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 MIP-1alpha-positive cells were frequently located near t

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

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) levels when c

11 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

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

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

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

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

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

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

18 3, IL-15, IL-17, Eotaxin, IP-10, MIG, MCP-1, MIP-1alpha, MIP-1beta, RANTES, tumor necrosis factor (TN

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 Macrophage inflammatory protein-1alpha (MIP-1alpha) is a proinflammatory cytokine that also inhi

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

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

53 ed), macrophage inflammatory protein-1alpha (MIP-1alpha), and MIP-1beta are the natural ligands of th

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

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

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

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

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

59 -17, macrophage inflammatory protein-1alpha (MIP-1alpha), monocyte chemoattractant protein-1 (MCP-1),

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 and macrophage inflammatory protein 1 alpha (MIP-1alpha).

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

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

89 1, macrophage inflammatory protein 1 alpha [MIP-1alpha], MIP-1beta) were significantly diminished or

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

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

92 ) and macrophage inflammatory-protein alpha, MIP-1alpha, both of which show correlation with severe R

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

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

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

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

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

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

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

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

101 -13; IFN-gamma; tumor necrosis factor-alpha; MIP-1alpha/beta; MCP-1 (monocyte chemotactic protein-1);

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

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

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

105 8/CXCL8 (P<0.001), MCP-3/CXCCL7 (P<0.05) and MIP-1alpha/CCL-3 (P<0.05) were significantly upregulated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 -2, keratinocyte cell-derived chemokine, and MIP-1alpha compared with wild-type cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

170 3(MIP-1alpha), CXCR3, CXCL10/IP-10, and CCL3/MIP-1alpha KO mice did not show a significant improvemen

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

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

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

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

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

176 5/MIP-1delta and CCL23/CKbeta8, but not CCL3/MIP-1alpha or CCL5/RANTES, were detected at relatively h

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

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

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

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

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

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

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

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

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

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

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

188 -13 stimulates select CC and CXC chemokines (MIP-1alpha/CCL-3, MIP-1beta/CCL-4, MIP-2/CXCL2/3, MCP-1/

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

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

191 a intracardiac inoculation, mice bearing CHO/MIP-1alpha tumors developed hypercalcemia and significan

192 aring CHO/EV tumors, with intramedullary CHO/MIP-1alpha tumors associated with significantly more tar

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

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

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

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

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

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

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

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

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

202 1B in MM cells and their capacity to express MIP-1alpha was examined.

203 Two cell populations expressed MIP-1alpha: physiologically activated microglia in white

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

230 17 and the lymphocyte chemokines IP-10, MIG, MIP-1alpha, MIP-1beta, and RANTES were decreased in the

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

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

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

234 uman type 5 adenovirus containing the murine MIP-1alpha cDNA (AdMIP-1alpha) was constructed to determ

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

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

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

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

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

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

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

242 by RUNX1/MOZ is discussed in the context of MIP-1alpha's role as an inhibitor of haematopoietic stem

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

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

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

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

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

248 both time- and dose-dependent expression of MIP-1alpha mRNA and protein within the lung.

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

250 ct of transient intrapulmonary expression of MIP-1alpha on leukocyte recruitment, activation, and bac

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

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

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

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

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

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

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

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

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

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

261 -1 receptor (CSF-1R)-dependent production of MIP-1alpha by macrophages was increased.

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

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

264 The regulation of MIP-1alpha expression by RUNX1/MOZ is discussed in the c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

286 not decrease tumor burden, we conclude that MIP-1alpha exerts a dual effect in myeloma, on osteoclas

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 urther demonstrate that MOZ can activate the MIP-1alpha promoter and that this activation is largely

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

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

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

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

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

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

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

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

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