Pneumonia
|
0.580 |
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
|
0.580 |
Biomarker
|
disease |
BEFREE |
Thus, macrophage-FABP4 has a novel role in pulmonary host defense against P. aeruginosa infection by facilitating crosstalk between macrophages and neutrophils via regulation of macrophage CXCL1 production.-Liang, X., Gupta, K., Rojas Quintero, J., Cernadas, M., Kobzik, L., Christou, H., Pier, G. B., Owen, C. A., Çataltepe, S. Macrophage FABP4 is required for neutrophil recruitment and bacterial clearance in Pseudomonas aeruginosa pneumonia.
|
30462529 |
2019 |
Pneumonia
|
0.580 |
AlteredExpression
|
disease |
BEFREE |
In contrast neutrophil infiltration in the lung is unaffected by platelet reduction, up-regulation of CXCL-1 (2·4-fold) and CCL5 (1·4-fold) acting as a compensatory mechanism in platelet-reduced mice during lung inflammation.
|
29325217 |
2018 |
Pneumonia
|
0.580 |
Biomarker
|
disease |
BEFREE |
CONCLUSIONS S100A9 and S100A12 may have a role in the pathogenesis of pneumonia: S100A9 and CXCL1 may contribute solely in mild pneumonia, and CCL5 and CXCL11 may contribute in severe pneumonia.
|
28381820 |
2017 |
Pneumonia
|
0.580 |
Biomarker
|
disease |
BEFREE |
Biologically significant amounts of GRO are present in vivo in the bronchoalveolar lavage fluid of rabbits with E. coli pneumonia; by in situ hybridization, GRO mRNA is detectable in infiltrating pulmonary leukocytes and bronchial epithelial cells.
|
8631900 |
1996 |
Pneumonia
|
0.580 |
Biomarker
|
disease |
BEFREE |
Our study reveals that p53-mediated induction of PAI-1 expression due to chronic CS exposure exacerbates lung inflammation through elaboration of CXCL1, CXCL2, and CXCR2.
|
26747783 |
2016 |
Pneumonia
|
0.580 |
Biomarker
|
disease |
BEFREE |
Mice deficient for chromosome 3 GBPs were unable to mount a rapid IL-1/chemokine (C-X-C motif) ligand 1 (CXCL1) response during Legionella-induced pneumonia, with defective bacterial clearance.
|
29972777 |
2018 |
Pneumonia
|
0.580 |
AlteredExpression
|
disease |
BEFREE |
AE inhibited PS colonization (p < 0.001) and lung inflammation (total cells, neutrophils, lymphocytes [p < 0.01] in bronchoalveolar lavage [BAL]), with significant differences in BAL levels of IL-1β (p < 0.001), IL-6 (p < 0.01), CXCL1 (p < 0.001), and TNF-α (p < 0.001), as well as parenchymal neutrophils (p < 0.001).
|
29843140 |
2018 |
Pneumonitis
|
0.350 |
AlteredExpression
|
disease |
BEFREE |
AE inhibited PS colonization (p < 0.001) and lung inflammation (total cells, neutrophils, lymphocytes [p < 0.01] in bronchoalveolar lavage [BAL]), with significant differences in BAL levels of IL-1β (p < 0.001), IL-6 (p < 0.01), CXCL1 (p < 0.001), and TNF-α (p < 0.001), as well as parenchymal neutrophils (p < 0.001).
|
29843140 |
2018 |
Pneumonitis
|
0.350 |
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 |
Pneumonitis
|
0.350 |
Biomarker
|
disease |
BEFREE |
Our study reveals that p53-mediated induction of PAI-1 expression due to chronic CS exposure exacerbates lung inflammation through elaboration of CXCL1, CXCL2, and CXCR2.
|
26747783 |
2016 |
Pneumonitis
|
0.350 |
AlteredExpression
|
disease |
BEFREE |
In contrast neutrophil infiltration in the lung is unaffected by platelet reduction, up-regulation of CXCL-1 (2·4-fold) and CCL5 (1·4-fold) acting as a compensatory mechanism in platelet-reduced mice during lung inflammation.
|
29325217 |
2018 |
Pneumonitis
|
0.350 |
Biomarker
|
disease |
BEFREE |
In order to study the role of GRO cytokines in lung inflammation, we cloned the predominant rabbit GRO cDNA (RabGRO) from alveolar macrophages, expressed bioactive recombinant protein (rRabGRO) in Escherichia coli, and developed a sensitive and specific enzyme-linked immunosorbent assay for RabGRO protein.
|
8631900 |
1996 |
Chronic Obstructive Airway Disease
|
0.340 |
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 |
Chronic Obstructive Airway Disease
|
0.340 |
Biomarker
|
disease |
BEFREE |
The analysis of gene expressions using a qPCR array revealed that many cytokines contributing to the pathogenesis and systemic inflammation in chronic obstructive pulmonary disease (COPD), including CCL2, CCL20, CSF2, CXCL1, CXCL10, IL1B and TNFα, were down-regulated by MA130 but not by a PKCζ-inactive control compound.
|
27516147 |
2016 |
Chronic Obstructive Airway Disease
|
0.340 |
Biomarker
|
disease |
BEFREE |
Neutrophils from patients with COPD showed enhanced chemotactic responses toward both CXCL1 and leukotriene B<sub>4</sub> compared with control cells.
|
30395484 |
2019 |
Chronic Obstructive Airway Disease
|
0.340 |
AlteredExpression
|
disease |
BEFREE |
Sputum CXCL1 levels in COPD and ACO patients were higher than in IP patients, whereas sputum CXCL8 levels were not.
|
30676127 |
2018 |
Juvenile arthritis
|
0.310 |
Biomarker
|
disease |
BEFREE |
Protein studies is revealed that JIA FLS release pro-inflammatory cytokines and chemokines, including IL-4, IL-6, IL-17, CXCL1, and CXCL6, and lose expression of important regulator signals, such as IL-10 and TIMP2.
|
28012239 |
2017 |
Esophageal Neoplasms
|
0.220 |
Biomarker
|
group |
BEFREE |
A key role for early growth response-1 and nuclear factor-kappaB in mediating and maintaining GRO/CXCR2 proliferative signaling in esophageal cancer.
|
19435811 |
2009 |
Esophageal Neoplasms
|
0.220 |
Biomarker
|
group |
BEFREE |
The expression levels of E‑cadherin were reduced, and those of snail family zinc finger 1, fibronectin, α‑smooth muscle actin and fibroblast secretory protein 1 increased in esophageal cancer cells following treatment with human recombinant EMMPRIN under hypoxic conditions.
|
26458866 |
2015 |
Lung diseases
|
0.220 |
Biomarker
|
group |
BEFREE |
The clinical importance of these chemokines was validated by association of CXCL1 and IL8 polymorphisms with changes in lung disease severity in patients with CF (n = 6365; IL8, P = .001; CXCL1, P = .001), confirming that targeting these chemokine pathways could help improve lung disease.
|
27799352 |
2017 |
Lung diseases
|
0.220 |
Biomarker
|
group |
BEFREE |
Enhanced CXCL1 production and angiogenesis in adenosine-mediated lung disease.
|
17227950 |
2007 |
Pneumonia, Bacterial
|
0.210 |
Biomarker
|
group |
BEFREE |
The reduced number of pulmonary macrophages and neutrophils observed in PGRN-deficient mice was related to a reduction of CCL2 and CXCL1 in the lungs after bacterial pneumonia.
|
28595330 |
2017 |
Alcoholic Liver Diseases
|
0.210 |
Biomarker
|
group |
BEFREE |
Increased production of interleukin-8 and CXCL1 by hepatocytes carrying the PNPLA3 148M variant contributes to a pro-inflammatory and tumorigenic milieu in patients with alcoholic liver disease.
|
31637480 |
2019 |
Malignant neoplasm of breast
|
0.100 |
Biomarker
|
disease |
BEFREE |
In stratified analyses, high density of FSP-1<sup>+</sup> or podoplanin<sup>+</sup> fibroblasts was significantly associated with worse OS; while α-SMA<sup>+</sup> or podoplanin<sup>+</sup> fibroblast infiltration was associated with worse DFS in breast cancer.
|
30405845 |
2018 |