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Novel pendrin inhibitor attenuates lipopolysaccharide-induced acute lung injury in mice
( Eun Hye Lee ),( Jae Young Choi ),( Mi Hwa Shin ),( Wan Namkung ),( Ji Soo Choi ),( Su Hwan Lee ),( Ah Young Leem ),( Sang Hoon Lee ),( Kyung Soo Chung ),( Song Yee Kim ),( Ji Ye Jung ),( Young Ae Ka 대한결핵 및 호흡기학회 2019 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.127 No.0
Background: Pendrin is encoded by SLC26A4 and its mutation leads to congenital hearing loss. Additionally, pendrin is up-regulated in inflammatory airway diseases such as chronic obstructive pulmonary disease, allergic rhinitis, and asthma. In this study, the effects of a novel pendrin inhibitor, YS-01, were investigated in an LPS-induced acute lung injury (ALI) mice model, and the mechanism underlying the effect of YS-01 was examined. Methods: LPS (10 mg/kg) was intranasally instilled in wild type (WT) and pendrin-null mice. Lung injury parameters were assessed in the lung tissue and bronchoalveolar lavage fluid (BALF). Pendrin levels in the BALF of 41 pneumonia/ARDS patients and 25 control (solitary pulmonary nodule) patients were also measured. Results: LPS instillation induced lung injury in WT mice but not in pendrin-null mice. YS-01 treatment dramatically attenuated lung injury and reduced BALF cell counts and protein concentration after LPS instillation in WT mice. Proinflammatory cytokines and NF-κB activation were suppressed by YS-01 treatment in LPS-induced ALI mice. However, the protective effects of pendrin inhibitor lost after SCN- instillation. Furthermore, pendrin expression was upregulated in pneumonia/ARDS patient compared to that in control patient BALF (mean, 24.86 vs. 6.83 ng/mL, p < 0.001). Conclusions: A novel Pendrin inhibitor, YS-01, suppressed lung injury in LPS-induced ALI mice and our data provide a new strategy for the treatment of inflammatory airway diseases including sepsis-induced ALI.