . mL(-1)) cultured in vitro in mouse peritoneal macrophages.

13 ated murine RAW264.7 macrophages, as well as peritoneal macrophages.

14 mmatory mediators in thioglycollate-elicited peritoneal macrophages.

15 ouse sera and livers, as well as in cultured peritoneal macrophages.

16 ce of palmitate on LPS-mediated responses in peritoneal macrophages.

17 asts (MEFs) and primary C/EBP-beta-deficient peritoneal macrophages.

18 lity of 0.776 in bovine MDM and 0.8 in mouse peritoneal macrophages.

19 d IL-1beta was confirmed to be attenuated in peritoneal macrophages.

20 take and trafficking in wild-derived MOLF/Ei peritoneal macrophages.

21 F4/80(+) circulating leukocytes and elicited peritoneal macrophages.

22 epithelial cells co-cultured with AEBP1(TG) peritoneal macrophages.

23 (iNOS) and S-nitrosylated in proinflammatory peritoneal macrophages.

24 lating Ly6C(high) inflammatory monocytes and peritoneal macrophages.

25 ed IL-27(p28) gene expression and release in peritoneal macrophages.

26 the inflamed peritoneum and develop into new peritoneal macrophages.

27 eukin (IL)-12 secretion response to TgPRF in peritoneal macrophages.

28 ydrolytic activity was replicated in primary peritoneal macrophages.

29 s specificity and are inactive toward murine peritoneal macrophages.

30 sis factor alpha (TNF-alpha) production from peritoneal macrophages.

31 ts were obtained for bone marrow-derived and peritoneal macrophages.

32 mediates phagocytosis of apoptotic cells by peritoneal macrophages.

33 different sizes on murine bronchoalveolar or peritoneal macrophages.

34 ns in established cells and in primary mouse peritoneal macrophages.

35 t pro-inflammatory cytokine interleukin-6 in peritoneal macrophages.

36 cription in Newcastle disease virus-infected peritoneal macrophages.

37 east tumors to identify peptides that target peritoneal macrophages.

38 hages and in vivo by thioglycolate-recruited peritoneal macrophages.

39 (keyhole limpet hemocyanin), on cultures of peritoneal macrophages.

40 induce apoptotic cell phagocytosis by murine peritoneal macrophages.

41 ecreased the uptake of spirochetes by murine peritoneal macrophages.

42 transcripts in Mecp2-deficient microglia and peritoneal macrophages.

43 of TLR pathway-specific genes compared with peritoneal macrophages.

44 alpha, although at much lower levels than in peritoneal macrophages.

45 rrow, blood, lung, and spleen, as well as in peritoneal macrophages.

46 o death and led to a contraction of resident peritoneal macrophages.

47 It induced peritoneal macrophage activation in mice, ~70% of cells

48 ats' peritoneal cavity, and their effects on peritoneal macrophages activation and in systemic inflam

49 In Candida albicans-infected resident peritoneal macrophages, activation of group IVA cytosoli

50 y and have limited effects on neutrophil and peritoneal macrophage activity.

51 bited and greatly impaired in the absence of peritoneal macrophages after depletion with clodronate e

52 nous transcriptional response of single-cell peritoneal macrophages after exposure to apoptotic cells

53 changes in circulating Ly6C(+) monocytes and peritoneal macrophages, along with increased CD36 expres

54 In contrast to monocytes or peritoneal macrophages, alveolar macrophages did not dis

55 ins, but in vitro complement killing assays, peritoneal macrophage and whole blood stimulations, phag

56 Peritoneal macrophages and atherosclerotic lesions from

57 We show that TIM-4(-/-) peritoneal macrophages and B-1 cells do not efficiently

58 roduction as well as caspase-1 activation by peritoneal macrophages and bone marrow-derived dendritic

59 nhibition of CD36 attenuated phagocytosis in peritoneal macrophages and brain M-MPhi These findings d

60 in polymerization, resulting in spreading of peritoneal macrophages and diminished uptake of E. coli.

61 in-1 ligation, while thioglycollate-elicited peritoneal macrophages and Flt3L-derived DC do not.

62 XC receptor 3 (CXCR3) expression on elicited peritoneal macrophages and granulocytes increases follow

63 differentiation of human monocytes and mouse peritoneal macrophages and hematopoietic progenitor cell

64 5-HT impaired efferocytosis by murine peritoneal macrophages and human alveolar macrophages.

65 for FR-alpha selectivity over FR-beta in rat peritoneal macrophages and human peripheral blood monocy

66 expressing ospC mutant spirochetes by murine peritoneal macrophages and human THP-1 macrophage-like c

67 egrative, and enlarged nuclear morphology of peritoneal macrophages and hyperphosphatemia were found

68 METHODS AND We quantified efferocytosis in peritoneal macrophages and in atherosclerotic lesions of

69 ression of TNFalpha and interleukin-1beta in peritoneal macrophages and increases the systemic inflam

70 varian cancer cells stimulated chemotaxis of peritoneal macrophages and induced macrophages to acquir

71 ed a significant but comparable reduction of peritoneal macrophages and lymphocytes, accompanied by a

72 DCAR was predominantly expressed in small peritoneal macrophages and monocyte-derived inflammatory

73 complexes that were efficiently taken up by peritoneal macrophages and other phagocytic cells.

74 We collected naive peritoneal macrophages and plasma, at multiple times of

75 cluding previously underappreciated roles of peritoneal macrophages and platelets.

76 Peritoneal macrophages and polymorphonuclear leukocytes

77 o suppressed the expression of iNOS in mouse peritoneal macrophages and primary human astrocytes.

78 ase in C5aR1 expression was also observed in peritoneal macrophages and several tissues from LysM-Cre

79 diaphragm tissue and in primary cultures of peritoneal macrophages and skeletal muscle fibroblasts.

80 Using both primary peritoneal macrophages and studies in advanced atheromat

81 dent chemokine production by pristane-primed peritoneal macrophages and suggest that C1q, and not C3,

82 ificantly augmented arginase-1 expression in peritoneal macrophages and SVF cells in both wild-type a

83 ne macrophages, such as primary alveolar and peritoneal macrophages and the macrophage cell line RAW2

84 Peritoneal macrophages and the stromal vascular fraction

85 equired for the homeostatic proliferation of peritoneal macrophages and their expansion during type 2

86 aride, (ii) enhancing phagocytic activity of peritoneal macrophages, and (iii) clearing bacterial per

87 We found that EPS specifically bind peritoneal macrophages, and because mice lacking MyD88 s

88 including CD19(+) B cells, CD11b(+)F4/80(+) peritoneal macrophages, and CD11c(+) bone marrow-derived

89 Normal brain tissue, cultured resident peritoneal macrophages, and cultured skin fibroblasts fr

90 d macrophages and in vivo by resident murine peritoneal macrophages, and diverted the anti-inflammato

91 IL-1beta response in mouse dendritic cells, peritoneal macrophages, and human PBMCs.

92 elevates RIP140 but lowers miR-33 levels in peritoneal macrophages, and increases the production of

93 e marrow chimeric mice, adoptive transfer of peritoneal macrophages, and myeloid-specific P2X7(-/-) m

94 ed in RAW264 macrophage-like cells or murine peritoneal macrophages, and their influence on LPS-induc

95 st (IL-1Ra) secretion in LPS-activated mouse peritoneal macrophages, and this response was regulated

96 M1-polarized murine macrophages, as well as peritoneal macrophages, and was associated with increase

97 Peritoneal macrophages are one of the most studied macro

98 ecretion of IL-1beta, IL-6, and KC (IL-8) by peritoneal macrophages as compared with WT controls.

99 f C5a, and could be demonstrated in cultured peritoneal macrophages as well as in the setting of anti

100 mmatory macrophages (thioglycollate-elicited peritoneal macrophages) as compared with bone marrow-der

101 C counteracts the LPS effect using a PMJ2-PC peritoneal macrophage cell line.

102 y, we identified a subpopulation of resident peritoneal macrophages characterized by high expression

103 In the OP-9 adipocyte peritoneal macrophage co-culture system, macrophages fro

104 0 were all significantly increased in murine peritoneal macrophages co-cultured with PbANKA-infected

105 eal exudate cells and decreased in PTEN(-/-) peritoneal macrophages compared with wild-type (WT) cell

106 z2-Cre x Gata6(flox/flox) mice, the resident peritoneal macrophage compartment, but not macrophages i

107 ase activity except in liver and in resident peritoneal macrophages, confirming endothelial specifici

108 s or knockdown of the CD36 receptor in mouse peritoneal macrophages, confirming the specific binding

109 effect of T3 is coupled to the modulation of peritoneal macrophage content, in a context not fully ex

110 ide increased liver injury and the levels of peritoneal macrophage cytokines, including IL-1beta, in

111 We demonstrate that primary resident peritoneal macrophages deficient for Btk and Tec secrete

112 e marrow-derived and thioglycollate-elicited peritoneal macrophages deficient for Btk and Tec secrete

113 Peritoneal macrophages deficient in ABCA1, ABCG1, or bot

114 CD200R1(-/-) peritoneal macrophages demonstrated a 70-75% decrease in

115 Efficacy studies in peritoneal macrophages demonstrated a high rate of conco

116 ver, IL-13 stimulation of alpha(M)-deficient peritoneal macrophages demonstrated an upregulated level

117 IL-1beta release was inhibited in peritoneal macrophages derived from CD44-deficient mice,

118 PEGs) stimulate potent cytokine responses in peritoneal macrophages, despite not being internalized.

119 files between bone marrow-derived (BMDM) and peritoneal macrophages differed drastically.

120 In resident peritoneal macrophages, docosapentaenoic acid (DPA) was

121 vitro of C5a to lipopolysaccharide-activated peritoneal macrophages dose dependently antagonized the

122 examethasone to lipopolysaccharide-activated peritoneal macrophages dose-dependently suppressed the e

123 hrine directly restrains MCP-1 production by peritoneal macrophages during infection.

124 Furthermore, murine peritoneal macrophages expressed an M2 marker arginase-1

125 ects of PD-1, we found the following: first, peritoneal macrophages expressed significantly higher le

126 Peritoneal macrophages expressed the 5-HT transporter an

127 In peritoneal macrophages, expression of NLRP3 and activati

128 they appear to facilitate the activation of peritoneal macrophages (F4-80(+)GR-1(-)) and F4-80(+)Gr-

129 eeding suppressed atherosclerosis, decreased peritoneal macrophage foam cell formation, and downregul

130 In this study, we report that peritoneal macrophages from a wild-derived inbred mouse

131 espite similar clearance of apoptotic cells, peritoneal macrophages from Abca1(-/-)Abcg1(-/-), Abcg1(

132 Peritoneal macrophages from ACE-KO mice were deficient i

133 We also observed that peritoneal macrophages from AIF-deficient mice showed an

134 Peritoneal macrophages from Apoe(-/-) mice or from Apoe(

135 cing, we characterized the transcriptomes of peritoneal macrophages from BALB/c and IL4Ralpha(-/-) mi

136 ROS generation in RAW 264.7 macrophages and peritoneal macrophages from BALB/c mice.

137 In isolated peritoneal macrophages from C/EBPbeta(-/-) mice, the ant

138 In contrast, a much lower percentage of peritoneal macrophages from C3(-/-) mice phagocytosed GP

139 so inhibited LPS-induced Cox-2 expression in peritoneal macrophages from C57BL/6 and NOD mice.

140 all interfering RNA knockdown of Arg2 and in peritoneal macrophages from C57BL/6 Arg2(-/-) mice.

141 and HFE:TFR1 complex (nonfunctional TFR1) in peritoneal macrophages from C57BL/6 mice, resulting in i

142 Peritoneal macrophages from CD36(-/-) mice exhibited dim

143 Primary, bone marrow-derived, and peritoneal macrophages from Chop(+/+) and Chop(-/-) were

144 Peritoneal macrophages from dyslipidemic animals were pr

145 f G2A deficiency in macrophages, we isolated peritoneal macrophages from G2A(+/+)ApoE(-/-) and G2A(-/

146 c submucosa of Gal3-deficient mice.In vitro, peritoneal macrophages from Gal3-deficient mice were ine

147 with results from gain-of-function studies, peritoneal macrophages from GX sPLA(2)-deficient mice ex

148 pt expression in tumor-associated as well as peritoneal macrophages from hrg(-/-) mice revealed an in

149 Finally, LPS-stimulated peritoneal macrophages from IL-10-deficient mice express

150 In vitro, peritoneal macrophages from IL-37Tg mice reduced LPS-ind

151 ed bactericidal NO production was reduced in peritoneal macrophages from Il10(-/-); Nod2(-/-) mice, c

152 the role of IRF-2 in apoptosis, responses of peritoneal macrophages from IRF-2(+/+) and IRF-2(-/-) mi

153 In contrast, peritoneal macrophages from IRF-7(-/-) mice showed signi

154 ation of anti-inflammatory genes in WAT, and peritoneal macrophages from KO mice displayed similarly

155 Peritoneal macrophages from M-JAK2(-/-) mice and Jak2 kn

156 Peritoneal macrophages from MARCO-deficient mice, but no

157 salpinx as severe as that of wild-type mice, peritoneal macrophages from mice deficient in TLR2 but n

158 OS and arginase-1 expression were reduced in peritoneal macrophages from mice receiving CTLA4-Ig, com

159 bone marrow-derived macrophages, and primary peritoneal macrophages from mice were used.

160 own-regulate PEA biosynthesis is impaired in peritoneal macrophages from mutant NAPE-PLD-deficient mi

161 umor-bearing animals express VEGFR2, whereas peritoneal macrophages from non-tumor-bearing animals do

162 Peritoneal macrophages from ob/ob and ob/ob;Ldlr(-/-) mi

163 of PI3K and have reduced PI3K activity, and peritoneal macrophages from PTEN(flox/flox)/LysMCre mice

164 Virtually no F4/80(+) peritoneal macrophages from saline-injected mice express

165 Peritoneal macrophages from TLR2(-/-) mice significantly

166 Peritoneal macrophages from transgenic lines displayed T

167 Furthermore, peritoneal macrophages from tumor-bearing animals expres

168 Similarly, peritoneal macrophages from vitamin D-deficient mice dis

169 A comparison of peritoneal macrophages from wild type and knock-out mice

170 We isolated peritoneal macrophages from wild-type, TLR2, TLR3, TLR4,

171 ed insulin resistance, and an improvement in peritoneal macrophage function.

172 Murine peritoneal macrophages generate 12-KETE-PEs, which are a

173 Finally, peritoneal macrophages harvested from mice with DIO and

174 Isolated peritoneal macrophages harvested from shifted mice exhib

175 monocyte-derived macrophage (MDM) and mouse peritoneal macrophages has been shown to be strongly ass

176 es, including murine bone marrow-derived and peritoneal macrophages, human monocyte-derived macrophag

177 Unexpectedly, we also found that in peritoneal macrophages, IFN-gammaR itself required tonic

178 In mouse peritoneal macrophages, IL-4 potency exceeds that of IL-

179 We examined the role of iPLA2beta in peritoneal macrophage immune function by comparing wild

180 a IL-1beta as well as IL-1beta production by peritoneal macrophages in a model of LPS-induced sepsis.

181 cantly higher levels of IRAK-M compared with peritoneal macrophages in a syngeneic mouse model of lun

182 (-/-) thymocytes failed to recruit wild-type peritoneal macrophages in a Transwell migration assay.

183 nes in the central clock, liver, thymus, and peritoneal macrophages in mice after chronic jet lag.

184 hat IL-4 activation of different lineages of peritoneal macrophages in mice is accompanied by lineage

185 Exiting of peritoneal macrophages in mice lacking integrin beta2 is

186 ion of coagulation factor V (FV) by resident peritoneal macrophages in mice promotes bacterial cleara

187 le for the major self-renewing population of peritoneal macrophages in mice.

188 lacental macrophages, THP-1 cells, and mouse peritoneal macrophages in vitro.

189 ctor kappaB in oxLDL uptake was validated in peritoneal macrophages in vivo.

190 bone marrow cells and reduced the number of peritoneal macrophages in wild-type mice but not EP2(-/-

191 gnificantly decreased phagocytic activity of peritoneal macrophages in WT (by 30%), but not in CD14(-

192 line RAW 264.7, and fresh amniotic fluid and peritoneal macrophages, including macrophages from TLR4

193 killing of Escherichia coli by monocytes and peritoneal macrophages incubated with lipopolysaccharide

194 naturally occurring mutation (med) in mouse peritoneal macrophages inhibited podosome formation.

195 atosis, but the mechanisms that induce naive peritoneal macrophages into TAMs are poorly understood.

196 s following cecal ligation and puncture, and peritoneal macrophage isolated from TK-/- mice exhibited

197 In peritoneal macrophages isolated from adult animals the b

198 Importantly, peritoneal macrophages isolated from Adv-IK17-scFv treat

199 Peritoneal macrophages isolated from APOE4 mice were def

200 64.7 mouse macrophages as well as in primary peritoneal macrophages isolated from both C3H/HeJ (TLR4-

201 ss I Ag presentation suppressed by ESAT-6 in peritoneal macrophages isolated from C57BL/6 mice.

202 Peritoneal macrophages isolated from CPEB knockout (KO)

203 ased in both LPS-treated RAW 264.7 cells and peritoneal macrophages isolated from LPS-challenged mice

204 as designed to evaluate UF in LPS stimulated peritoneal macrophages isolated from mice.

205 Peritoneal macrophages isolated from myeKlf2(-/-) mice s

206 Peritoneal macrophages isolated from PC1/3 KO mice also

207 Cytokine analysis was performed on infected peritoneal macrophages isolated from these mice, and imm

208 or the self-renewal and maintenance of large peritoneal macrophages (LPMs), but not that of other tis

209 bolism were evaluated in nonactivated murine peritoneal macrophages (MPhi0) and macrophages stimulate

210 and P. aeruginosa was inhibited in Lum(-/-) peritoneal macrophages (MPhis).

211 In mice deficient in GATA6+ peritoneal macrophages, neutrophils infiltrated more rob

212 ursors, and also the numbers of the resident peritoneal macrophages, observations consistent with CSF

213 es of death explained the marked decrease in peritoneal macrophage observed.

214 ment, was up-regulated in the ears or in the peritoneal macrophages of Lmna(Dhe/+) mice.

215 Peritoneal macrophages of mice lacking TNF have a dimini

216 mRNA levels were significantly higher in the peritoneal macrophages of the HIV-1Tg rat than those in

217 howed a diminished capacity to infect murine peritoneal macrophages, only the Deltaasl null mutant wa

218 ar cAMP in AMs, but this was not observed in peritoneal macrophages or elicited peritoneal neutrophil

219 L-12p40 production by thioglycolate-elicited peritoneal macrophages or GM-CSF plus IL-4-induced bone

220 Depletion of peritoneal macrophages or neutralization of endogenous I

221 eased cholesterol delivery to either primary peritoneal macrophages or Raw264.7 cells.

222 Peritoneal macrophages (PEM) are derived from circulatin

223 LPS-induced TNF-alpha production by resident peritoneal macrophages (PerMphi) in type 2 diabetic (db/

224 ulated platelets also significantly enhanced peritoneal macrophage phagocytosis of both methicillin-r

225 or M2 activation of RAW264.7 macrophages and peritoneal macrophages (PM) on subsequent HSV-1 infectio

226 sion of alphavbeta3, but primary cultures of peritoneal macrophages (PMo) required activation of TLR4

227 USP21 also restricted antiviral responses in peritoneal macrophages (PMs) and bone marrow-derived den

228 Peritoneal macrophages (PMs) regulate inflammation and c

229 nvestigated the functions and origins of two peritoneal macrophage populations in mice: small and lar

230 5-HT transporter inhibited 5-HT uptake into peritoneal macrophages, prevented 5-HT-induced phosphory

231 Depletion of resident peritoneal macrophages prior to, or concomitant injectio

232 SMase-deficient (asm(-/-)) mice and isolated peritoneal macrophages produce severalfold more TNFalpha

233 Peritoneal macrophages produced IFN-gamma when stimulate

234 ta6 deficiency also resulted in dysregulated peritoneal macrophage proliferative renewal during homeo

235 In mouse resident peritoneal macrophages, prostacyclin, prostaglandin E2 a

236 We report that naive, primary peritoneal macrophages rapidly upregulate the expression

237 In vivo, amlodipine and verapamil suppressed peritoneal macrophage recruitment in response to thiogly

238 Cultured mouse peritoneal macrophages release large numbers of ~30-nm c

239 those in the infected mice, and depletion of peritoneal macrophages rendered the mice significantly m

240 ate lymphoid cell (ILC3) numbers and altered peritoneal macrophage responses.

241 SBM treatment of peritoneal macrophages resulted in the upregulation of p

242 Stimulated peritoneal macrophages revealed suppression of COX-2-der

243 THP-1 cells, and genetic deletion of RAGE in peritoneal macrophages, revealed that hypoxia-induced up

244 In addition, Tim-4(-/-) resident peritoneal macrophages (rPMs) phagocytose necrotic cells

245 sm of arachidonoyltaurine by murine resident peritoneal macrophages (RPMs) was also profiled.

246 In contrast to splenic APCs, peritoneal macrophages secreted NO, failed to activate n

247 more, C1q-deficient pristane-primed resident peritoneal macrophages secreted significantly less CCL3,

248 The SHIP-deficient peritoneal macrophages show evidence of IgG receptor sti

249 Likewise, cultures of primary peritoneal macrophages show that VLDLR deficiency reduce

250 19 compared with WT mice, and RELMalpha(-/-) peritoneal macrophages showed deficient IL-23p19 inducti

251 accharide-stimulated thioglycollate-elicited peritoneal macrophages showed increased inflammatory gen

252 , expression arrays conducted on HRG-treated peritoneal macrophages showed induction of genes involve

253 sed on studies in which (i) biotinylation of peritoneal macrophages showed that endogenous ABCG1 is i

254 Analyses of isolated inflammatory peritoneal macrophages showed that IL-4-induced fusion o

255 e, investigation of the activation status of peritoneal macrophages showed that the expression of gen

256 d higher survival within the THP-1 and mouse peritoneal macrophages, simultaneously increasing the in

257 rophage populations in mice: small and large peritoneal macrophages (SPM and LPM, respectively).

258 lective mobilization of unconventional small peritoneal macrophages (SPMs) that, in comparison with l

259 creased phosphorylation of ERK1/2 and Akt in peritoneal macrophages stimulated ex vivo by LPS.

260 ofiling microarray analysis in primary mouse peritoneal macrophages stimulated with LXR ligands.

261 rain mononuclear cells, blood monocytes, and peritoneal macrophages, suggesting that cell surface CD3

262 ation, carotid artery TF activity as well as peritoneal macrophage TF activity/expression.

263 Enano had a higher binding affinity to mouse peritoneal macrophages than Enano.

264 in GP-F88A permissive IC-21 cells and mouse peritoneal macrophages than in RAW 264.7 cells.

265 In mouse peritoneal macrophages, the activity of TACE was the rat

266 tion and resulted in increased cAMP level in peritoneal macrophages through G protein-coupled E-serie

267 localization and functional polarization of peritoneal macrophages through the reversible induction

268 nt with the expression of these receptors in peritoneal macrophages (TLR2/4, C5aR) and mesothelial ce

269 consistent with that of GPCR, allowing mouse peritoneal macrophages to migrate toward its ligand CCL5

270 m the Golgi and recycling endosomes of mouse peritoneal macrophages to newly formed phagosomes and re

271 genes were specifically modified by exposing peritoneal macrophages to PS or PC liposomes in vivo.

272 In vitro, exposure of primary peritoneal macrophages to saturated fatty acids also alt

273 equired for bone marrow macrophages, but not peritoneal macrophages, to phagocytose apoptotic neutrop

274 Gata6 in the macrophage compartment affected peritoneal macrophages, using Lyz2-Cre x Gata6(flox/flox

275 p. injection, percent phagocytosis of GPs by peritoneal macrophages was comparable in wild-type and D

276 lyso-PS(high) neutrophils (95% viable) by WT peritoneal macrophages was quantitatively similar to UV-

277 oneally with dl922-947 and beta3 null murine peritoneal macrophages, we confirm a role for macrophage

278 With the use of mouse bone marrow and peritoneal macrophages, we demonstrate that classical ac

279 Ex vivo stimulation studies using murine peritoneal macrophages were also used to elucidate the p

280 rophage-like RAW264.2 cells or mouse primary peritoneal macrophages were challenged with nicotine; an

281 Peritoneal macrophages were collected for determination

282 opment of cellular dysfunction; second, when peritoneal macrophages were depleted (using clodronate l

283 LPS)-induced inflammatory responses in mouse peritoneal macrophages were examined.

284 Murine peritoneal macrophages were incubated in the presence of

285 Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras

286 Infections of mouse peritoneal macrophages were performed with Chlamydia mur

287 phages (SPMs) that, in comparison with large peritoneal macrophages, were enriched for IL-17 receptor

288 urthermore, we showed that Arhgef1-deficient peritoneal macrophages when either injected into the lun

289 of cytosolic phospholipase A(2) in resident peritoneal macrophages, which are specifically primed fo

290 on causes a decrease in the thiol content of peritoneal macrophages, which can influence IL-12 produc

291 yl-beta-cyclodextrin (MbetaCD) to load mouse peritoneal macrophages with [(13)C]cholesterol.

292 ed by in vitro studies in which treatment of peritoneal macrophages with a nuclear factor-kappaB inhi

293 macrophages and correlated FoxO1 activity in peritoneal macrophages with IL-1beta production profiles

294 stimulation of murine bone marrow-derived or peritoneal macrophages with IL-33 failed to promote argi

295 n this model in that in vitro stimulation of peritoneal macrophages with killed LAC-4 induced a simil

296 In vitro stimulation of LGALS3(-/-) peritoneal macrophages with lipopolysaccharide (LPS) and

297 In vitro incubation of mouse peritoneal macrophages with lipopolysaccharide (LPS) in

298 Ex vivo stimulation of peritoneal macrophages with LPS elicited proinflammatory

299 dies demonstrate that stimulation of primary peritoneal macrophages with macrophage-stimulating prote

300 cholesterol crystal-activated cultured mouse peritoneal macrophages, with a maximum effect at approxi