[The role of interleukin-1β on the pulmonary fibrosis in mice exposed to crystalline silica].
OBJECTIVE
This study was designed to evaluate the role of interleukin (IL)-1β in the development of fibrosis in mice exposed to silica.


METHODS
The total of 96 Male C57BL/6 mice were divided into four groups. (1) blank control group, (2) PBS group in which mice were instilled with PBS only, (3) silica + IL-1β mAb group in which mice were instilled with 2.5 mg silica dust and 40 µg anti-IL-1β mAb, (4) silica group in which mice were instilled with 2.5 mg silica dust and 40 µg IgG. The final volume of suspension or PBS instilled into the mouse was 50 µl. At 7, 28 and 84 days after treatment, 8 mice were sacrificed in each group. Then BALF was collected for the count of inflammatory cells and cytokines determination. The lung tissues were collected for the detecting of mRNA levels of fibrogenic molecules.


RESULTS
The collagen deposition induced by silica in the lung tissues was partly inhibited by anti-IL-1β. A intensely pulmonary cytokines such as IL-1β, TNF-α, MCP-1 were induced by crystalline silica exposure, and partly inhibited by anti-IL-1β. The levels of TGF-β and fibronectin in silica exposed mice were significantly elevated than those in control mice at days 28 and 84 after treatment (P < 0.01). And the mRNA levels of TGF-β, collagen I and fibronectin were significantly decreased in silica+IL-1β mAb group when compared with those in silica group at days 7, 28 and 84 (P < 0.01). There was a significant decrease of the ratios of IFN-γ/IL-4 in both silica+anti-IL-1β mAb and silica groups when compared with those in control mice at the above three time points (P < 0.01). However, the IFN-γ/IL-4 ratios in silica+anti-IL-1β group were significantly higher than those in silica group at 7, 28 and 84 days (P < 0.05 or P < 0.01).


CONCLUSIONS
IL-1β may promote the pulmonary fibrosis in mice exposed to silica.
MOE Key Lab of Environmental and Health, School of Public Health, Tongji Medical College, Huazhong University of Science & Technology, Wuhan 430030, China.
Jia-li
JL
Guo
Xiu-qing
XQ
Cui
Yi
Y
Rong
Ting
T
Zhou
Yun
Y
Zhou
Zhi-hong
ZH
Zhang
Na-li
NL
Gu
Wei-hong
WH
Chen
D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D024042:Collagen Type I / Q000378:metabolism; D004195:Disease Models, Animal; D005353:Fibronectins / Q000378:metabolism; D007371:Interferon-gamma / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism / Q000502:physiology*; D015847:Interleukin-4 / Q000378:metabolism; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D011658:Pulmonary Fibrosis / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D012822:Silicon Dioxide / Q000633:toxicity*; D016212:Transforming Growth Factor beta / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D000911:Antibodies, Monoclonal; D024042:Collagen Type I; D005353:Fibronectins; D053583:Interleukin-1beta; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4; D012822:Silicon Dioxide; D007371:Interferon-gamma