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1 emokines (keratinocyte-derived chemokine and macrophage inflammatory protein-2).
2 and-5, chemokine (C-X-C motif) ligand-1, and macrophage inflammatory protein 2.
3 al marker of neutrophils), and the chemokine macrophage inflammatory protein 2.
4 ukin receptor 1 messenger RNA and release of macrophage inflammatory protein-2.
5 ression of the neutrophil chemotactic factor macrophage inflammatory protein-2.
6 n-1beta, monocyte chemotactic protein-1, and macrophage inflammatory protein-2.
7 and reduced expression of the CXC chemokine, macrophage inflammatory protein-2.
8 l-phenylalanine, zymosan-activated serum, or macrophage inflammatory protein-2.
9 d a striking increase in binding of IL-8 and macrophage inflammatory protein-2.
10 protein-1, KC growth-regulated protein, and macrophage inflammatory protein-2.
11 neutrophil-selective CXC chemokines, KC and macrophage inflammatory protein-2.
12 nflammatory protein-1alpha but not RANTES or macrophage inflammatory protein-2.
13 okine-induced neutrophil chemoattractant and macrophage-inflammatory protein 2.
14 he related, but distinct rat alpha-chemokine macrophage-inflammatory protein 2.
15 onary production of IL-1beta, TNF-alpha, and macrophage-inflammatory protein-2.
16 CL10/IP-10 and increased expression of CXCL2/macrophage-inflammatory protein-2.
17 1beta, a major proinflammatory cytokine, and macrophage inflammatory protein 2, a chemokine involved
18 f LPA in mice resulted in elevated levels of macrophage inflammatory protein-2, a murine homolog of I
19 coli challenge than control mice; moreover, macrophage-inflammatory protein-2 Ab pretreatment preven
20 ng homogenate cytokines TNF-alpha, IL-12, or macrophage-inflammatory protein-2 after K. pneumoniae ad
22 gulation of interleukin-6 (IL-6), IL-10, and macrophage inflammatory protein 2 alpha in the intestine
23 in peritoneal neutrophils, and inhibition of macrophage inflammatory protein-2 also resulted in incre
24 ein kinase phosphorylation and expression of macrophage inflammatory protein 2 (an interleukin-8 homo
25 mor necrosis factor alpha and CXC chemokines macrophage inflammatory protein 2 and KC by neutrophils
26 and lipopolysaccharide was also detected for macrophage inflammatory protein 2 and KC mRNA expression
27 tion resulting in increased airway levels of macrophage inflammatory protein 2 and KC, and higher lun
29 addition, mRNA levels of the CXC chemokines macrophage inflammatory protein 2 and keratinocyte-deriv
30 nal concentrations of inflammatory mediators macrophage inflammatory protein 2 and tumor necrosis fac
31 stimulated production of the CXC chemokines macrophage inflammatory protein-2 and cytokine-induced n
32 ion of the macrophage-derived CXC chemokines macrophage inflammatory protein-2 and KC (IL-8), and of
33 RNA and the protein levels of CXC chemokines macrophage inflammatory protein-2 and KC as well as the
34 ndicate that increases in the CXC chemokines macrophage inflammatory protein-2 and KC precede poor ou
37 ne-induced neutrophil chemoattractant-1, and macrophage inflammatory protein-2 and more sustained ele
38 sociated with significantly lower amounts of macrophage inflammatory protein-2 and reduced numbers of
39 rease in lung levels of the C-X-C chemokine, macrophage inflammatory protein-2 and the C-C chemokines
40 y cytokines tumor necrosis factor- alpha and macrophage inflammatory protein-2 and with a decrease in
41 entrations of NF-kappaB-dependent chemokines macrophage-inflammatory protein 2 and KC and increased n
42 ding, RelA nuclear translocation, and MIP-2 (macrophage inflammatory protein 2) and keratinocyte-deri
43 TNFalpha, macrophage inflammatory protein 1, macrophage inflammatory protein 2, and IFNgamma upon sti
44 terleukin 6, monocyte chemotactic protein 1, macrophage inflammatory protein 2, and inducible nitric
46 ing tumor necrosis factor alpha (TNF-alpha), macrophage inflammatory protein 2, and monocyte chemoatt
47 stimulated gamma interferon, interleukin 6, macrophage inflammatory protein 2, and monocyte chemoatt
49 1beta, IL-6, monocyte chemotactic protein 1, macrophage inflammatory protein 2, and nitrite levels we
50 including keratinocyte-derived chemokine and macrophage inflammatory protein 2, and severe lung neutr
51 ion caused enhanced production of TNF-alpha, macrophage inflammatory protein-2, and cytokine-induced
52 bronchoalveolar lavage levels of TNF-alpha, macrophage inflammatory protein-2, and cytokine-inducibl
53 ediators, including TNF-alpha, IL-1beta, and macrophage inflammatory protein-2, and decreases interst
54 phil-associated tumor necrosis factor-alpha, macrophage inflammatory protein-2, and endothelial-depen
56 ion of proinflammatory cytokines (TNF-alpha, macrophage inflammatory protein-2, and IL-1beta), as wel
57 chemokines, and receptors, such as IL-12p40, macrophage inflammatory protein-2, and IL-6; Ag presenta
58 atory mediators, including TNF-alpha, murine macrophage inflammatory protein-2, and KC/N51, in bronch
59 s, such as interleukin-1beta, interleukin-6, macrophage inflammatory protein-2, and keratinocyte chem
60 veolar lavage fluid concentrations of G-CSF, macrophage inflammatory protein-2, and keratinocyte-deri
61 by Northern blot analysis, binding to [125I]macrophage inflammatory protein-2, and macrophage inflam
62 s onset, mean levels of TNF-alpha, IL-1beta, macrophage inflammatory protein-2, and RANTES were decre
63 RANTES, monocyte chemoattractant protein 1, macrophage-inflammatory protein 2, and cytokine-induced
64 RANTES, monocyte chemoattractant protein 1, macrophage-inflammatory protein 2, and cytokine-induced
65 is showed that protein levels for IL-1 beta, macrophage-inflammatory protein 2, and macrophage-inflam
66 chemokines, including TNF-alpha, IL-1alpha, macrophage-inflammatory protein-2, and KC, but inhibits
67 NF-kappaB-regulated neutrophilic chemokine, macrophage-inflammatory protein-2, and the inflammatory
68 ary neutrophil accumulation, lung IL-1 beta, macrophage-inflammatory protein-2, and TNF-alpha cytokin
70 educed expression of molecules such as IL-6, macrophage-inflammatory protein-2, and vascular endothel
71 lcium flux, induced by the chemokines KC and macrophage inflammatory protein-2, are defective in G6PT
72 with marked early reduction in the level of macrophage inflammatory protein 2 as well as reduced lev
73 Interestingly, the C-X-C chemokine murine macrophage inflammatory protein-2, as well as the C-C ch
74 okine interleukin-6 and the chemokine MIP-2 (macrophage inflammatory protein 2) but impair levels of
75 ibroblasts had less mRNA for IL-1, IL-6, and macrophage-inflammatory protein-2, but TLR4-deficient ce
76 y inhibition of the murine chemokines KC and macrophage inflammatory protein-2 caused a reduction in
77 t indicates reduction in the level of KC and macrophage inflammatory protein-2 chemokine expression i
78 macrophages, both alarmins increased MIP-2 (macrophage inflammatory protein-2) chemokine expression,
79 ne-induced neutrophil chemoattractant-1, and macrophage inflammatory protein-2 contents were increase
80 2,3 (mouse growth-related oncogene-alpha and macrophage-inflammatory protein-2), CXCL10 (IFN-gamma-in
81 We measured levels of myeloperoxidase and macrophage inflammatory protein 2 (CXCL2), trypsinogen a
83 of neutrophil chemoattractant CXC chemokines macrophage inflammatory protein-2/CXCL8 and cytokine-ind
84 In vivo neutralization of highly induced macrophage inflammatory protein 2 did not affect clinica
85 -kappa B and the expression of the chemokine macrophage inflammatory protein-2 did not differ between
86 s through a mechanism that involves CD1d and macrophage inflammatory protein 2 expression by CD8 alph
87 cyte derived cytokine and was independent of macrophage inflammatory protein 2 expression, whereas su
88 eater monocyte chemoattractant protein-1 and macrophage inflammatory protein-2 expression; (2) more m
89 hemoattractant protein-1, interleukin-6, and macrophage inflammatory protein-2 following stimulation
91 ereas tolerogenic APCs secrete the chemokine macrophage-inflammatory protein-2 for the purpose of rec
92 ydrate, which potently induces TNF-alpha and macrophage-inflammatory protein-2 generation from alveol
93 ha and beta, murine macrophage elastase, and macrophage-inflammatory protein-2 genes, while down-regu
94 C chemokine, monocyte chemotactic protein-1, macrophage inflammatory protein-2, granulocyte colony-st
95 genes encoding interleukin-1beta [IL-1beta], macrophage inflammatory protein 2, IL-12, and gamma inte
96 hemoattractant protein-1, interleukin-6, and macrophage inflammatory protein-2, important for neutrop
98 ed a synergistic rise in local production of macrophage inflammatory protein 2 in nasal lavage fluid
99 elevation of tumor necrosis factor alpha and macrophage inflammatory protein 2 in the lung but not in
100 n p47phox-/- mice, LPS-induced production of macrophage inflammatory protein 2 in the lungs and neutr
101 more polymorphonuclear leukocytes (PMN) and macrophage inflammatory protein 2 in the lungs, whereas
102 mpanied by decreased levels of IFN-gamma and macrophage inflammatory protein-2 in anti-IL-18-treated
103 less tumor necrosis factor-alpha, IL-6, and macrophage inflammatory protein-2 in bronchial alveolar
104 nduced neutrophil chemoattractant (CINC) and macrophage inflammatory protein-2 in bronchoalveolar lav
105 neutrophilic influx or the concentration of macrophage inflammatory protein-2 in lung lavage fluid.
106 polymorphonuclear leukocytes, TNF-alpha, and macrophage inflammatory protein-2 in the lavage fluid fo
109 g neutrophil-specific chemokine genes KC and macrophage-inflammatory protein-2, in viable fibroblasts
110 [125I]macrophage inflammatory protein-2, and macrophage inflammatory protein-2-induced calcium respon
111 lung, and decreased levels of blood amylase, macrophage inflammatory protein-2, interleukin 6, and hi
112 n of the important activating cytokines TNF, macrophage inflammatory protein-2, interleukin-12, and g
113 l production of KC and the related chemokine macrophage inflammatory protein-2 is decreased in both B
114 aB-regulated genes, such as IkappaBalpha and macrophage inflammatory protein 2, is minimally affected
115 cell line NR8383 expressed greater levels of macrophage inflammatory protein 2, KC, and tumor necrosi
116 -10, IL-12p70, GM-CSF, IFN-gamma, TNF-alpha, macrophage inflammatory protein-2, KC, macrophage inflam
118 leukocyte counts, murine GRO-alpha (KC), and macrophage inflammatory protein-2 levels were significan
121 ophages, together with an increase of KC and macrophage-inflammatory protein-2 levels in the lung tis
122 pha, macrophage inflammatory protein-1alpha, macrophage inflammatory protein-2, macrophage chemotacti
123 erleukin-1beta, neutrophil chemokine KC, and macrophage inflammatory protein-2 messenger RNA by polym
124 erleukin-1beta, neutrophil chemokine KC, and macrophage inflammatory protein-2 messenger RNA expressi
125 sed expression of the chemoattractants CXCL2/macrophage inflammatory protein 2 (MIP-2) and CXCL1/kera
127 was associated with decreased expression of macrophage inflammatory protein 2 (MIP-2) and MIP-1alpha
128 -induced neutrophil chemoattractant (KC) and macrophage inflammatory protein 2 (MIP-2) in murine plas
129 necrosis factor alpha and chemokines JE and macrophage inflammatory protein 2 (MIP-2) in the lungs o
132 junctival injection with an antibody against macrophage inflammatory protein 2 (MIP-2), a powerful ch
133 tor alpha (TNF-alpha), interleukin-6 (IL-6), macrophage inflammatory protein 2 (MIP-2), and CXCL5/LIX
134 Tumor necrosis factor alpha, interleukin-6, macrophage inflammatory protein 2 (MIP-2), and keratinoc
135 nes, such as keratinocyte-derived chemokine, macrophage inflammatory protein 2 (MIP-2), and lipopolys
136 expression of the ELR(+) CXC chemokines, KC, macrophage inflammatory protein 2 (MIP-2), and lipopolys
137 vels of Keratinocyte-derived chemokine (KC), macrophage inflammatory protein 2 (MIP-2), and MIP-1alph
139 nt study demonstrated that the CXCR2 ligands macrophage inflammatory protein 2 (MIP-2), CXCL1, and CX
140 tion during fecal peritonitis, the levels of macrophage inflammatory protein 2 (MIP-2), IL-10, and MC
141 evels of interleukin-1beta (IL-1beta), IL-2, macrophage inflammatory protein 2 (MIP-2), IL-6, IL-1 re
142 a, IL-22, or IL-17, including genes encoding macrophage inflammatory protein 2 (MIP-2), inducible nit
143 lpha (IL-1alpha) and IL-6 and the chemokines macrophage inflammatory protein 2 (MIP-2), monocyte chem
144 recruitment accompanied by induction of KC, macrophage inflammatory protein 2 (MIP-2), NOS-2, interl
145 x calcium, undergo chemotaxis in response to macrophage inflammatory protein 2 (MIP-2), stain for the
146 xpress the murine homologue of CXCL1, murine macrophage inflammatory protein 2 (MIP-2), under the tra
147 phage colony-stimulating factor (GM-CSF) and macrophage inflammatory protein 2 (MIP-2), was examined,
148 ulator of proinflammatory cytokines, such as macrophage inflammatory protein 2 (MIP-2), which, in tur
151 dulation/and or potentiation of RANTES/CCL5, macrophage inflammatory protein 2 (MIP-2)/CXCL2, IP-10/C
152 rum levels of the neutrophil chemoattractant macrophage inflammatory protein 2 (MIP-2); however, pulm
153 red for 10 days increased neutrophil counts, macrophage inflammatory protein-2 (MIP-2) and chemokine
154 il recruitment, bronchoalveolar lavage (BAL) macrophage inflammatory protein-2 (MIP-2) and cytokine-i
155 e evaluated the roles of two rat chemokines, macrophage inflammatory protein-2 (MIP-2) and cytokine-i
156 o induced mRNA expression of the chemokines, macrophage inflammatory protein-2 (MIP-2) and eotaxin in
157 d that Helicobacter pylori maximally induced macrophage inflammatory protein-2 (MIP-2) and inducible
159 aeruginosa challenge, corneal PMN number and macrophage inflammatory protein-2 (MIP-2) and KC levels
160 ides rapidly up-regulated the CXC chemokines macrophage inflammatory protein-2 (MIP-2) and KC within
163 sma levels of the neutrophil chemoattractant macrophage inflammatory protein-2 (MIP-2) and pulmonary
164 ages with increasing amounts of NaCl induced macrophage inflammatory protein-2 (MIP-2) and tumor necr
165 induced neutrophil chemoattractant (KC), and macrophage inflammatory protein-2 (MIP-2) are rodent che
166 The mRNAs encoding TNF-alpha, COX-2 and macrophage inflammatory protein-2 (MIP-2) bound to hnRNP
167 We studied the expression of the chemokine, macrophage inflammatory protein-2 (MIP-2) by the rat sma
169 nocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-2 (MIP-2) expression in
171 all isolate (PCBG) stimulates the release of macrophage inflammatory protein-2 (MIP-2) from isolated
173 lavage concentrations of IL-8 in humans and macrophage inflammatory protein-2 (MIP-2) in mice occurr
174 nant mouse sICAM-1 induces the production of macrophage inflammatory protein-2 (MIP-2) in mouse astro
175 d neutrophil chemoattractant-1 (CINC-1), and macrophage inflammatory protein-2 (MIP-2) in newborn rat
178 myl-methionyl-leucyl-phenylalanine (fMLP) or macrophage inflammatory protein-2 (MIP-2) next to a venu
179 s in keratinocyte-derived chemokine (KC) and macrophage inflammatory protein-2 (MIP-2) production as
180 phils and macrophages, blocked TNF-alpha and macrophage inflammatory protein-2 (MIP-2) release, and e
181 23 cell line tumor necrosis factor alpha and macrophage inflammatory protein-2 (MIP-2) secretion, but
182 hat neutrophils mobilized in response to rat macrophage inflammatory protein-2 (MIP-2) shed l-selecti
183 own to cause release of cytokines, including macrophage inflammatory protein-2 (MIP-2), a functional
185 ine-induced neutrophil chemoattractant (KC), macrophage inflammatory protein-2 (MIP-2), and epithelia
186 B accompanied by increases in inducible NOS, macrophage inflammatory protein-2 (MIP-2), and ICAM-1 ex
187 in mice, keratinocyte-derived cytokine (KC), macrophage inflammatory protein-2 (MIP-2), and TNF-alpha
188 ion of ELR-containing CXC chemokines such as macrophage inflammatory protein-2 (MIP-2), epithelial ne
189 uced production of several cytokines such as macrophage inflammatory protein-2 (MIP-2), ILs, TNFalpha
190 e synthesis and secretion of the chemokines, macrophage inflammatory protein-2 (Mip-2), KC, and Mip-1
191 rfusion increased expression of TNFalpha and macrophage inflammatory protein-2 (MIP-2), leading to he
192 IP-10), monokine induced by INF-gamma (MIG), macrophage inflammatory protein-2 (MIP-2), lipopolysacch
193 n increase in mRNA for the T-cell chemokines macrophage inflammatory protein-2 (MIP-2), MIP-1beta, an
194 ulation of proinflammatory cytokines such as macrophage inflammatory protein-2 (MIP-2), upregulation
198 ly neutrophil response to SR, with increased macrophage inflammatory protein-2 (MIP-2, murine equival
201 duced neutrophil chemoattractant-1 (CINC-1), macrophage-inflammatory protein-2 (MIP-2), ICAM-1, IL-10
202 ating factor (G-CSF) and chemokines, such as macrophage-inflammatory protein-2 (MIP-2; CXCL2), can in
203 tor alpha [TNF-alpha], interleukin-6 [IL-6], macrophage inflammatory protein-2 [MIP-2], and MIP-1alph
204 ut it reduced levels of bacteremia and serum macrophage inflammatory protein-2) (MIP-2), interleukin-
205 f N-methyl-d-aspartate (NMDA) attenuated the macrophage inflammatory protein 2 (MIP2)-induced protect
206 ion, stimulates the Kupffer cells to produce macrophage inflammatory protein-2 (MIP2) and up-regulate
207 tokine-induced neutrophil chemoattractant-1, macrophage inflammatory protein-2, monocyte chemoattract
208 of several inflammatory chemokines including macrophage-inflammatory protein-2, monocyte chemoattract
209 ha; IFN-inducible protein-10; interleukin-6; macrophage inflammatory protein-2; monocyte chemotactic
210 clear neutrophil number, bacterial load, and macrophage inflammatory protein-2 mRNA and protein level
212 or necrosis factor alpha, interleukin-6, and macrophage inflammatory protein 2 not inhibited by polym
213 es, to significantly stimulate production of macrophage-inflammatory protein 2 or IL-8, TNF-alpha, an
214 concentration of both IL-6 (P = 0.0003) and macrophage inflammatory protein-2 (P = 0.0001) in the la
215 nsulin-like growth factor-binding protein 6, macrophage inflammatory protein 2 precursor, macrophage
216 Dectin-1 is required for P. carinii-induced macrophage inflammatory protein 2 production by alveolar
217 r the tumor necrosis factor-alpha, IL-6, and macrophage inflammatory protein-2 production in LPS-stim
218 ificantly increased neutrophil infiltration, macrophage inflammatory protein-2 production, and lung m
219 ssue destruction appears to be by increasing macrophage inflammatory protein-2 production, resulting
220 , macrophage-inflammatory protein-1alpha and macrophage-inflammatory protein-2 production and prevent
222 showed that keratinocyte-derived chemokine, macrophage inflammatory protein 2, RANTES, tumor necrosi
223 peptidoglycan-stimulated Akt activation and macrophage inflammatory protein-2 release correlated clo
224 atment of primary wild-type hepatocytes with macrophage inflammatory protein-2 revealed that low conc
225 istic regression model indicated that KC and macrophage inflammatory protein-2, rodent homologues of
227 of airway keratinocyte-derived chemokine and macrophage inflammatory protein-2 significantly improves
228 ver, CXC chemokines with ELR motifs, KC, and macrophage-inflammatory protein 2, significantly increas
229 a], tumor necrosis factor alpha), chemokine (macrophage inflammatory protein 2), Th1/Th2 indicator (I
230 erleukin (IL-12) and C-X-C chemokines KC and macrophage inflammatory protein 2 than similarly treated
231 the keratinocyte-derived chemokine, RANTES, macrophage inflammatory protein 2, tumor necrosis factor
232 utrophil influx, cytokine and chemokine (KC, macrophage inflammatory protein 2, tumor necrosis factor
233 ion of LIX, tumor necrosis factor alpha, and macrophage inflammatory protein 2 was confirmed at the p
234 a, IL-6, monocyte chemotactic protein 1, and macrophage inflammatory protein 2 was decreased on the f
235 the proinflammatory mediators TNF-alpha and macrophage inflammatory protein-2 was inhibited in a dos
237 mortalized murine melanocytes overexpressing macrophage inflammatory protein-2, was inhibited or enha
238 e synthase, tumor necrosis factor alpha, and macrophage inflammatory protein-2, was significantly att
239 hesion molecule 1, Toll-like receptor 4, and macrophage inflammatory protein 2 were all up-regulated.
240 ntrations of tumor necrosis factor alpha and macrophage inflammatory protein 2 were measured by enzym
241 ntaining sequences based on beta-amyloid and macrophage inflammatory protein 2 were synthesized and c
242 okine-induced neutrophil chemoattractant and macrophage inflammatory protein-2 were greatly reduced i
243 hemokines keratinocyte-derived chemokine and macrophage inflammatory protein-2 were significantly low
244 significantly lower levels of TNF-alpha and macrophage-inflammatory protein-2 were detected in genit
245 pulmonary levels of IL-1beta, TNF-alpha, or macrophage-inflammatory protein-2 were not decreased aft
246 olecule 1, keratinocyte chemoattractant, and macrophage inflammatory protein 2, which favored neutrop
247 , macrophage-inflammatory protein-1beta, and macrophage-inflammatory protein-2, with concurrent inhib
248 t cytokines such as interleukin-1a, MIG, and macrophage inflammatory protein-2 within the tumor and t
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