ライフサイエンスコーパス: MIP-1alpha

1 MIP-1alpha expression by gingival epithelial cells may b

2 MIP-1alpha expression in PMNs and gingival epithelial ce

3 MIP-1alpha had a specificity of 96.8% and a sensitivity

4 MIP-1alpha induced osteoclast formation at an optimal co

5 MIP-1alpha levels were also related to increasing probin

6 MIP-1alpha was highly expressed in the basal epithelial

7 MIP-1alpha(-/-) mice with ALI had less acute lung inflam

8 P = .01), IP-10 (P = .0001), MDC (P < .001), MIP-1alpha, (P < .001), MIP-1beta (P = .005), MCP-1 (P =

9 F (P<0.01), GM-CSF (P<0.01), MCP-1 (P<0.05), MIP-1alpha (P<0.01) and TGF-beta1 (P<0.01) levels when c

10 F (P<0.01), GM-CSF (P<0.01), MCP-1 (P<0.05), MIP-1alpha (P<0.01) and TGF-beta1 (P<0.01) which are key

11 ted genes macrophage inflammatory protein-1 (MIP-1alpha), MIP-2 and MMP-12, were decreased in macroph

12 Macrophage inflammatory protein-1 (MIP-1), MIP-1alpha (CCL3) and MIP-1beta (CCL4) are chemokines cr

13 mia-reperfusion induced expression of MCP-1, MIP-1alpha, and MIP-1beta mRNA in the retinal vessels 3

14 Mice treated with MCP-1, MIP-1alpha, and RANTES neutralizing antibodies had a sig

15 ion of genes encoding IL-1beta, IL-6, MCP-1, MIP-1alpha, CXCR4, and TLR2 induced in RAW264.7 cells by

16 uated the release of IL-6, IL-8, TNF, MCP-1, MIP-1alpha, IFN-gamma, LTB-4, MMP-8 and -9, and IL-1Ra w

17 Levels of IP-10, HGF, IL-6, MCP-1, MIP-1alpha, IL-12p70, IL-18, VEGF-A, PDGF-BB and IL-1RA

18 okines include IL-1beta, IL-6, IL-10, MCP-1, MIP-1alpha, MIP-1beta, MMP-2, and TNF-alpha.

19 3, IL-15, IL-17, Eotaxin, IP-10, MIG, MCP-1, MIP-1alpha, MIP-1beta, RANTES, tumor necrosis factor (TN

20 ory cytokines (IL-1beta, IL-6, IL-17, MCP-1, MIP-1alpha, MIP-2, RANTES, and TNF-alpha), inflammatory

21 ins, including; IL-6, IL-10, MCP-1, sVCAM-1, MIP-1alpha, IP-10, GM-CSF, M-CSF, TNF-alpha, IFN-gamma,

22 (MCP-1 [monocyte chemoattractant protein 1], MIP-1alpha/beta [macrophage inflammatory protein 1alpha/

23 ssed markedly reduced levels of IL-2, IL-10, MIP-1alpha, and GM-CSF.

24 emokines (interleukin-2 [IL-2], IL-6, IL-10, MIP-1alpha, and RANTES) that together enhanced beta-cell

25 ls of MCP-1, IFN-gamma-inducible protein-10, MIP-1alpha, and MIP-1beta mRNA transcripts, had greater

26 tion, secretion of IFN-gamma, GM-CSF, IL-13, MIP-1alpha, MIP-1beta, CCL5, and TNF-alpha, and massive

27 y by macrophage inflammatory protein 1alpha (MIP-1alpha) and regulated on normal T-cell expressed and

28 and macrophage inflammatory protein 1alpha (MIP-1alpha) in the bladder.

29 gher macrophage inflammatory protein 1alpha (MIP-1alpha) levels early in infection.

30 ic CD3e and monocyte-induced protein 1alpha (MIP-1alpha) mRNA induction.

31 and macrophage inflammatory protein 1alpha (MIP-1alpha) paralleled NF-kappaB activation, while incre

32 n of macrophage-inflammatory protein 1alpha (MIP-1alpha), a leukocyte chemokine, in astrocytes.

33 ding macrophage inflammatory protein 1alpha (MIP-1alpha), CCL3 and CCL3L1, were found to be upregulat

34 and macrophage inflammatory protein 1alpha (MIP-1alpha), in response to SHFV infection were observed

35 ines macrophage inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, and RANTES, interfere with HIV-1

36 ha), macrophage inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, hepatocyte growth factor (HGF),

37 pha, macrophage inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, MIP-2, interferon gamma-inducibl

38 s of macrophage inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, monokine induced by interferon (

39 inds macrophage inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, RANTES, and members of the monoc

40 ine, macrophage inflammatory protein 1alpha (MIP-1alpha), monocyte chemoattractant protein 1, and reg

41 ines macrophage inflammatory protein 1alpha (MIP-1alpha), RANTES, and IP-10 were individually cloned

42 and macrophage inflammatory protein 1alpha (MIP-1alpha), were individually cloned into RABV.

43 kine macrophage inflammatory protein 1alpha (MIP-1alpha).

44 kine macrophage inflammatory protein 1alpha (MIP-1alpha).

45 for macrophage inflammatory protein 1alpha (MIP-1alpha)/CCL3 and RANTES/CCL5, exhibited high constit

46 L2), macrophage inflammatory protein 1alpha (MIP-1alpha/CCL3), and RANTES (CCL5), in a pattern that w

47 and macrophage inflammatory protein 1alpha (MIP-1alpha; CCL3) to their receptors CCR1 and CCR5, resp

48 nes, macrophage inflammatory protein-1alpha (MIP-1alpha) and MIP-1beta.

49 kine macrophage inflammatory protein-1alpha (MIP-1alpha) and the DC-specific growth factor fms-like t

50 ines macrophage inflammatory protein-1alpha (MIP-1alpha) and thymus- and activation-related chemokine

51 the macrophage inflammatory protein-1alpha (MIP-1alpha) are reported in inflammatory bone diseases i

52 Macrophage inflammatory protein-1alpha (MIP-1alpha) is a chemokine that leads to leukocyte recru

53 and macrophage inflammatory protein-1alpha (MIP-1alpha) than in C57BL/6J mice.

54 CL3 (macrophage inflammatory protein-1alpha (MIP-1alpha)), CCL4 (MIP-1beta), CCL5 (RANTES), CXCL2 (MI

55 -10, macrophage inflammatory protein-1alpha (MIP-1alpha), and MIP-1beta, the pattern of which varied

56 eta, macrophage inflammatory protein-1alpha (MIP-1alpha), and MIP-1beta.

57 ding macrophage inflammatory protein-1alpha (MIP-1alpha), fms-like tyrosine kinase 3 ligand (Flt3L),

58 CCL3/macrophage inflammatory protein-1alpha (MIP-1alpha), increased expression of phosphorylated, dis

59 -8), macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, and growth-related oncogene beta

60 ha), macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, and IL-9, as well as IL-10, more

61 -17, macrophage inflammatory protein-1alpha (MIP-1alpha), monocyte chemoattractant protein-1 (MCP-1),

62 gand macrophage inflammatory protein-1alpha (MIP-1alpha/CCL3).

63 asma macrophage inflammatory protein-1alpha (MIP-1alpha; also called CCL3), but only minimally affect

64 ine (macrophage inflammatory protein 1alpha [MIP-1alpha] and MIP-2) transcripts from joints.

65 ta], macrophage inflammatory protein 1alpha [MIP-1alpha], and tumor necrosis factor alpha [TNF-alpha]

66 ies (macrophage inflammatory protein 1alpha [MIP-1alpha], MIP-1beta, RANTES) and CXC families (growth

67 with monocyte production of IL-8, IL-1alpha, MIP-1alpha, and IL-10 being comparable to that seen in t

68 milar increases were observed for IL-1alpha, MIP-1alpha, and prostaglandin E2.

69 mmatory cytokine responses (e.g., IL-1alpha, MIP-1alpha, TNF, IL-6, and IL-8) as well as regulated a

70 lpha, tumor necrosis factor alpha, IL-1beta, MIP-1alpha, and KC produced by PMNs.

71 and chemokines (TNF-alpha, MCP-1, IL-1beta, MIP-1alpha, IL-6, Leptin, and IL-18) and metformin signi

72 bundant amounts of CC chemokines (MIP-1beta, MIP-1alpha, and RANTES) but not IL-2.

73 and chemokines (IP-10/CXCL-10, MCP-1/CCL-2, MIP-1alpha/CCL-3, RANTES/CCL-5, and interleukin 8) than

74 terferon) and chemokine (RANTES, MIG, MCP-2, MIP-1alpha, and interleukin-8) expression was examined.

75 ssion of chemokines/cytokines such as CCL-3 (MIP-1alpha) and granulocyte-macrophage colony-stimulatin

76 acrophage inflammatory protein-1alpha/CCL-3 (MIP-1alpha/CCL-3), MIP-1beta/CCL-4, and RANTES/CCL-5, am

77 ristic cytokines, including IFN-gamma, IL-4, MIP-1alpha, and IL-6.

78 kines such as TNF-alpha, IL-1beta, and IL-6, MIP-1alpha and MIP-1beta also were significantly higher

79 roduction of proinflammatory cytokines IL-6, MIP-1alpha, IL-1beta, and KC increased over the course o

80 IL-10, IL-6, MIP-1alpha, MIP-1beta, and MCP-2 were associated with in

81 g reduction in pulmonary neutrophilia, IL-6, MIP-1alpha, MIP-1beta, CXCL1, and CXCL5 in AlloTbet mice

82 of proinflammatory factors IFN-alpha, IL-6, MIP-1alpha, RANTES, and KC, up-regulate the expression o

83 produced significantly less TNF-alpha, IL-6, MIP-1alpha/CCL3, and IFN-gamma-induced protein 10/CXCL10

84 of the proinflammatory factors MCP-1, IL-8, MIP-1alpha, and IL-6, as well as the antiinflammatory IL

85 retion of TNF-alpha and the chemokines IL-8, MIP-1alpha, and RANTES was also observed under these con

86 emonstrated a poor correlation between IL-8, MIP-1alpha, MIP-1beta, and GRO-beta mRNA levels and prot

87 educed when neutralizing antibodies to IL-8, MIP-1alpha, or RANTES were added to culture supernatants

88 6), macrophage inflammatory protein 1 alpha (MIP-1alpha), IL-1 receptor (IL-1R), or tumor necrosis fa

89 1), macrophage inflammatory protein 1-alpha (MIP-1alpha), and MIP-1beta, which chemoattract genetical

90 ine macrophage inflammatory protein 1-alpha (MIP-1alpha/CCL3).

91 1, macrophage inflammatory protein 1 alpha [MIP-1alpha], MIP-1beta) were significantly diminished or

92 f chemokine ligand 10 [CXCL10], MIP-1 alpha [MIP-1alpha]/CCL3), which segregated participants who die

93 gher levels of alpha interferon (IFN-alpha), MIP-1alpha, and MIP-1beta in plasmacytoid DCs (pDCs) exp

94 ntly down-regulated production of IFN-alpha, MIP-1alpha, IL-12p70, and IL-1alpha following activation

95 ll infiltration, tissue and serum TNF-alpha, MIP-1alpha and MIP-2 levels, tissue lipid peroxidation,

96 ne production (MCP-1, RANTES, KC, TNF-alpha, MIP-1alpha, and IFN-gamma) was significantly attenuated

97 lts in enhanced LPS-induced IL-6, TNF-alpha, MIP-1alpha, and MIP-1beta expression in human primary mo

98 gands enhanced early secretion of TNF-alpha, MIP-1alpha, and MIP-2 and increased late TGF-beta1 secre

99 egree of hepatic damage and serum TNF-alpha, MIP-1alpha, and MIP-2 levels.

100 of the proinflammatory cytokines TNF-alpha, MIP-1alpha, IL-12, and IFN-gamma in pancreata, endotoxin

101 hat IL-1beta, IL-6, IL-10, IL-12, TNF-alpha, MIP-1alpha, keratinocyte-derived chemokine, and MCP-1 mR

102 lones secreted IL-4, IL-5, IL-13, TNF-alpha, MIP-1alpha, MIP-1beta, and RANTES.

103 -13; IFN-gamma; tumor necrosis factor-alpha; MIP-1alpha/beta; MCP-1 (monocyte chemotactic protein-1);

104 Although MIP-1alpha is an important chemokine in the recruitment

105 matory intra-aneurysmal tissue healing in an MIP-1alpha- and MIP-2-dependent pathway.

106 or IL-1beta (p < 0.03), IL-8 (p < 0.03), and MIP-1alpha (p < 0.003), and borderline significance for

107 8/CXCL8 (P<0.001), MCP-3/CXCCL7 (P<0.05) and MIP-1alpha/CCL-3 (P<0.05) were significantly upregulated

108 Immunoreactive MCP-1 and MIP-1alpha were detected in the GCL, INL, and the retina

109 ines (monocyte chemoattractant protein-1 and MIP-1alpha) and proteases (MMP-2, MMP-9, and cathepsins-

110 a, PDGF-A, and FGF-7), chemokines (MCP-1 and MIP-1alpha), and extracellular matrix (collagen-I and al

111 /monocyte chemotactic protein 1 (MCP-1), and MIP-1alpha followed NF-kappaB activation leading to sign

112 nsferase, TNF-alpha, IL-6, IL-10, MCP-1, and MIP-1alpha and Kupffer cell cytokine production was obse

113 e ligands IFN-gamma-inducible protein 10 and MIP-1alpha were increased (61.4 +/- 13.9 to 1103.7 +/- 2

114 ibrosis by reducing lung levels of IP-10 and MIP-1alpha.

115 the NF-kappaB-dependent chemokines IP-10 and MIP-1alpha.

116 f IFN-gamma-inducible protein-10 (IP-10) and MIP-1alpha.

117 kines, including TNF-alpha, IL-6, IL-10, and MIP-1alpha, than did WT mice.

118 nd chemokines, such as TNF-alpha, IL-12, and MIP-1alpha.

119 , including interleukin-12p70 (IL-12p70) and MIP-1alpha, which were positively correlated with the ma

120 ta, with IL-6, IL-8, IL-1alpha, IL-1beta and MIP-1alpha/beta production significantly elevated.

121 decreased production of IL-6, IL-1beta, and MIP-1alpha but not TNF-alpha, suggesting a role for IL-1

122 TNF, MIP-1beta, and MIP-1alpha were produced predominantly by monocytes and

123 These cells produced IL-2 and MIP-1alpha, but much less IL-4 and IFN-gamma than CD73-

124 crophage inflammatory protein 2 (MIP-2), and MIP-1alpha in bronchoalveolar lavage fluid and an increa

125 e in the production of TNF-alpha, MIP-2, and MIP-1alpha in IgG IC-stimulated macrophages.

126 in C/EBP induction and TNF-alpha, MIP-2, and MIP-1alpha production induced by IgG IC.

127 olony-stimulating factor [GM-CSF], IL-4, and MIP-1alpha) responses of the treated mice was observed,

128 Indeed, production of IL-1alpha, IL-6, and MIP-1alpha was reduced in IL-18 knock-out (ko) mouse emb

129 ines and chemokines (IL-1beta, KC, IL-6, and MIP-1alpha) were greater in eyes of TNFalpha(-/-) mice t

130 of virus replication and spread in IL-6- and MIP-1alpha-deficient mice were not different from those

131 n MMP inhibitor, decreases both baseline and MIP-1alpha-induced DC transmigration.

132 -2, keratinocyte cell-derived chemokine, and MIP-1alpha compared with wild-type cells.

133 n of IL-8, macrophage-derived chemokine, and MIP-1alpha was also observed after costimulation.

134 we show that all three beta-chemokines, and MIP-1alpha in particular, inhibit postentry steps of the

135 CD16-dependent degranulation and MIP-1alpha secretion were not fully inhibited, suggestin

136 response (KC, 2.6-fold; MCP-1, 2.6-fold; and MIP-1alpha, 4.4-fold increase over WT values).

137 Mucosal NK cells produced IFN-gamma and MIP-1alpha/CCL3 but lacked several markers of activation

138 otein 10, monokine induced by IFN-gamma, and MIP-1alpha, specifically in those patients that experien

139 nd there was earlier transcription of KC and MIP-1alpha in B10 x C2D mice.

140 ines (TNF-alpha, IL-6, IL-10, MCP-1, KC, and MIP-1alpha), lung neutrophil infiltration, and edema wer

141 nd increased pulmonary expression of MIG and MIP-1alpha.

142 kines such as IL-1beta, IL-5, IL-12 p70, and MIP-1alpha was increased in OLFM4 KO mice compared with

143 Salivary PGE2 and MIP-1alpha discriminate gingivitis from health, and pati

144 ted GM-CSF-induced STAT5 phosphorylation and MIP-1alpha production in normal PBMCs.

145 e, whereas the native chemokines (RANTES and MIP-1alpha) fail to displace bound fluorescent analogs e

146 TNF and MIP-1alpha were significantly higher in the SM compared

147 In both groups, mRNA levels for TNFalpha and MIP-1alpha were elevated, no significant change was seen

148 fficking-only EDN (in BAL fluid and WBC) and MIP-1alpha (in WBC) levels were higher for TPE patients

149 C57BL/6J wild type (WT) and MIP-1alpha-deficient (KO) mice were used either as contr

150 ng mice, administration of neutralizing anti-MIP-1alpha antibodies reduced tumor load assessed by mon

151 As MIP-1alpha-mediated inflammation is a common response to

152 nate chemokines CCL3 and CCL4 (also known as MIP-1alpha and MIP-1beta) are produced.

153 tion of the CC chemokine CCL3 (also known as MIP-1alpha), which recruits monocytes to the area in whi

154 Baseline MIP-1alpha and MIP-1beta did not significantly differ be

155 Because MIP-1alpha is temporally expressed with neutrophils at s

156 CCR5, binding MIP-1alpha/CCL3 and RANTES/CCL5, was up-regulated on ST

157 Blocking MIP-1alpha and MIP-2 with antagonist antibody causes a s

158 Furthermore, blocking MIP-1alpha expression in an in vivo model of human MM pr

159 Peripheral blood MIP-1alpha and MIP-1beta levels were significantly eleva

160 Both MIP-1alpha and MIP-1beta form high-molecular-weight aggr

161 L-23p19, and IL-17), chemokines (MCP-1/CCL2, MIP-1alpha/CCL3, and RANTES/CCL5), and chemotactic facto

162 atory cytokines and receptors (IL-22, CCL27, MIP-1alpha, IP-10, CCR4, CCR5, and CXCR3), immune dysfun

163 hed levels of IFN-gamma, CCL2 (MCP-1), CCL3 (MIP-1alpha), and CCL5 (RANTES) in the cerebrospinal flui

164 ession of the chemokines CCL2 (MCP-1), CCL3 (MIP-1alpha), CCL4 (MIP-1beta), CCL5 (RANTES), and CXCL10

165 oinflammatory cytokines Cxcl2 (MIP-2), Ccl3 (MIP-1alpha), and Ccl4 (MIP-1beta).

166 umor necrosis factor and the chemokine CCL3 (MIP-1alpha), were released multidirectionally.

167 M1 and the human and murine chemokines CCL3 (MIP-1alpha), CCL2 (MCP-1), and CCL5 (RANTES).

168 ed chemokine gene promoters, the human CCL3 (MIP-1alpha) and CCL4 (MIP-1beta), were transfected into

169 ad reduced content of the CCR1 ligands CCL3 (MIP-1alpha) and CCL5 (RANTES) compared with injured kidn

170 : mu-opioid receptor/HEK293 cells with CCL3 (MIP-1alpha) induced internalization of mu-opioid recepto

171 pe (WT) hosts, allografts in CCR5, CCR2/CCL3(MIP-1alpha), CXCR3, CXCL10/IP-10, and CCL3/MIP-1alpha KO

172 umor necrosis factor alpha (TNF-alpha), CCL3/MIP-1alpha, and CCL4/MIP-1beta production and lower neut

173 mpaired IL-1alpha, IL-1beta, TNF-alpha, CCL3/MIP-1alpha, CCL4/MIP-1beta, and CXCL1/KC production, whi

174 sCD14 (P = .04), sCD163 (P = .02), and CCL3/MIP-1alpha (P = .02), suggesting increased macrophage/mi

175 3(MIP-1alpha), CXCR3, CXCL10/IP-10, and CCL3/MIP-1alpha KO mice did not show a significant improvemen

176 The chemokine CCL3/MIP-1alpha is a risk factor in the outcome of multiple m

177 secretion of the CCR5-binding chemokine CCL3/MIP-1alpha.

178 Although chemokines CCL3/MIP-1alpha and CCL5/RANTES are considered to be primary

179 ttracting, HIV-1-inhibitory chemokines, CCL3/MIP-1alpha and CCL4/MIP-1beta, were induced in human pri

180 nuated (p < 0.05) 0.02 muM HagB-induced CCL3/MIP-1alpha, CCL4/MIP-1beta, and TNFalpha responses.

181 5/MIP-1delta and CCL23/CKbeta8, but not CCL3/MIP-1alpha or CCL5/RANTES, were detected at relatively h

182 iggers the production of high levels of CCL3/MIP-1alpha, CCL4/ MIP-1beta, and CCL5/RANTES but not of

183 d MIP-1beta, but not in CCR1(-/-), CCR2(-/-)/MIP-1alpha(-/-), or MIP-1alpha(-/-) mice.

184 tural ligands of the HIV-1 coreceptors CCR5 (MIP-1alpha/beta and RANTES) and CXCR4 (SDF-1).

185 s coupled with lower levels of the chemokine MIP-1alpha and Th1 cytokines IL-12 and TNF-alpha.

186 MCP-1 was the most abundant chemokine, MIP-1alpha was the least abundant, and RANTES levels wer

187 The CC chemokines MIP-1alpha, MIP-1beta, and RANTES and their receptors CC

188 inflammatory cytokines (including chemokines MIP-1alpha, MIP-1beta, and IP-10).

189 No differential expression of chemokines MIP-1alpha or MIP-2 or Th2 cytokines IL-4 or IL-5 was ob

190 ha, IL-1beta, IL-6, and IL-12b), chemokines (MIP-1alpha; MCP-3; growth-related oncogenes 1 and 2; and

191 TNF-alpha, IL-1alpha, IL-6) and chemokines (MIP-1alpha, MCP-1) and increased the production of the a

192 rted, circulating levels of beta-chemokines (MIP-1alpha, MIP-1beta, and RANTES) and their respective

193 -13 stimulates select CC and CXC chemokines (MIP-1alpha/CCL-3, MIP-1beta/CCL-4, MIP-2/CXCL2/3, MCP-1/

194 iated decreases in IL-13-induced chemokines (MIP-1alpha/CCL-3, MIP-1beta/CCL-4, MIP-2/CXCL-1, RANTES/

195 imal IL-13 stimulation of select chemokines (MIP-1alpha/CCL3, MIP-1beta/CCL4, MCP-1/CCL-2), matrix me

196 Mice bearing intramuscular CHO/MIP-1alpha tumors developed lytic lesions at distant ske

197 it inhibitor, PLX3397, decreased circulating MIP-1alpha and ameliorated the extramedullary hematopoie

198 upernatant from resistant EC cells contained MIP-1alpha and MIP-1beta and was sufficient to confer R5

199 0, IL-12, CRP, TNF-alpha, IFN-gamma, GM-CSF, MIP-1alpha, and Eotaxin-1 in patients with MDD based on

200 its potential to generate IFN-gamma, GM-CSF, MIP-1alpha, MIP-1beta, and RANTES.

201 atory protein 2 (MIP-2)/CXCL2, IP-10/CXCL10, MIP-1alpha/CCL3, granulocyte colony-stimulating factor (

202 atively regulates pro-inflammatory cytokines MIP-1alpha and IL-17A.

203 Genetically deleting MIP-1alpha in MMP-8(-/-) mice reduced the increased lung

204 arization, degranulation, and CD16-dependent MIP-1alpha secretion by NK cell clones that expressed in

205 pha, thus depolymerization mutations enhance MIP-1alpha to arrest monocytes onto activated human endo

206 1B in MM cells and their capacity to express MIP-1alpha was examined.

207 mmunogenicity of recombinant RABV expressing MIP-1alpha (rHEP-MIP1alpha) was determined.

208 (P < .001) and osteoclast-activating factor MIP-1alpha (P < .05) also were significantly elevated in

209 m levels of the pro-osteoclastogenic factor, MIP-1alpha, were elevated and CSF-1 receptor (CSF-1R)-de

210 sensitivity to 2 other suppressive factors (MIP-1alpha and IFNgamma) to which FA hematopoietic proge

211 ctic protein 1 (4.5-folds), MIG (4.4-folds), MIP-1alpha (3.4-folds), and IL-8 (3.1-folds).

212 hese findings indicate an important role for MIP-1alpha in the recruitment and activation of selected

213 inflammatory cytokines and chemokines, e.g., MIP-1alpha/beta.

214 ne-bound MMP-8 on activated PMNs had greater MIP-1alpha-degrading activity than soluble MMP-8.

215 gation is a polymerization process and human MIP-1alpha and MIP-1beta form rod-shaped, double-helical

216 Recombinant human MIP-1alpha isoforms LD78beta and LD78alpha were expresse

217 the conserved sequence elements in the human MIP-1alpha promoter are two consensus RUNX sites.

218 f producing interleukin-8 (IL-8), Exodus II, MIP-1alpha, MIP-1beta, and IL-1alpha and preferentially

219 We observed an increase in MIP-1alpha (macrophage inflammatory protein-1alpha)/CCL3

220 of Sandhoff disease involves an increase in MIP-1alpha that induces monocytes to infiltrate the CNS,

221 Soluble MMP-8 cleaved and inactivated MIP-1alpha in vitro, but membrane-bound MMP-8 on activat

222 er injury during ALI in mice by inactivating MIP-1alpha.

223 lated other proinflammatory genes, including MIP-1alpha and MIF, and growth factors such as platelet-

224 These findings indicate MIP-1alpha may play an important role in early and later

225 ced by IL-1beta and LPS, but neither induced MIP-1alpha expression in gingival fibroblasts or osteobl

226 cells demonstrated that Met-RANTES inhibited MIP-1alpha and MIP-1beta at 50% inhibition concentration

227 inflammatory or antimicrobial responses (KC, MIP-1alpha, TNF-alpha, IL-6, IL-12p70, and NO) in the lu

228 c oxide synthase (Nos2), lipocalin-2 (Lcn2), MIP-1alpha, MIP-1beta, and keratinocyte-derived cytokine

229 induced elevated expression of CCR5 ligands MIP-1alpha and RANTES in the microvasculature, increased

230 the CCR5 chemokine receptor and its ligands MIP-1alpha/CCL3 and MIP-1beta/CCL4.

231 nd Actinobacillus actinomycetemcomitans LPS, MIP-1alpha mRNA and secreted protein levels were quantif

232 her levels of chemokines such as MIP2, MCP1, MIP-1alpha, and MCP1, and display more infiltrating neut

233 acrophage migration inhibitory factor [MIF], MIP-1alpha, and MIP-2alpha) was measured using real-time

234 17 and the lymphocyte chemokines IP-10, MIG, MIP-1alpha, MIP-1beta, and RANTES were decreased in the

235 ell lines that expressed less than 200 pg/mL MIP-1alpha.

236 erial lipopolysaccharides (LPSs) to modulate MIP-1alpha expression in epithelial cells, fibroblasts,

237 F) from LPS-treated MMP-8(-/-) mice had more MIP-1alpha than BALF from LPS-treated WT mice, but simil

238 Older age and increased nasal MIP-1alpha levels were of borderline statistical signifi

239 roduction of IFN-gamma and TNF-alpha but not MIP-1alpha, MIP-1beta, and RANTES.

240 The ability of MIP-1alpha to facilitate formation of multinuclear bone

241 In the absence of MIP-1alpha, acute inflammatory responses were attenuated

242 Binding of MIP-1alpha to cognate receptors decreases activation-ind

243 Concentrations of MIP-1alpha and PGE2 were significantly higher (2.8 times

244 ss significantly increased concentrations of MIP-1alpha, MIP-1beta, IP-10, and MIG proteins in the co

245 h MM who produce increased concentrations of MIP-1alpha, the relative level of AML-1B is significantl

246 Deletion of MIP-1alpha expression resulted in a substantial decrease

247 We also evaluated the effect of MIP-1alpha as an osteoclast activating factor.

248 resulted in a higher level of expression of MIP-1alpha at the site of inoculation, increased recruit

249 Furthermore, the transgenic expression of MIP-1alpha during bacterial pneumonia resulted in enhanc

250 ene LTD(4) strongly stimulates expression of MIP-1alpha in macrophages and MIP-2 (also called CXCL2)

251 Our data thus demonstrate that expression of MIP-1alpha not only reduces viral pathogenicity but also

252 Expression of MIP-1alpha; MIP-1beta; regulated on activation, normal T

253 n MM cell lines that produced high levels of MIP-1alpha (> 1 ng/mL per 10(6) cells per 72 hours), but

254 acterized by increased circulating levels of MIP-1alpha and MIP-1beta and decreased RANTES.

255 Furthermore, it increased levels of MIP-1alpha, MIP-1beta, and CCR5 transcripts in the corne

256 e model, it was found that overexpression of MIP-1alpha further decreased RABV pathogenicity by induc

257 Previously, we showed that overexpression of MIP-1alpha in mouse brain further decreased rabies virus

258 eta-mediated functions promote production of MIP-1alpha (or CCL3) by mediating the recruitment of MIP

259 NK cells, as well as decreased production of MIP-1alpha and IFN-gamma in liver.

260 l proliferation, and decreased production of MIP-1alpha and RANTES.

261 rollers, we observed increased production of MIP-1alpha and/or MIP-1beta at the protein level.

262 -1 receptor (CSF-1R)-dependent production of MIP-1alpha by macrophages was increased.

263 tes of infection, we examined proteolysis of MIP-1alpha in vitro by the neutrophil-derived serine pro

264 ha (or CCL3) by mediating the recruitment of MIP-1alpha-producing macrophages to the liver during ear

265 e MDC/CCL22 chemokine and down-regulation of MIP-1alpha/CCL3, RANTES/CCL5, MIP-1beta/CCL4, and MCP-1/

266 g to monocytes and triggering the release of MIP-1alpha and MIP-1beta.

267 ymerization buries receptor-binding sites of MIP-1alpha, thus depolymerization mutations enhance MIP-

268 The superior sensitivity and specificity of MIP-1alpha, which correlated well with probing depths an

269 MCP-1 production preceded that of MIP-1alpha during infection and was dependent on IFN-alp

270 creased at 2 weeks post-surgery and those of MIP-1alpha and MIP-2alpha at 3 weeks.

271 aneurysms causes significant upregulation of MIP-1alpha and MIP-2 expression by cytokine array assay.

272 LI treatment induced massive upregulation of MIP-1alpha, IP-10, and IFN-alpha in normal blood mononuc

273 in CCR1(-/-), CCR2(-/-)/MIP-1alpha(-/-), or MIP-1alpha(-/-) mice.

274 associated cytokines including IL-12 (p40), MIP-1alpha (CCL3), and IFN inducible protein-10 (IP-10,

275 l cytokines macrophage inflammatory proteins MIP-1alpha, MIP-1alphaP (CCL3L1), and MIP-1beta; granulo

276 cox-2(-/-) macrophages toward MCP-1, RANTES, MIP-1alpha, or MIP-1beta, as well as cell adhesion to IC

277 production of interleukin-8 (IL-8), RANTES, MIP-1alpha, and MIP-1beta, whereas only IL-8 and RANTES

278 ng proteins (Lyn), chemokines (IL-8, RANTES, MIP-1alpha, and MIP-1beta) and transcription factors (ea

279 is a G protein-coupled receptor for RANTES, MIP-1alpha, MIP-1beta, and MCP-2 that functions as the f

280 Expression of mRNA for RANTES, MIP-1alpha, MIP-1beta, and SDF-1 and secretion of the ch

281 The ability of recombinant MIP-1alpha to induce osteoclast formation was determined

282 hamsters but altered neutrophil recruitment, MIP-1alpha and MIP-2 chemokine expression, and vascular

283 Thus, interventions that reduce MIP-1alpha levels following T-H should be useful in decr

284 ever, same depolymerization mutations render MIP-1alpha ineffective in mouse peritoneal cell recruitm

285 ells and IL-12 to mice led to enhanced serum MIP-1alpha.

286 hemokine (C-C motif) ligand 3 (CCL3, synonym MIP-1alpha) were significantly diminished in mice with a

287 njury than WT mice with ALI, confirming that MIP-1alpha promotes acute lung inflammation and injury i

288 Together, these results establish that MIP-1alpha is sufficient to induce MM-like destructive l

289 We now report that MIP-1alpha increases the transmigration of bone marrow-d

290 burden and bone destruction, suggesting that MIP-1alpha is an important mediator of MM bone disease.

291 The MIP-1alpha, MIP-1beta, and RANTES chemokines are natural

292 tory markers were markedly attenuated in the MIP-1alpha KO mice following T-H.

293 therapy in conjunction with blockade of the MIP-1alpha/CCR1 inflammatory cascade may ultimately prov

294 Thus, MIP-1alpha plays an important role in mediating the acut

295 at TAFA proteins appear distantly related to MIP-1alpha, a member of the CC-chemokine family.

296 and MMP-8 approached healthy levels, whereas MIP-1alpha and PGE2 concentrations remained significantl

297 flammatory cells, it remains unknown whether MIP-1alpha plays any role in the development of systemic

298 oncentrations, alone and in combination with MIP-1alpha, readily discriminated gingivitis from health

299 e phosphorylation in T cells stimulated with MIP-1alpha in a time-dependent manner.

300 These mice without MIP-1alpha showed improved neurologic status and a longe