Degenerative polyarthritis
|
0.330 |
AlteredExpression
|
disease |
BEFREE |
Comparative expression pattern analysis revealed the involvement of catabolic enzymes (MMP1, -2, -13, ADAM10), chemokines (IL8, CCL2, CXCL2, CXCL12, CCXL14), and genes associated with cell death (TNFSF10, PMAIPI, AHR) and skeletal development (GPNMB, FRZB) including transcription factors (WIF1, DLX5, TWIST1) and growth factors (IGFBP1, -3, TGFB1) consistent with published data from human OA cartilage.
|
24635637 |
2014 |
Degenerative polyarthritis
|
0.330 |
AlteredExpression
|
disease |
BEFREE |
Except for interleukin-1β (IL-1β) and CXCL2, the mRNA (messenger RNA) expression of all other chemokine (IL-8, CXCL1, CXCL3, CXCL6, CCL3, and CCL3L1), matrix-degrading (matrix metalloproteinase [MMP]-13 and ADAMTS-4), and structural matrix (COL2A1 [collagen, type II, alpha] and ACAN [aggregan]) genes was higher overall in cartilage from hips with femoroacetabular impingement compared with hips with osteoarthritis and normal controls.
|
23965695 |
2013 |
Degenerative polyarthritis
|
0.330 |
Biomarker
|
disease |
BEFREE |
While these differences may represent differential behaviour of synovial fibroblasts in in vitro culture, these observations suggest that TFPI2, GRObeta (CXCL2), MnSOD and GCP-2 (CXCL6) may represent new targets for treatments specifically tailored to osteoarthritis.
|
15292528 |
2004 |
Rheumatoid Arthritis
|
0.320 |
AlteredExpression
|
disease |
BEFREE |
We found that early arthritis triggered by obesity is due to elevated joint MIP2/interleukin-8 levels detected in CIA as well as in the RA and mouse adipose tissues and the effect of this chemokine on neutrophil recruitment.
|
27797749 |
2017 |
Rheumatoid Arthritis
|
0.320 |
Biomarker
|
disease |
BEFREE |
Plasminogen (PLG) and related DEGs such as chemokine (C-X-C motif) ligand 2 (CXCL2), laminin, alpha 3 (LAMA3), complement component 7 (C7), and coagulation factor X (F10) were identified in 4 submodules.Our results indicate that DLG1, GUCY1A2, GRIN2A, KCNA1, PLG, CXCL2, LAMA3, C7, and F10 may play key roles in the progression of RA and may serve as putative therapeutic targets for treating RA.
|
28767591 |
2017 |
Chronic Obstructive Airway Disease
|
0.310 |
Biomarker
|
disease |
BEFREE |
Within this context, we now show increased expression of the C-X-C chemokines (CXCL1 and CXCL2) and their receptor CXCR2, and the intercellular cellular adhesion molecule-1 (ICAM-1), in the lung tissues of patients with COPD.
|
26747783 |
2016 |
Esophageal Neoplasms
|
0.310 |
AlteredExpression
|
group |
BEFREE |
The analyses pointed out the potential importance of CXCL2, and monitoring CXCL2 with quantitative videomicroscopy indicated that its biologic activity was silenced in OE21 esophageal cancer cells.
|
21509778 |
2011 |
Malignant neoplasm of esophagus
|
0.310 |
AlteredExpression
|
disease |
BEFREE |
The analyses pointed out the potential importance of CXCL2, and monitoring CXCL2 with quantitative videomicroscopy indicated that its biologic activity was silenced in OE21 esophageal cancer cells.
|
21509778 |
2011 |
Pneumonia
|
0.260 |
Biomarker
|
disease |
BEFREE |
Thus, our data indicate that PLAG may represent a potential therapeutic agent for resolution of LPS-induced lung inflammation through effective MIP-2 modulation.
|
31620122 |
2019 |
Pneumonia
|
0.260 |
Biomarker
|
disease |
BEFREE |
TNF-α, MIP-2α, and injury score at 6 h IRB returned to control. p38 activation contributes to IRB-induced pulmonary inflammation.
|
29974374 |
2018 |
Pneumonia
|
0.260 |
Biomarker
|
disease |
BEFREE |
We then treated mice with PvdQ during lethal <i>P. aeruginosa</i> pulmonary infection and that resulted in a 5-fold reduction of lung bacterial load and a prolonged survival of the infected animals with the median survival time of 57 hin comparison to 42 h for the PBS-treated group.In a sublethal <i>P. aeruginosa</i> pulmonary infection, PvdQ treatment resulted in less lung inflammation as well as decrease of CXCL2 and TNF-α levels at 24 h post-bacterial-infection by 15 and 20%, respectively.
|
29755959 |
2018 |
Pneumonia
|
0.260 |
Biomarker
|
disease |
BEFREE |
We found that loss of ACE2 function in mouse lung in the setting of endotoxin inhalation led to activation of the DABK/BKB1R axis, release of proinflammatory chemokines such as C-X-C motif chemokine 5 (CXCL5), macrophage inflammatory protein-2 (MIP2), C-X-C motif chemokine 1 (KC), and TNF-α from airway epithelia, increased neutrophil infiltration, and exaggerated lung inflammation and injury.
|
28935640 |
2018 |
Pneumonia
|
0.260 |
AlteredExpression
|
disease |
BEFREE |
We additionally show that chronic CS exposure in mice promoted AMPK phosphorylation and expression of MIP-2α (an IL-8 homolog) in LECs and lungs, as well as lung inflammation, all of which were reduced by Compound C treatment.
|
21376115 |
2011 |
Pneumonia
|
0.260 |
Biomarker
|
disease |
BEFREE |
Given the bioactivities of MIP-1 alpha and beta and MIP-2 and the recent studies demonstrating their association with lung inflammation, it is likely these chemokines play a significant role in respiratory tract defenses and may contribute to the pathogenesis of inflammatory lung disease.
|
7882902 |
1995 |
Lung diseases
|
0.210 |
Biomarker
|
group |
BEFREE |
Given the bioactivities of MIP-1 alpha and beta and MIP-2 and the recent studies demonstrating their association with lung inflammation, it is likely these chemokines play a significant role in respiratory tract defenses and may contribute to the pathogenesis of inflammatory lung disease.
|
7882902 |
1995 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The underlying mechanism for this transformation by ttIL-12 treatment was induction of expression of CXCL9 and reduction of expression of CXCL2 and CCL22 in tumors.
|
31208461 |
2019 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In addition, tumors with higher CXCL2 expression included significantly more numbers of multiple tumors than the lower expression group.
|
30564899 |
2019 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In the validation cohort, however, only the changes in the plasma levels of CXCL2 and MMP2 after treatment were associated with PFS (p = 0.003 and p = 0.006, respectively), and these changes were maintained during the course of anti-PD-1 therapy in patients who showed better clinical outcomes, even in those with tumor pseudoprogression.
|
30307035 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Addition of MMM to colon tumors <i>in vivo</i> significantly enhances tumor growth in control tumors and restores tumor growth in the presence of MK2 inhibition.
|
30298062 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Chemokine (C-X-C motif) ligand 1 and CXCL2 produced by tumor promote the generation of monocytic myeloid-derived suppressor cells.
|
30259595 |
2018 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Tumor cell growth in Emilin2 null mice was impaired as well as the expression of MIP-2.
|
29483644 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In animal studies, we found that overexpressing CXCL2 by lentivirus also apparently inhibited the size and weight of subcutaneous tumours in nude mice.
|
30293547 |
2018 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Furthermore, we showed that MDSC recruitment to the primary tumor and metastatic sites occurs via direct ΔNp63-dependent activation of the chemokines CXCL2 and CCL22.
|
30295647 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Snail knockdown reduces the expression of CXCR2 ligands (CXCL1 and CXCL2), chemokines that attract MDSCs to the tumor via CXCR2.
|
29703902 |
2018 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Analysis of immune cells revealed that CXCR2 ligands (CXCL1, CXCL 2 and CXCL5) expressed by TNFα-activated MSCs efficiently recruited CXCR2<sup>+</sup> neutrophils into tumor.
|
27375023 |
2017 |