ライフサイエンスコーパス: peritoneal macrophage

1 east tumors to identify peptides that target peritoneal macrophages.

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

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

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

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

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

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

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

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

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

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

12 the inflamed peritoneum and develop into new peritoneal macrophages.

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

14 ydrolytic activity was replicated in primary peritoneal macrophages.

15 s specificity and are inactive toward murine peritoneal macrophages.

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

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

18 mediates phagocytosis of apoptotic cells by peritoneal macrophages.

19 different sizes on murine bronchoalveolar or peritoneal macrophages.

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

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

22 cription in Newcastle disease virus-infected peritoneal macrophages.

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

24 pha, or C/EBPalpha was replicated in primary peritoneal macrophages.

25 killing of bacteria by blood neutrophils and peritoneal macrophages.

26 induce apoptotic cell phagocytosis by murine peritoneal macrophages.

27 release from LPS-stimulated Kupffer cells or peritoneal macrophages.

28 c activation of MSP-1 at the cell surface of peritoneal macrophages.

29 and in vivo in thioglycolate-elicited murine peritoneal macrophages.

30 terial load and isolation and study of CD11b peritoneal macrophages.

31 ecreased the uptake of spirochetes by murine peritoneal macrophages.

32 transcripts in Mecp2-deficient microglia and peritoneal macrophages.

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

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

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

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

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

38 , Gata6 is expressed selectively in resident peritoneal macrophages.

39 stantial alterations in the transcriptome of peritoneal macrophages.

40 KO was required for stimulation of elicited peritoneal macrophages.

41 rophage-dense atherosclerotic lesions and in peritoneal macrophages.

42 ve microenvironment via paracrine effects on peritoneal macrophages.

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

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

45 8.5 mug . mL(-1)) cultured in vitro in mouse peritoneal macrophages.

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

47 mmatory mediators in thioglycollate-elicited peritoneal macrophages.

48 ficient in 20:4 (10 +/- 1 mol %) compared to peritoneal macrophages (26 +/- 1 mol %).

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

50 yrosine kinase receptor RON are required for peritoneal macrophage activation.

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

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

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

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

55 Peritoneal macrophages and atherosclerotic lesions from

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

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

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

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

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

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

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

63 5-HT impaired efferocytosis by murine peritoneal macrophages and human alveolar macrophages.

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

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

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

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

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

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

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

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

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

73 cluding previously underappreciated roles of peritoneal macrophages and platelets.

74 Peritoneal macrophages and polymorphonuclear leukocytes

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

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

77 Using both primary peritoneal macrophages and studies in advanced atheromat

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

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

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

81 Peritoneal macrophages and the stromal vascular fraction

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

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

84 We demonstrate MT-SP1 expression in peritoneal macrophages, and biochemical methods confirm

85 ney cells (MARC-145 and Vero), primary mouse peritoneal macrophages, and canine DH82 (histocytosis) c

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

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

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

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

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

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

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

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

94 Peritoneal macrophages are one of the most studied macro

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

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

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

98 Depletion of peritoneal macrophages, but not neutrophils or natural k

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

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

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

102 0 were all significantly increased in murine peritoneal macrophages co-cultured with PbANKA-infected

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

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

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

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

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

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

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

110 Peritoneal macrophages deficient in ABCA1, ABCG1, or bot

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

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

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

114 anisms with Dectin-Fc increased alveolar and peritoneal macrophage-dependent killing of PC.

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

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

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

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

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

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

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

122 splenocytes, bone marrow cells, or enriched peritoneal macrophages, either for prevention against su

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

124 Peritoneal macrophages expressed the 5-HT transporter an

125 In peritoneal macrophages, expression of NLRP3 and activati

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

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

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

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

130 Peritoneal macrophages from ACE-KO mice were deficient i

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

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

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

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

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

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

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

138 We studied 2 types of cells, resident peritoneal macrophages from CD-1 mice and the murine mac

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

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

141 Peritoneal macrophages from dyslipidemic animals were pr

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

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

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

145 found that compared with HO-1(+/+) controls, peritoneal macrophages from HO-1(-/-) and HO-1(+/-) mice

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

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

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

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

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

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

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

153 Peritoneal macrophages from MARCO-deficient mice, but no

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

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

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

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

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

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

160 Peritoneal macrophages from PPARalpha(-/-) mice had incr

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

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

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

164 Peritoneal macrophages from transgenic lines displayed T

165 Furthermore, peritoneal macrophages from tumor-bearing animals expres

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

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

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

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

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

171 In the present study, peritoneal macrophages harvested from green fluorescent

172 Finally, peritoneal macrophages harvested from mice with DIO and

173 Isolated peritoneal macrophages harvested from shifted mice exhib

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

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

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

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

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

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

180 Exiting of peritoneal macrophages in mice lacking integrin beta2 is

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

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

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

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

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

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

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

188 cell lines (RAW 264.7 and J774A.1) and mouse peritoneal macrophages induced by thioglycollate were an

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

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

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

192 In peritoneal macrophages isolated from adult animals the b

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

194 Peritoneal macrophages isolated from APOE4 mice were def

195 64.7 mouse macrophages as well as in primary peritoneal macrophages isolated from both C3H/HeJ (TLR4-

196 Peritoneal macrophages isolated from CPEB knockout (KO)

197 ased IL-12 expression were observed in mouse peritoneal macrophages isolated from EL knockout mice.

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

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

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

201 Peritoneal macrophages isolated from PC1/3 KO mice also

202 Peritoneal macrophages isolated from SR-BI/BII-knockout

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

204 To further define the role of VIP, peritoneal macrophages (Mphi) and PMN from BALB/c and B6

205 Over 25 years ago, it was observed that peritoneal macrophages (Mphi) isolated from mice given h

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

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

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

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

210 that MOR expression was up-regulated in the peritoneal macrophages of F344 control rats by exposure

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

212 Peritoneal macrophages of mice lacking TNF have a dimini

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

214 ct of decreased or absent HO-1 expression in peritoneal macrophages on oxidative stress and inflammat

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

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

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

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

219 ntly increased in J744 macrophages and mouse peritoneal macrophages overexpressing human EL.

220 Peritoneal macrophages (PEM) are derived from circulatin

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

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

223 innate immune response, we examined a mouse peritoneal macrophage (PM) cell line (RAW) and resident

224 ogs on resident alveolar macrophage (AM) and peritoneal macrophage (PM) innate immune functions.

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

229 dified lysozyme protein, dendritic cells and peritoneal macrophages presented citrullinated peptides

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 ere treated intravenously with anti-H2B Fab, peritoneal macrophage recruitment in response to thiogly

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

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

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

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

243 olipid remodeling in murine primary resident peritoneal macrophages (RPMs) during zymosan phagocytosi

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 d using cultured normal rat Kupffer cells or peritoneal macrophages stimulated by lipopolysaccharide

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

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

262 uing eicosanoid generation in mouse resident peritoneal macrophages, suggesting a role for the enzyme

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

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

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

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

267 nd eicosanoid production from resident mouse peritoneal macrophages through activation of group IVA c

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

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

270 TIM-4(+) peritoneal macrophages, TIM-1(+) kidney cells, and TIM-4

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

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

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

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

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

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

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

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

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

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 Resident peritoneal macrophages were isolated from db/db mice and

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

287 Infections of mouse peritoneal macrophages were performed with Chlamydia mur

288 ct effect on macrophage production of IL-12, peritoneal macrophages were pretreated with farnesol pri

289 In the present study, RAW cells and mouse peritoneal macrophages were treated with Toll-like recep

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

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

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

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

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

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

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