Abstract
Acute Lung Injury is characterized by severe inflammation. Vitamin D3 was discussed to reduce inflammation in ALI, but the mechanism is not well understood. This study assessed the effect of different calcitriol administration strategies on inflammation and the lung microbiota composition in ALI. In a mouse model, the alveolus and airway pathology were assessed by immunohistology. mRNA expression was determined by RT-qPCR and protein expressions was detected by Western-blotting. The composition of microbiota was performed by 16s DNA high-throughput sequencing. Short-term vitamin D3 supplementation prevented Lipopolysaccharide-induced ALI by preventing pro-inflammatory cytokines including IL-1β, IL-6, and TNF-α. In contrast, long-term treatment over 3 days, 6 days or 10 days had no such effect. Short-term vitamin D3, but not long-term pretreatment significantly reduced the phosphorylation of STAT3 and SOCS3, but upregulated the phosphorylation of IκBα. Furthermore, an increased relative abundance of Rodentibacter genus in LPS-challenged mice bronchoalveolar lavage fluid was observed, which was sensitive to short-term vitamin D3 treatment, effectively alleviating the Rodentibacter abundance. Correlation analysis showed that the load of Rodentibacter positively correlated with the IL-1β, IL-6, and TNF-α gene expression. The data support that a single administration of vitamin D3 may work as an adjuvant therapy for acute lung inflammation. This article is protected by copyright. All rights reserved.
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