Asthma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In an experimental model of fungal-associated allergic airway inflammation, we demonstrate that IL-1R1 signaling promotes type 1 (IFN-γ, CXCL9, CXCL10) and type 17 (IL-17A, IL-22) responses that were associated with neutrophilic inflammation and increased airway hyperreactivity.
|
31550242 |
2019 |
Asthma
|
0.100 |
Biomarker
|
disease |
BEFREE |
ST2 OE also enhanced HRV1B-induced IP-10, a chemokine involved in asthma exacerbations.In the <i>M. pneumoniae</i>-infected mouse model, ST2 deficiency, in contrast to sufficiency, significantly reduced the levels of neutrophils following acute (≤24 h) infection, while in the HRV1B-infected mouse model, ST2 deficiency significantly reduced the levels of proinflammatory cytokines KC, IP-10, and IL-33 in bronchoalveolar lavage (BAL) fluid.
|
31061143 |
2019 |
Asthma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Following PIV3 infection, IP-10 protein release and mRNA expression were significantly higher in asthmatics compared to healthy controls (median 36.03-fold).
|
29411555 |
2018 |
Asthma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Therefore, eosinophils are likely to contribute to the development of asthma exacerbation through several mechanisms, including activation by Th2 cytokines, such as IL-5 or GM-CSF or by virus infection-related proteins, such as CXCL10, and interaction with other cells, such as neutrophils.
|
30323811 |
2018 |
Asthma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
High baseline serum CXCL10 and IL-12 levels may be useful in predicting a good omalizumab response in severe asthmatics.
|
29413515 |
2018 |
Asthma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Serum IP-10 levels higher than 38.9pg/ml (sensitivity: 85%, specificity: 47%, p=0.002) were predictive of virus-induced asthma.
|
27955890 |
2017 |
Asthma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We show high levels of CXCL10 mRNA closely associated with IFNG levels in the BAL cells of 50% of severe asthmatics and also in the airways of mice subjected to a severe asthma model, both in the context of high-dose CS treatment.
|
28679952 |
2017 |
Asthma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Air-liquid interface cultures of human bronchial epithelial cells (HBEC) of control subjects (cHBEC) or severe asthma patients (saHBEC) were co-cultured with monocyte-derived dendritic cells (moDC).Increased release of CXCL8, TSLP and IL-33 from saHBEC contrasted with cHBEC producing CXCL10 and CCL2.
|
28275176 |
2017 |
Asthma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our data suggested ASMCs in the asthma microenvironment promoted the migration of mast cells via secretion of ATP and the expression of CXCL10/CXCR3 axis.
|
25272186 |
2014 |
Asthma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings suggest that CRS associated with asthma may become intractable through the over-production of CXCL10 in response to viral infection.
|
24153332 |
2013 |
Asthma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We aimed to investigate the role of cytokine-induced MAPK activation in CXCL10 production by ASM cells from people with and without asthma.
|
22387292 |
2012 |
Asthma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The median (IQR) T-bet expression after normalization with beta-actin was suppressed in asthmatics versus controls [asthmatics 0 x 71 (0 x 59) versus controls 1 x 07 (1 x 14), P=0 x 03].The median (IQR) of plasma RANTES was elevated, whereas IP-10 was suppressed in asthmatics versus controls (RANTES: 13658 x 0 (13673 x 3) versus 6299 x 5 (19407 x 8) pg/ml, P=0 x 03; IP-10: 1047 x 6 (589 x 8) versus 1306 x 4 (759 x 9) pg/ml, P=0 x 001).
|
17302903 |
2007 |
Asthma
|
0.100 |
Biomarker
|
disease |
LHGDN |
Increased serum IP-10 levels were predictive of virus-induced asthma (odds ratio, 44.3 [95% CI, 3.9-100.3]).
|
17628646 |
2007 |
Asthma
|
0.100 |
AlteredExpression
|
disease |
LHGDN |
Our data implicate TSLP, TARC/CCL17, MDC/CCL22, and IP-10/CXCL10 in asthma pathogenesis.
|
15944327 |
2005 |
Asthma
|
0.100 |
Biomarker
|
disease |
LHGDN |
These results suggest that inhibition of the CXCL10/CXCR3 axis offers a novel target for the treatment of asthma.
|
15879427 |
2005 |
Asthma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We sought to investigate the effect of a 2-week course of oral corticosteroid (methylprednisolone, 40 mg/d) on the expression of CXC chemokines (IL-8 and IFN-gamma-inducible protein 10 [IP-10]) and CC chemokines (eotaxin and monocyte chemotactic proteins [MCPs] 1-4) in endoscopic biopsy specimens of 13 patients with moderate-to-severe asthma.
|
15696082 |
2005 |
Asthma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus IP-10 may play a role in the pathogenesis of HRV-induced colds and in HRV-induced exacerbations of COPD and asthma.
|
15764644 |
2005 |
Asthma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We used in situ hybridization and immunohistochemistry to examine the expression and cellular provenance of TSLP, Th2-attracting (thymus and activation-regulated chemokine (TARC)/CCL17, macrophage-derived chemokine (MDC)/CCL22, I-309/CCL1) and Th1-attracting (IFN-gamma-inducible protein 10 (IP-10)/CXCL10, IFN-inducible T cell alpha-chemoattractant (I-TAC)/CXCL11) chemokines and expression of their receptors CCR4, CCR8, and CXCR3 in bronchial biopsies from 20 asthmatics and 15 normal controls.
|
15944327 |
2005 |