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. 2022 Jan 24;18(4):1521–1538. doi: 10.7150/ijbs.66477

Figure 5.

Figure 5

PyrBDs activate the p38 MAPK pathway to promote MLE-12 cell activation. (A) The number of MsEVs was determined by flow cytometry. With the occurrence of pyroptosis, alveolar macrophages derived a large number of MsEVs (PyrBDs). Data are expressed as the mean ± SD, n = 3. (B) PRM for whole-protein analysis of PyrBDs, from which DAMP-related molecular proteins were screened. The results are expressed as log2 fold change (n = 4). (C) TNF-α, IL-6, and IL-1β content of PyrBDs. Compared with MsEVs derived from normal alveolar macrophages (N-AM-MsEVs), MsEVs derived from pyroptotic alveolar macrophages (AM-PyrBDs) contained high levels of TNF-α, IL-6, and IL-1β. Data are expressed as the mean ± SD, n = 6, ***P < 0.001. (D) Immunoblot analysis for icam-1. AM-PyrBDs and ALI-MsEVs (derived from ALI-1h mice) groups showed the promoted expression of icam-1 in MLE-12 cells. N-MsEVs, isolated from BALF of normal mouse; N-AM-MsEVs, derived from normal alveolar macrophages; (E) Immunoblot analysis of phospho-p38 MAPK, p38 MAPK, phospho-NF-κB p65, NF-κB p65, and icam-1. Quantification of the related protein expression showed significant upregulation of phospho-p38 MAPK (F), phospho-NF-κB p65 (G), and icam-1 (H), which was reversed by the inhibitor SB 203580. Data are expressed as the mean ± SD, n = 3. *P < 0.05; **P < 0.01.