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. 2021 Mar 9;64(6):722–733. doi: 10.1165/rcmb.2020-0387OC

Figure 1.

Figure 1.

B-cells from patients with idiopathic pulmonary fibrosis (IPF) respond to microbial antigens by releasing a proinflammatory and profibrotic milieu that induced fibroblast migration and activation. (A and B) Peripheral B-cells from patients with IPF were either left unstimulated or were stimulated with CpG (A) or β-glucan (Gluc) (B), as indicated. IL-6, MMP-7, and IL-8 were measured in the cell supernatant by ELISA. (C) Images of quiescent IPF fibroblasts stained with Wright-Giemsa migrating toward B-cell–conditioned media (BCM). BCM was obtained from B-cell supernatant from unstimulated cells or B-cells stimulated with CpG (CpG-BCM) or Gluc (Gluc-BCM) for 48 hours. CpG and Gluc in regular media were used as controls. Migrated IPF fibroblasts were manually counted using ImageJ software. (D) Cell lysate of IPF fibroblasts stimulated with TGFβ, CpG, Gluc, CpG-BCM, or Gluc-BCM (as indicated) and immunoblotted for FN1 (fibronectin), αSMA (α-smooth muscle actin), PAI1 (plasminogen activator inhibitor-1), or β-actin. Data are representative of three independent experiments. *P < 0.05 and ***P < 0.001. Med = media; MMP-7 = matrix metallopeptidase-7; NTC = unstimulated B-cells; TGFβ = transforming growth factor β.