Publication | Open Access
CXCL10/IP-10 Neutralization Can Ameliorate Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome in Rats
72
Citations
30
References
2017
Year
Acute Lung InjuryInflammatory Lung DiseaseRespiratory Distress Syndrome (Pulmonary Critical Care)Lung InflammationImmunologyImmune RegulationRenal InflammationCxcl10/ip-10 NeutralizationInflammationSepsisPulmonary PharmacologyChronic InflammationCxcl10 NeutralizationRespiratory Distress Syndrome (Neonatal Medicine)Inflammatory MediatorsInflammatory DiseaseInflammatory CellsCytokineAnti-inflammatoryImmunosuppressionMedicineMatrikines
The role of C-X-C motif chemokine 10 (CXCL10), a pro-inflammatory factor, in the development of acute respiratory distress syndrome (ARDS) remains unclear. In this study, we explored the role of CXCL10 and the effect of CXCL10 neutralization in lipopolysaccharide (LPS)-induced ARDS in rats. The expression of CXCL10 and its receptor chemokine receptor 3(CXCR3) increased after LPS induction. Moreover, neutralization of CXCL10 ameliorated the severity of ARDS by reducing pulmonary edema, inhibiting the release of inflammatory mediators (IFN-γ, IL-6 and ICAM-1) and limiting inflammatory cells (neutrophils, macrophages, CD8+ T cells) influx into the lung, with a reduction in CXCR3 expression in neutrophils and macrophages. Therefore, CXCL10 could be a potential therapeutic target in LPS-induced ARDS.
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