Objective To investigate the relationship between lipopolysaccharide (LPS) and the expression of monocarboxylate transporter‑1 (MCT1), and its effect on epithelial‑mesenchymal transformation (EMT) of alveolar epithelial cells, and to explore the potential mechanism of EMT during LPS‑induced pulmonary fibrosis. Methods ① According to the random number table method, 24 C57BL/6 mice were divided into two groups (n=12): a control (Con1) group and a LPS stimulated (LPS1) group. Mice in the LPS1 group were intraperitoneally injected with 5 mg·kg−1·d−1 LPS for 3 d. Those in the Con1 group were intraperitoneally injected with the equal volume of normal saline, and the mice were sacrificed 7 days after modeling. The amounts of MCT1 and EMT marker proteins (E‑cadherin and Vimentin) in lung tissue were detected by Western blot and immunofluorescence. The content of serum lactate was detected by enzyme‑linked immunosorbent assay (ELISA), and the degree of lung fibrosis was evaluated by Masson staining. ② According to the random number table method, MLE‑12 cells were divided into four groups (in triplicate for each group): a PBS control (Con2) group, a lactate (Lac2) group, a lipopolysaccharide (LPS2) group and a lactate+lipopolysaccharide (Lac+LPS2) group. These groups were stimulated with PBS, 10 mmol/L lactate, 1 mg/L LPS, and 10 mmol/L lactate+1 mg/L LPS for 48 h, respectively. Their levels of MCT1, E‑cadherin and Vimentin were detected by Western blot and immunofluorescence, and the pH value of the supernatant in each group was measured. Results ① Compared with the Con1 group, the LPS1 group showed decreases in MCT1 level (P<0.05) and E‑cadherin level (P<0.05), as well as increases in Vimentin level (P<0.05) in lung tissue; it also presented reduced E‑cadherin fluorescence intensity, enhanced Vimentin fluorescence intensity, and reduced MCT1 fluorescence intensity in lung tissue, with fibrosis in lung tissue and elevation in the content of serum lactate (P<0.05). ② Compared with the Con2 group, the Lac2 group presented significant increases in MCT1 protein level (P<0.05), while no statistical difference was found in the levels of E‑cadherin and Vimentin and pH value (P>0.05). The LPS2 group and the Lac+LPS2 group showed remarkable decreases in MCT1 protein level (P<0.05) and E‑cadherin level (P<0.05), increases in Vimentin level (P<0.05) and decreases in pH value (P<0.05). Compared with the Lac2 group, the Lac+LPS2 group showed remarkable decreases in MCT1 and E‑cadherin levels (P<0.05), increases in Vimentin level (P<0.05), and decreases in pH value (P<0.05). Compared with the Con2 group, the Lac2 group showed enhanced MCT1 fluorescence intensity, without remarkable changes in E‑cadherin and Vimentin; the LPS2 group and the Lac+LPS2 group presented reduced MCT1 and E‑cadherin fluorescence intensity, and enhanced Vimentin fluorescence intensity. Compared with the Lac2 group, the Lac+LPS2 group presented remarkably reduced MCT1 and E‑cadherin fluorescence intensity, and enhanced Vimentin fluorescence intensity. Conclusion During the process of LPS‑induced pulmonary fibrosis, LPS can inhibit the expression of MCT1 in mouse alveolar epithelial cells, resulting in impaired lactate clearance and extracellular fluid acidification, thereby promoting EMT and lung fibrosis.