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. 2019 Jul 3;10:2040622319860653. doi: 10.1177/2040622319860653

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© The Author(s), 2019

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 5. — LGG regulated the systemic inflammatory response.

(a) ELISA analysis of serum levels of RANKL, TNF-α, and IL-17 (n = 10 mice per group). (b) FACS analysis of the ratios of Treg and Th17 cells in the CD4⁺ T cell subset and the Treg:Th17 ratio in the spleen (n = 6 mice per group). (c) Representative FACS plots on ratio of Treg cells in the CD4⁺ T cell subset of the spleen. (d) Representative FACS plots of the ratio of Th17 cells in the CD4⁺ T cell subset of the spleen. Data are expressed as mean ± SD. All data were normally distributed according to the Shapiro–Wilk normality test and analyzed using two-way ANOVA and post hoc tests applying the LSD correction for multiple comparisons.

^*p < 0.05 compared with the Sham group.

^#p < 0.05 compared with the LGG+TDF group.

^%p < 0.05 compared with the E. coli+TDF group.

^$p < 0.05 compared with the TDF group.

ANOVA, analysis of variance; ELISA, enzyme-linked immunosorbent assay; FACS, fluorescence activate cell sorting; IL-17, interleukin-17; LGG, Lactobacillus rhamnosus GG; LSD, least significant difference; RANKL, receptor activator of nuclear factor kappa-B ligand; SD, standard deviation; TDF, tenofovir disoproxil fumarate; Th17, T-helper 17 cell; TNF-α, tumor necrosis factor alpha; TRAP, tartrate-resistant acid phosphatase; Treg, regulatory T cell; ZOL, zoledronic acid.