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. 2021 May 4;12:668002. doi: 10.3389/fimmu.2021.668002

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Copyright © 2021 Mao, Luo, Geng, Xu, Liao, Zhong, Ma, Tan, Xia, Duan, Song, Long, Liu, Yang, Wu and Jin

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Melatonin protects against chronic LPS-induced mouse lung destruction by the targeting MT1/MT2 receptor. (A–D) Melatonin inhibited BALT formation and bronchial thickening as well as alveolar enlargement compared with LPS treatment. Mice receiving luzindole (MT1/MT2 inhibitor) intraperitoneal injection showed diminished protective effects of melatonin in their lungs. N = 5–7 in each group. (E, F) Micro-CT indicated that mice treated with melatonin had less destruction in their lungs under chronic LPS exposure. However, luzindole (MT1/MT2 inhibitor) increased the amount of destruction in the lungs even when mice were treated with melatonin. N = 5–7 in each group. (G–J) Melatonin preserved the number of cilia and normal morphology of mitochondrial autophagosomes in mouse bronchial epithelial cells under LPS exposure. However, luzindole (MT1/MT2 inhibitor) intraperitoneal injection reduced the cilia and increased the percentage of abnormal mitochondria and mitochondrial autophagosomes, although mice received melatonin orally daily. N = 4 in each group. The green arrow shows cilia, the yellow arrow shows mitochondrial autophagosomes, the red arrow shows autophagosomes, and the black arrow shows lysosomes. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.