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J Pharmacol Sci ; 155(3): 94-100, 2024 Jul.
Article in English | MEDLINE | ID: mdl-38797538

ABSTRACT

Interleukin (IL-19) belongs to the IL-10 family of cytokines and plays diverse roles in inflammation, cell development, viral responses, and lipid metabolism. Acute lung injury (ALI) is a severe respiratory condition associated with various diseases, including severe pneumonia, sepsis, and trauma, lacking established treatments. However, the role of IL-19 in acute inflammation of the lungs is unknown. We reported the impact of IL-19 functional deficiency in mice crossed with an ALI model using HCl. Lungs damages, neutrophil infiltration, and pulmonary edema induced by HCl were significantly worse in IL-19 knockout (KO) mice than in wild-type (WT) mice. mRNA expression levels of C-X-C motif chemokine ligand 1 (CXCL1) and IL-6 in the lungs were significantly higher in IL-19 KO mice than in WT mice. Little apoptosis was detected in lung injury in WT mice, whereas apoptosis was observed in exacerbated area of lung injury in IL-19 KO mice. These results are the first to show that IL-19 is involved in acute inflammation of the lungs, suggesting a novel molecular mechanism in acute respiratory failures. If it can be shown that neutrophils have IL-19 receptors and that IL-19 acts directly on them, it would be a novel drug target.


Subject(s)
Acute Lung Injury , Hydrochloric Acid , Interleukins , Mice, Knockout , Animals , Acute Lung Injury/etiology , Acute Lung Injury/pathology , Acute Lung Injury/genetics , Interleukins/genetics , Interleukins/metabolism , Mice, Inbred C57BL , Interleukin-6/metabolism , Interleukin-6/genetics , Disease Models, Animal , Neutrophil Infiltration , Chemokine CXCL1/genetics , Chemokine CXCL1/metabolism , Male , Lung/pathology , Lung/metabolism , Apoptosis/genetics , Apoptosis/drug effects , Mice , Neutrophils , Pulmonary Edema/etiology , Gene Expression
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