RT Journal Article
SR Electronic
T1 The Involvement of NLRX1 in Pulmonary Hyperoxic Acute Injury
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP PA723
DO 10.1183/13993003.congress-2021.PA723
VO 58
IS suppl 65
A1 Hye Rin Kim
A1 Mi Na Kim
A1 Eun Gyul Kim
A1 Jae Woo Lee
A1 Kyung Won Kim
A1 Myung Hyun Sohn
YR 2021
UL http://erj.ersjournals.com/content/58/suppl_65/PA723.abstract
AB Introduction: Hyperoxia is frequently used for a treatment in acute respiratory failure, but it can also induce acute lung injury (ALI). Nucleotide-binding domain and leucine-rich-repeat-containing family member X1 (NLRX1) is ubiquitously expressed and localized in mitochondria. And it is related to reactive oxygen species production, inflammation and apoptosis, which are the features of hyperoxic acute lung injury (HALI). However, the regulation and contribution of NLRX1 in HALI have not been addressed. Thus, we studied to demonstrate a role of NLRX1 in hyperoxia.Methods: A murine model of ALI induced by hyperoxia was generated in wild-type mice and NLRX1-null mutant(-/-) mice. Mice were exposed to over 95% O2 for 24, 48 and 72 hours. Lung injury signaling was invested by real-time PCR, bicinchoninic acid (BCA) assay and lactate dehydrogenase (LDH) assay. Survival of wild-type and NLRX1 knock-out mice was assessed after continuous O2 exposure.Results: Hyperoxia exposed wild-type mice showed exacerbated protein leak and cell death by BCA and LDH assay compared to room air exposed mice in time dependent manner. And mRNA expression levels of pro-inflammatory cytokine such as IL-1β, TNF-α and IL-6 were also increased in wild-type mice after exposing over 95% O2 for 72 hours. However, lung injury induced by hyperoxia was significantly diminished in NLRX1 knock-out mice. In the case of survival test, NLRX1-null mutant mice showed prolonged survival compared to wild-type mice under hyperoxic condition.Conclusion: Genetic deficient of NLRX1 alleviate the pulmonaty acute injury induced by hyperoxia.FootnotesCite this article as: European Respiratory Journal 2021; 58: Suppl. 65, PA723.This abstract was presented at the 2021 ERS International Congress, in session “Prediction of exacerbations in patients with COPD”.This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).