Fig 2: The blockade of CCL5 in vivo. a The serum levels of CCL3 and CCL5 in 10-week-old mice were measured by an ELISA (n = 5). b Mouse anti-CCL5 neutralizing antibodies (mCCL5 neu ab, 500 μg per mouse) were injected (once per week for 2 weeks) into 6-week-old male C57BL/6J mice (n = 5). IgG was administered to the control group. c, d μCT images (scale bars, 100 μm) and parameters (n = 5 mice per group) are shown. e Representative images of the distal femurs from the control IgG and mCCL5 ab groups. HE- (scale bars, 100 μm) and TRAP-stained sections (scale bars, 50 μm) are shown in the upper and lower panels, respectively (n = 5). f Quantitative bone histomorphometric analyses were conducted of the trabecular bones in the distal femurs of control IgG and mouse CCL5 neutralizing antibody-injected mice. *P < 0.05 (by Student’s t-test) in comparison to control and mCCL5-neuAb mice. All values are shown as the mean ± SD, n = 5

Fig 3: Effect of L. salivarius FFIG58 (positive strain) and FFIG79 (negative strain) on the long-term modulation of the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, chemokine C-C motif ligand 2 (CCL2), chemokine C-C motif ligand 3 (CCL3), chemokine C-X-C motif ligand 2 (CXCL2), and chemokine C-X-C motif ligand 10 (CXCL10) in pneumococcal pneumonia. Infant mice were nasally primed with FFIG58 or FFIG79 during two consecutive days, then stimulated with three once-daily doses of poly(I:C) and finally challenged with S. pneumoniae serotype 6B five and thirty days after the last administration of poly(I:C). Infant mice treated with PBS (vehicle), stimulated with poly(I:C), and then challenged with S. pneumoniae were used as controls. The levels of TNF-α, IL-1β, CCL2, CCL3, CXCL2, and CXCL10 in bronchoalveolar lavages (BALs) were determined on day 2 post-pneumococcal-challenge. Asterisks indicate significant differences between lactobacilli-treated and control groups; * (p < 0.05) and ** (p < 0.01).