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. 2009 Sep 3;180(11):1114–1121. doi: 10.1164/rccm.200901-0023OC

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Figure 5. — Cytokine secretion by Hermansky-Pudlak syndrome type 1 (HPS-1) and normal cultured alveolar macrophages and suppression by pirfenidone in HPS-1 cells. (A) Concentrations (pg/ml) of monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein-1α (MIP-1a), and regulated upon activation, normal T cell expressed and secreted (RANTES) were significantly higher in conditioned medium from alveolar macrophages cultured for 24 hours from subjects with HPS-1 pulmonary fibrosis (HPSPF) (n = 18) compared with healthy research volunteers (NV) (n = 6). (B) Concentrations of MIP-1α, MCP-1, RANTES, macrophage colony-stimulating factor (M-CSF), macrophage inflammatory protein (MIP)-4, and IFN-γ (IFNg), but not granulocyte-macrophage colony-stimulating factor (GM-CSF) or IL12p40, in conditioned medium from alveolar macrophages from subjects with HPS-1 pulmonary fibrosis (n = 6) cultured for 24 hours were lower with increasing concentrations of pirfenidone.

Figure 5. — Cytokine secretion by Hermansky-Pudlak syndrome type 1 (HPS-1) and normal cultured alveolar macrophages and suppression by pirfenidone in HPS-1 cells. (A) Concentrations (pg/ml) of monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein-1α (MIP-1a), and regulated upon activation, normal T cell expressed and secreted (RANTES) were significantly higher in conditioned medium from alveolar macrophages cultured for 24 hours from subjects with HPS-1 pulmonary fibrosis (HPSPF) (n = 18) compared with healthy research volunteers (NV) (n = 6). (B) Concentrations of MIP-1α, MCP-1, RANTES, macrophage colony-stimulating factor (M-CSF), macrophage inflammatory protein (MIP)-4, and IFN-γ (IFNg), but not granulocyte-macrophage colony-stimulating factor (GM-CSF) or IL12p40, in conditioned medium from alveolar macrophages from subjects with HPS-1 pulmonary fibrosis (n = 6) cultured for 24 hours were lower with increasing concentrations of pirfenidone.