Classical dendritic cells (
cDCs) are involved in the pathogenesis of inflammatory
lung diseases; however, their contributions in
acute respiratory distress syndrome (ARDS), which is pathophysiologically inflammatory, remain unknown. The present study aimed to explore the regulatory effects of pulmonary
cDCs on acute
lung inflammation and injury in
lipopolysaccharide (LPS)‑induced ARDS. Fms‑like
tyrosine kinase 3‑ligand (FLT3L) and
lestaurtinib, a specific activator and an inhibitor of FLT3 signaling respectively, were used separately for the pretreatment of C57BL/6 mice for 5 consecutive days. ARDS was induced by intratracheal injection of LPS, and mice were sacrificed 6 and 24 h later. Flow cytometry was used to measure the aggregation and maturation of pulmonary
cDCs. The ratio of
lung wet weight to
body weight (LWW/BW) and histopathological analyses were assessed to evaluate lung
edema and
lung injury.
Tumor necrosis factor‑α and
interleukin (IL)‑6 levels were measured by ELISA to evaluate acute
lung inflammation. The levels of interferon‑γ, IL‑1β, IL‑4 and IL‑10, and the expression of the
transcription factors T‑box‑expressed‑in‑T‑cells (T‑bet) and GATA
binding protein 3, were quantified by ELISA, RT‑qPCR and western blotting to evaluate the balance of the Th1/Th2 response.
Myeloperoxidase (MPO) activity was measured to evaluate neutrophil infiltration. The results demonstrated that the aggregation and maturation of pulmonary
cDCs reached a peak at 6 h after LPS challenge, followed by a significant decrease at 24 h. FLT3L pretreatment further stimulated the aggregation and maturation of pulmonary
cDCs, resulting in elevated lung MPO activity and increased T‑bet expression, which in turn led to aggravated LWW/BW, acute
lung inflammation and injury. However,
lestaurtinib pretreatment inhibited the aggregation and maturation of pulmonary
cDCs, decreased lung MPO activity and T‑bet expression, and eventually improved LWW/BW, acute
lung inflammation and injury. The present results suggested that pulmonary
cDCs regulated acute
lung inflammation and injury in LPS‑induced ARDS through the modulation of neutrophil infiltration and balance of the Th1/Th2 response.