Abstract
Cigarette smoke exposure (SE) during pregnancy is the largest modifiable risk factor for the development of asthma. We have previously shown that maternal L-Carnitine treatment reduces renal and brain adverse impacts in SE offspring, but its effect on the lung is unknown. Here, in order to investigate the effect of maternal L-Carnitine supplementation on lungproinflammatory signalling pathwayswe measured inflammasome NLRP3 activation, signalling pathway activation (ERK1,2, JNK1,2, MAPK, and NF-KB), and markers of autophagy (LC3A/B-I, II) and mitophagy (Drp-1 and Opa-1). Female Balb/c mice (8 weeks) were exposed to cigarette smoke before mating for 6 weeks, during gestation and lactation. Half SE mothers were given L-Carnitine supplementation through drinking water during gestation and lactation. Lung samples were collected at postnatal day 1 and 13 weeks from both male and female offspring. At P1, there was an increase in phospho-ERK1,2, total ERK1,2, total JNK1,2, phospho-P38 MAPK and P38 MAPK, phospho-NFKB, NFKB and NLPR3 protein levels in male offspring. The mitochondrial fission marker Drp-1 and autophagosome markers (LCA3A/B-I,II) were increased in SE offspring, L-Carnitine significantly reduced protein levels of phospho-ERK1 and Drp-1. At 13 weeks, there was an increase in autophagosome markers (LCA3A/B-I,II) and MAPK signaling pathway markers (phospho-ERK2, total ERK2, total P38 MAPK and phospho-NFKB), which were partially normalized by L-Carnitine treatment. Maternal SE did not affect the female offspring with no changes found after L-Carnitine treatment. L-Carnitine supplementation during pregnancy may alleviate the adverse impact of maternal smoking in the male offspring’s lung.
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