Objective: To study the effects of IL-17 antibody on adipose tissue inflammation and macrophage accumulation in obese mice induced by BPA.
Methods: 4-week-old male C57 BL/6 mice were fed with high fat diet( HFD) and were randomly divided into solvent control group, IgG treatment group, IL-17 antibody treatment group, 1000 nmol/L BPA group, IgG + 1000 nmol/L BPA group, IL-17 antibody + 1000 nmol/L BPA group, with 8 mice in each group. The BPA exposed group administered 1000 nmol/L BPA by drinking water. The mice in IL-17 treatment group were intraperitoneally injected with 100 μg IL-17 antibody and the mice in IgG treatment group were intraperitoneally injected with 100 μg IgG each week. Mice were sacrificed and epididymal fat pad was obtained after 16 weeks. Histopathological section was used to observe the cells morphological changes and inflammation in epididymal adipose tissue. Immunohistochemistry( IHC) was used to detect the expression of IL-17、TNF-α and IL-1β in epididymal adipose tissue. Immunofluorescence( IF) was used to detect the location of macrophage in the epididymal adipose tissue. One-Way ANOVA was used to compare the mean values of the two groups, and the Tukey method was used for pairwise comparison.
Results: The obesity rate [( 40. 68 ± 9. 43) %]and body weight [( 41. 95 ±2. 81) g]of mice in 1000 nmol/L BPA group higher than the mice in solvent control group( body weight [( 38. 44 ± 4. 23) g], the obesity rate [( 28. 90 ± 14. 19) % ]), the difference was statistically significant( body weight F = 5. 895, P < 0. 05, the obesity rate F = 5. 895, P < 0. 05). Epididymal adipose tissue inflammatory cell infiltration increased. The expression of IL-17( F = 28. 225, P < 0. 05) and IL-1β( F = 57. 878, P < 0. 05) were upregulated. And the macrophage accumulation was increased( F = 90. 829, P < 0. 05). Compared with the 1000 nmol/L BPA group, IgG treatment groups( the obesity rate[( 35. 98 ± 10. 73) % ]) had less effect on the mice. IL-17 treatment( the obesity rate[( 23. 03 ± 12. 50) % ]) inhibited BPA-induced increased in obesity rate of mice. Also, the inflammatory infiltration and macrophage accumulation of the adipose tissue were reduced( F = 90. 829, P < 0. 05). And the expression of IL-17( F = 28. 225, P < 0. 05), TNF-α( F = 4. 199, P < 0. 05) and IL-1β( F = 57. 878, P < 0. 05) inflammatory factors were decreased.
Conclusion: IL-17 antibody can improve BPA-induced mice obesity by reducing adipose tissue macrophage accumulation and reducing adipose tissue inflammation.
Keywords: IL-17 antibody; bisphenol A; inflammation; macrophage; obesity.