Objective: To investigate the changes in the levels of inflammatory cytokines in bronchoalveolar lavage fluid (BALF) in rats exposed to silica dust.
Methods: Experimental rats were randomly divided into control group and three experimental groups (doses of dust: 15, 30, and 60 mg/ml), with 42 rats in each group. Each rat in the control group was treated with 1 ml of normal saline by intratracheal instillation, while each rat in the experimental groups was exposed to 1 ml of silica suspension by a single intratracheal instillation. Seven rats in each group were killed at 1, 3, 7, 14, 21, and 28 days after exposure, and then BALF was collected. Enzyme-linked immunosorbent assay was used to measure the levels of interleukin (IL)-1, IL-6, IL-16, macrophage inflammatory protein-1 alpha (MIP-1α), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β).
Results: The levels of cytokines in each experimental group were higher than those in the control group at any time point. In the early stage of exposure (day 1-3), BALF IL-1 level increased significantly with the increase in dust dose, and on day 14, BALF IL-6 and IL-16 levels increased significantly with the increase in dust dose; the levels of IL-1, IL-6, and IL-16 in the experimental groups reached the peak on day 14. There were significant differences in the levels of MIP-1α and MCP-1 between the experimental groups (FMIP-1α = 30.106, P<0.01; FMCP-1 = 17.193, P<0.01). In each group, the level of MCP-1 varied significantly at different time points (F = 0.618, P>0.05). On day 1-14, BALF TNF-α level increased with the increase in dust dose, with a significant dose-response relationship (P < 0.05). In each experimental group, TNF-α level reached the peak on day 14. On days 14, 21, and 28, the high-dose group had significantly higher BALF TGF-β levels than the low-dose group (P<0.05); on days 14 and 28, the high-dose group had significantly higher BALF TGF-β levels than the middle-dose group (P<0.05).
Conclusion: IL-1, IL-6, IL-16, MIP-1α, MCP-1, and TNF-α play a role in the development and progression of silicosis inflammation. TGF-β may be related to (related to; associated with; correlated with) fibrosis.
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