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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 ression of the neutrophil chemotactic factor macrophage inflammatory protein-2.
5 n-1beta, monocyte chemotactic protein-1, and macrophage inflammatory protein-2.
6 and reduced expression of the CXC chemokine, macrophage inflammatory protein-2.
7 l-phenylalanine, zymosan-activated serum, or macrophage inflammatory protein-2.
8 ukin receptor 1 messenger RNA and release of 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 CL10/IP-10 and increased expression of CXCL2/macrophage-inflammatory protein-2.
16 onary production of IL-1beta, TNF-alpha, and 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 e chemotactic protein 2 (GCP-2; p < 0.0001), macrophage inflammatory protein 2-alpha (GRObeta; p = 0.
24 in peritoneal neutrophils, and inhibition of macrophage inflammatory protein-2 also resulted in incre
25 ein kinase phosphorylation and expression of macrophage inflammatory protein 2 (an interleukin-8 homo
26 mor necrosis factor alpha and CXC chemokines macrophage inflammatory protein 2 and KC by neutrophils
27 and lipopolysaccharide was also detected for macrophage inflammatory protein 2 and KC mRNA expression
28 tion resulting in increased airway levels of macrophage inflammatory protein 2 and KC, and higher lun
30 addition, mRNA levels of the CXC chemokines macrophage inflammatory protein 2 and keratinocyte-deriv
31 nal concentrations of inflammatory mediators macrophage inflammatory protein 2 and tumor necrosis fac
32 stimulated production of the CXC chemokines macrophage inflammatory protein-2 and cytokine-induced n
33 ion of the macrophage-derived CXC chemokines macrophage inflammatory protein-2 and KC (IL-8), and of
34 RNA and the protein levels of CXC chemokines macrophage inflammatory protein-2 and KC as well as the
35 ndicate that increases in the CXC chemokines macrophage inflammatory protein-2 and KC precede poor ou
38 ne-induced neutrophil chemoattractant-1, and macrophage inflammatory protein-2 and more sustained ele
39 sociated with significantly lower amounts of macrophage inflammatory protein-2 and reduced numbers of
40 rease in lung levels of the C-X-C chemokine, macrophage inflammatory protein-2 and the C-C chemokines
41 y cytokines tumor necrosis factor- alpha and macrophage inflammatory protein-2 and with a decrease in
42 entrations of NF-kappaB-dependent chemokines macrophage-inflammatory protein 2 and KC and increased n
43 ding, RelA nuclear translocation, and MIP-2 (macrophage inflammatory protein 2) and keratinocyte-deri
44 TNFalpha, macrophage inflammatory protein 1, macrophage inflammatory protein 2, and IFNgamma upon sti
45 terleukin 6, monocyte chemotactic protein 1, macrophage inflammatory protein 2, and inducible nitric
47 ing tumor necrosis factor alpha (TNF-alpha), macrophage inflammatory protein 2, and monocyte chemoatt
48 stimulated gamma interferon, interleukin 6, macrophage inflammatory protein 2, and monocyte chemoatt
50 1beta, IL-6, monocyte chemotactic protein 1, macrophage inflammatory protein 2, and nitrite levels we
51 including keratinocyte-derived chemokine and macrophage inflammatory protein 2, and severe lung neutr
52 ion caused enhanced production of TNF-alpha, macrophage inflammatory protein-2, and cytokine-induced
53 bronchoalveolar lavage levels of TNF-alpha, macrophage inflammatory protein-2, and cytokine-inducibl
54 ediators, including TNF-alpha, IL-1beta, and macrophage inflammatory protein-2, and decreases interst
55 phil-associated tumor necrosis factor-alpha, macrophage inflammatory protein-2, and endothelial-depen
57 ion of proinflammatory cytokines (TNF-alpha, macrophage inflammatory protein-2, and IL-1beta), as wel
58 chemokines, and receptors, such as IL-12p40, macrophage inflammatory protein-2, and IL-6; Ag presenta
59 atory mediators, including TNF-alpha, murine macrophage inflammatory protein-2, and KC/N51, in bronch
60 s, such as interleukin-1beta, interleukin-6, macrophage inflammatory protein-2, and keratinocyte chem
61 veolar lavage fluid concentrations of G-CSF, macrophage inflammatory protein-2, and keratinocyte-deri
62 by Northern blot analysis, binding to [125I]macrophage inflammatory protein-2, and macrophage inflam
63 s onset, mean levels of TNF-alpha, IL-1beta, macrophage inflammatory protein-2, and RANTES were decre
64 RANTES, monocyte chemoattractant protein 1, macrophage-inflammatory protein 2, and cytokine-induced
65 RANTES, monocyte chemoattractant protein 1, macrophage-inflammatory protein 2, and cytokine-induced
66 is showed that protein levels for IL-1 beta, macrophage-inflammatory protein 2, and macrophage-inflam
67 chemokines, including TNF-alpha, IL-1alpha, macrophage-inflammatory protein-2, and KC, but inhibits
68 NF-kappaB-regulated neutrophilic chemokine, macrophage-inflammatory protein-2, and the inflammatory
69 ary neutrophil accumulation, lung IL-1 beta, macrophage-inflammatory protein-2, and TNF-alpha cytokin
71 educed expression of molecules such as IL-6, macrophage-inflammatory protein-2, and vascular endothel
72 lcium flux, induced by the chemokines KC and macrophage inflammatory protein-2, are defective in G6PT
73 with marked early reduction in the level of macrophage inflammatory protein 2 as well as reduced lev
74 Interestingly, the C-X-C chemokine murine macrophage inflammatory protein-2, as well as the C-C ch
75 okine interleukin-6 and the chemokine MIP-2 (macrophage inflammatory protein 2) but impair levels of
76 ibroblasts had less mRNA for IL-1, IL-6, and macrophage-inflammatory protein-2, but TLR4-deficient ce
77 y inhibition of the murine chemokines KC and macrophage inflammatory protein-2 caused a reduction in
78 t indicates reduction in the level of KC and macrophage inflammatory protein-2 chemokine expression i
79 macrophages, both alarmins increased MIP-2 (macrophage inflammatory protein-2) chemokine expression,
80 ne-induced neutrophil chemoattractant-1, and macrophage inflammatory protein-2 contents were increase
81 2,3 (mouse growth-related oncogene-alpha and macrophage-inflammatory protein-2), CXCL10 (IFN-gamma-in
82 We measured levels of myeloperoxidase and macrophage inflammatory protein 2 (CXCL2), trypsinogen a
84 of neutrophil chemoattractant CXC chemokines macrophage inflammatory protein-2/CXCL8 and cytokine-ind
85 In vivo neutralization of highly induced macrophage inflammatory protein 2 did not affect clinica
86 -kappa B and the expression of the chemokine macrophage inflammatory protein-2 did not differ between
87 y increased pulmonary edema, elevated plasma macrophage inflammatory protein 2, enhanced neutrophil l
88 s through a mechanism that involves CD1d and macrophage inflammatory protein 2 expression by CD8 alph
89 cyte derived cytokine and was independent of macrophage inflammatory protein 2 expression, whereas su
90 eater monocyte chemoattractant protein-1 and macrophage inflammatory protein-2 expression; (2) more m
91 hemoattractant protein-1, interleukin-6, and macrophage inflammatory protein-2 following stimulation
93 ereas tolerogenic APCs secrete the chemokine macrophage-inflammatory protein-2 for the purpose of rec
94 ydrate, which potently induces TNF-alpha and macrophage-inflammatory protein-2 generation from alveol
95 ha and beta, murine macrophage elastase, and macrophage-inflammatory protein-2 genes, while down-regu
96 C chemokine, monocyte chemotactic protein-1, macrophage inflammatory protein-2, granulocyte colony-st
97 genes encoding interleukin-1beta [IL-1beta], macrophage inflammatory protein 2, IL-12, and gamma inte
98 hemoattractant protein-1, interleukin-6, and macrophage inflammatory protein-2, important for neutrop
100 ed a synergistic rise in local production of macrophage inflammatory protein 2 in nasal lavage fluid
101 elevation of tumor necrosis factor alpha and macrophage inflammatory protein 2 in the lung but not in
102 n p47phox-/- mice, LPS-induced production of macrophage inflammatory protein 2 in the lungs and neutr
103 more polymorphonuclear leukocytes (PMN) and macrophage inflammatory protein 2 in the lungs, whereas
104 mpanied by decreased levels of IFN-gamma and macrophage inflammatory protein-2 in anti-IL-18-treated
105 less tumor necrosis factor-alpha, IL-6, and macrophage inflammatory protein-2 in bronchial alveolar
106 nduced neutrophil chemoattractant (CINC) and macrophage inflammatory protein-2 in bronchoalveolar lav
107 neutrophilic influx or the concentration of macrophage inflammatory protein-2 in lung lavage fluid.
108 polymorphonuclear leukocytes, TNF-alpha, and macrophage inflammatory protein-2 in the lavage fluid fo
111 g neutrophil-specific chemokine genes KC and macrophage-inflammatory protein-2, in viable fibroblasts
112 [125I]macrophage inflammatory protein-2, and macrophage inflammatory protein-2-induced calcium respon
113 lung, and decreased levels of blood amylase, macrophage inflammatory protein-2, interleukin 6, and hi
114 n of the important activating cytokines TNF, macrophage inflammatory protein-2, interleukin-12, and g
115 l production of KC and the related chemokine macrophage inflammatory protein-2 is decreased in both B
116 aB-regulated genes, such as IkappaBalpha and macrophage inflammatory protein 2, is minimally affected
117 cell line NR8383 expressed greater levels of macrophage inflammatory protein 2, KC, and tumor necrosi
118 -10, IL-12p70, GM-CSF, IFN-gamma, TNF-alpha, macrophage inflammatory protein-2, KC, macrophage inflam
120 leukocyte counts, murine GRO-alpha (KC), and macrophage inflammatory protein-2 levels were significan
123 ophages, together with an increase of KC and macrophage-inflammatory protein-2 levels in the lung tis
124 pha, macrophage inflammatory protein-1alpha, macrophage inflammatory protein-2, macrophage chemotacti
125 erleukin-1beta, neutrophil chemokine KC, and macrophage inflammatory protein-2 messenger RNA by polym
126 erleukin-1beta, neutrophil chemokine KC, and macrophage inflammatory protein-2 messenger RNA expressi
127 sed expression of the chemoattractants CXCL2/macrophage inflammatory protein 2 (MIP-2) and CXCL1/kera
129 was associated with decreased expression of macrophage inflammatory protein 2 (MIP-2) and MIP-1alpha
130 responses, Interleukin-6 (IL-6) in serum and Macrophage Inflammatory Protein 2 (MIP-2) in liver signi
131 -induced neutrophil chemoattractant (KC) and macrophage inflammatory protein 2 (MIP-2) in murine plas
132 necrosis factor alpha and chemokines JE and macrophage inflammatory protein 2 (MIP-2) in the lungs o
135 junctival injection with an antibody against macrophage inflammatory protein 2 (MIP-2), a powerful ch
136 tor alpha (TNF-alpha), interleukin-6 (IL-6), macrophage inflammatory protein 2 (MIP-2), and CXCL5/LIX
137 Tumor necrosis factor alpha, interleukin-6, macrophage inflammatory protein 2 (MIP-2), and keratinoc
138 nes, such as keratinocyte-derived chemokine, macrophage inflammatory protein 2 (MIP-2), and lipopolys
139 expression of the ELR(+) CXC chemokines, KC, macrophage inflammatory protein 2 (MIP-2), and lipopolys
140 vels of Keratinocyte-derived chemokine (KC), macrophage inflammatory protein 2 (MIP-2), and MIP-1alph
142 nt study demonstrated that the CXCR2 ligands macrophage inflammatory protein 2 (MIP-2), CXCL1, and CX
143 tion during fecal peritonitis, the levels of macrophage inflammatory protein 2 (MIP-2), IL-10, and MC
144 evels of interleukin-1beta (IL-1beta), IL-2, macrophage inflammatory protein 2 (MIP-2), IL-6, IL-1 re
145 a, IL-22, or IL-17, including genes encoding macrophage inflammatory protein 2 (MIP-2), inducible nit
146 lpha (IL-1alpha) and IL-6 and the chemokines macrophage inflammatory protein 2 (MIP-2), monocyte chem
147 recruitment accompanied by induction of KC, macrophage inflammatory protein 2 (MIP-2), NOS-2, interl
148 x calcium, undergo chemotaxis in response to macrophage inflammatory protein 2 (MIP-2), stain for the
149 xpress the murine homologue of CXCL1, murine macrophage inflammatory protein 2 (MIP-2), under the tra
150 phage colony-stimulating factor (GM-CSF) and macrophage inflammatory protein 2 (MIP-2), was examined,
151 (FKS) stimulate mouse macrophages to secret macrophage inflammatory protein 2 (MIP-2), which suggest
152 ulator of proinflammatory cytokines, such as macrophage inflammatory protein 2 (MIP-2), which, in tur
155 dulation/and or potentiation of RANTES/CCL5, macrophage inflammatory protein 2 (MIP-2)/CXCL2, IP-10/C
156 rum levels of the neutrophil chemoattractant macrophage inflammatory protein 2 (MIP-2); however, pulm
157 red for 10 days increased neutrophil counts, macrophage inflammatory protein-2 (MIP-2) and chemokine
158 il recruitment, bronchoalveolar lavage (BAL) macrophage inflammatory protein-2 (MIP-2) and cytokine-i
159 e evaluated the roles of two rat chemokines, macrophage inflammatory protein-2 (MIP-2) and cytokine-i
160 o induced mRNA expression of the chemokines, macrophage inflammatory protein-2 (MIP-2) and eotaxin in
161 d that Helicobacter pylori maximally induced macrophage inflammatory protein-2 (MIP-2) and inducible
163 aeruginosa challenge, corneal PMN number and macrophage inflammatory protein-2 (MIP-2) and KC levels
164 ides rapidly up-regulated the CXC chemokines macrophage inflammatory protein-2 (MIP-2) and KC within
167 sma levels of the neutrophil chemoattractant macrophage inflammatory protein-2 (MIP-2) and pulmonary
168 ages with increasing amounts of NaCl induced macrophage inflammatory protein-2 (MIP-2) and tumor necr
169 induced neutrophil chemoattractant (KC), and macrophage inflammatory protein-2 (MIP-2) are rodent che
170 The mRNAs encoding TNF-alpha, COX-2 and macrophage inflammatory protein-2 (MIP-2) bound to hnRNP
171 We studied the expression of the chemokine, macrophage inflammatory protein-2 (MIP-2) by the rat sma
173 nocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-2 (MIP-2) expression in
175 all isolate (PCBG) stimulates the release of macrophage inflammatory protein-2 (MIP-2) from isolated
177 lavage concentrations of IL-8 in humans and macrophage inflammatory protein-2 (MIP-2) in mice occurr
178 nant mouse sICAM-1 induces the production of macrophage inflammatory protein-2 (MIP-2) in mouse astro
179 d neutrophil chemoattractant-1 (CINC-1), and macrophage inflammatory protein-2 (MIP-2) in newborn rat
182 myl-methionyl-leucyl-phenylalanine (fMLP) or macrophage inflammatory protein-2 (MIP-2) next to a venu
183 s in keratinocyte-derived chemokine (KC) and macrophage inflammatory protein-2 (MIP-2) production as
184 phils and macrophages, blocked TNF-alpha and macrophage inflammatory protein-2 (MIP-2) release, and e
185 23 cell line tumor necrosis factor alpha and macrophage inflammatory protein-2 (MIP-2) secretion, but
186 hat neutrophils mobilized in response to rat macrophage inflammatory protein-2 (MIP-2) shed l-selecti
187 own to cause release of cytokines, including macrophage inflammatory protein-2 (MIP-2), a functional
189 ine-induced neutrophil chemoattractant (KC), macrophage inflammatory protein-2 (MIP-2), and epithelia
190 B accompanied by increases in inducible NOS, macrophage inflammatory protein-2 (MIP-2), and ICAM-1 ex
191 in mice, keratinocyte-derived cytokine (KC), macrophage inflammatory protein-2 (MIP-2), and TNF-alpha
192 ion of ELR-containing CXC chemokines such as macrophage inflammatory protein-2 (MIP-2), epithelial ne
193 uced production of several cytokines such as macrophage inflammatory protein-2 (MIP-2), ILs, TNFalpha
194 e synthesis and secretion of the chemokines, macrophage inflammatory protein-2 (Mip-2), KC, and Mip-1
195 rfusion increased expression of TNFalpha and macrophage inflammatory protein-2 (MIP-2), leading to he
196 IP-10), monokine induced by INF-gamma (MIG), macrophage inflammatory protein-2 (MIP-2), lipopolysacch
197 n increase in mRNA for the T-cell chemokines macrophage inflammatory protein-2 (MIP-2), MIP-1beta, an
198 ulation of proinflammatory cytokines such as macrophage inflammatory protein-2 (MIP-2), upregulation
203 ly neutrophil response to SR, with increased macrophage inflammatory protein-2 (MIP-2, murine equival
206 duced neutrophil chemoattractant-1 (CINC-1), macrophage-inflammatory protein-2 (MIP-2), ICAM-1, IL-10
207 ating factor (G-CSF) and chemokines, such as macrophage-inflammatory protein-2 (MIP-2; CXCL2), can in
208 tor alpha [TNF-alpha], interleukin-6 [IL-6], macrophage inflammatory protein-2 [MIP-2], and MIP-1alph
209 ut it reduced levels of bacteremia and serum macrophage inflammatory protein-2) (MIP-2), interleukin-
210 f N-methyl-d-aspartate (NMDA) attenuated the macrophage inflammatory protein 2 (MIP2)-induced protect
211 ion, stimulates the Kupffer cells to produce macrophage inflammatory protein-2 (MIP2) and up-regulate
212 sion of keratinocyte derived chemokine (Kc), macrophage inflammatory protein-2 (Mip2), granulocyte-ma
213 tokine-induced neutrophil chemoattractant-1, macrophage inflammatory protein-2, monocyte chemoattract
214 of several inflammatory chemokines including macrophage-inflammatory protein-2, monocyte chemoattract
215 ha; IFN-inducible protein-10; interleukin-6; macrophage inflammatory protein-2; monocyte chemotactic
216 clear neutrophil number, bacterial load, and macrophage inflammatory protein-2 mRNA and protein level
218 or necrosis factor alpha, interleukin-6, and macrophage inflammatory protein 2 not inhibited by polym
219 es, to significantly stimulate production of macrophage-inflammatory protein 2 or IL-8, TNF-alpha, an
220 concentration of both IL-6 (P = 0.0003) and macrophage inflammatory protein-2 (P = 0.0001) in the la
221 nsulin-like growth factor-binding protein 6, macrophage inflammatory protein 2 precursor, macrophage
222 Dectin-1 is required for P. carinii-induced macrophage inflammatory protein 2 production by alveolar
223 r the tumor necrosis factor-alpha, IL-6, and macrophage inflammatory protein-2 production in LPS-stim
224 ificantly increased neutrophil infiltration, macrophage inflammatory protein-2 production, and lung m
225 ssue destruction appears to be by increasing macrophage inflammatory protein-2 production, resulting
226 , macrophage-inflammatory protein-1alpha and macrophage-inflammatory protein-2 production and prevent
228 showed that keratinocyte-derived chemokine, macrophage inflammatory protein 2, RANTES, tumor necrosi
229 peptidoglycan-stimulated Akt activation and macrophage inflammatory protein-2 release correlated clo
230 atment of primary wild-type hepatocytes with macrophage inflammatory protein-2 revealed that low conc
231 istic regression model indicated that KC and macrophage inflammatory protein-2, rodent homologues of
233 of airway keratinocyte-derived chemokine and macrophage inflammatory protein-2 significantly improves
234 ver, CXC chemokines with ELR motifs, KC, and macrophage-inflammatory protein 2, significantly increas
235 a], tumor necrosis factor alpha), chemokine (macrophage inflammatory protein 2), Th1/Th2 indicator (I
236 erleukin (IL-12) and C-X-C chemokines KC and macrophage inflammatory protein 2 than similarly treated
237 the keratinocyte-derived chemokine, RANTES, macrophage inflammatory protein 2, tumor necrosis factor
238 utrophil influx, cytokine and chemokine (KC, macrophage inflammatory protein 2, tumor necrosis factor
239 ion of LIX, tumor necrosis factor alpha, and macrophage inflammatory protein 2 was confirmed at the p
240 a, IL-6, monocyte chemotactic protein 1, and macrophage inflammatory protein 2 was decreased on the f
241 the proinflammatory mediators TNF-alpha and macrophage inflammatory protein-2 was inhibited in a dos
243 mortalized murine melanocytes overexpressing macrophage inflammatory protein-2, was inhibited or enha
244 e synthase, tumor necrosis factor alpha, and macrophage inflammatory protein-2, was significantly att
245 hesion molecule 1, Toll-like receptor 4, and macrophage inflammatory protein 2 were all up-regulated.
246 ntrations of tumor necrosis factor alpha and macrophage inflammatory protein 2 were measured by enzym
247 ntaining sequences based on beta-amyloid and macrophage inflammatory protein 2 were synthesized and c
248 okine-induced neutrophil chemoattractant and macrophage inflammatory protein-2 were greatly reduced i
249 hemokines keratinocyte-derived chemokine and macrophage inflammatory protein-2 were significantly low
250 significantly lower levels of TNF-alpha and macrophage-inflammatory protein-2 were detected in genit
251 pulmonary levels of IL-1beta, TNF-alpha, or macrophage-inflammatory protein-2 were not decreased aft
252 olecule 1, keratinocyte chemoattractant, and macrophage inflammatory protein 2, which favored neutrop
253 , macrophage-inflammatory protein-1beta, and macrophage-inflammatory protein-2, with concurrent inhib
254 t cytokines such as interleukin-1a, MIG, and macrophage inflammatory protein-2 within the tumor and t