Correlations between saturation and lung weight, birth weight, LW/BW ratio and PW/BW ratio.

Correlations between saturation and lung weight, birth weight, LW/BW ratio and PW/BW ratio.</p

Immunohistochemical analysis of VDR in fetal rat lung.

Immunohistochemistry was performed on lung tissues from each dietary group at both E19 (VDL group (n = 31); control group (n = 27)) and E22 (VDL group (n = 35); control group (n = 19)) using the monoclonal D-6 antibody and counterstained with Mayer’s hematoxylin. Representative images of lung tissue from E19 (A) and E22 (B) (Magnification x28). Arrows indicate positive ATII cells. Positive (C) and negative (D) control sections with omission of the monoclonal D-6 antibody in the duodenum (Magnification x5). The expression of VDR in the lung was evaluated as the density of positive ATII cells (cells/μm2) (E).</p

Effects of vitamin D on mRNA levels of surfactant proteins.

Quantitative real-time PCR analysis of surfactant protein A-D mRNA transcripts in fetal rat lung at E19, VDL group (n = 15); control group (n = 12) and at E22, VDL group (n = 15); control group (n = 11). Data were normalized against GAPDH. Results were calculated as mean ± SEM values.</p

Survival-rate of pups from mothers stratified by s-25(OH)D <25 nmol/L.

Kaplan-Meier survival analysis of both A) E19 (s-25(OH)D <25 nmol/L (n = 58); ≥25 nmol/L (n = 43)) and B) E22 (s-25(OH)D <25 nmol/L (n = 58); ≥25 nmol/L (n = 28)) pups. Comparison of survival curves using log-rank (Mantel-Cox) test.</p

The final size of regenerating splenic tissue is determined by the number of LTβR expressing cells at distant sites.

(A) Weight of splenic regenerates eight weeks of implantation into 4 types of recipients: i) WT mice that expressed LTβR in spleen (+) as well in other tissues (+); ii) splenectomized WT mice that expressed LTβR not in the spleen (-) but only in other tissues (+); iii) LTβR deficient mice that received WT splenic implants 8 weeks earlier, therefore expressing LTβR only within the regenerated splenic tissue (+) but not in other tissues (-); iv) LTβR deficient mice expressing LTβR neither in the spleen (-) nor in other tissues (-). Indicated are means and standard deviation (n = 5–9, ** = p < 0.01). (B) Cell number of splenic regenerates eight weeks of implantation into 4 types of recipients. Indicated are means and standard deviation (n = 5–9, ** = p < 0.01). (C) Indicated is the weight of the splenic implant and the weight of the resulting regenerate 8 weeks after implantation. There was no correlation between both parameters (Spearman-ρ = -0.1). The broken line indicates the mean. Each dot represents one animal. These experiments were 2 times independently performed.</p

The two faces of the LTβR signaling pathway.

After LTα1β2 expressed by activated B and T cell binds to LTβR, stromal cells up-regulate the secretion of chemokines (e.g. CCL19, CCL21, CXCL13) and the expression of adhesion molecules (e.g. ICAM-1, VCAM-1, MAdCAM-1). This further attracts LTα1β2 expressing cells and establishes a positive feed-back loop that is essential for the development and maintenance of secondary lymphoid organs (left side, green). The present study now indicates that ligation of the LTβR also leads to production of growth inhibitory factor(s) which upon binding to unknown receptors expressed by not yet characterized cells might counteract the positive feed-back loop. Interference with stromal cell turnover and/or angiogenesis might be possible targets (right side, red). When reaching a threshold level, LTβR dependent supportive and suppressive activities are in balance and secondary lymphoid organs homeostasis is achieved.</p

Maternal data.

Maternal data.</p

LTβR dependent growth suppressive activity also affects fully developed splenic tissue.

<p>(A) WT recipients without prior splenectomy were either sham operated or received WT or LTβR^-/- splenic implants. Eight weeks later weight (left side) and cell number (right side) of the endogenous spleen was determined. Only WT splenic regenerates significantly reduced weight and cell number of the endogenous WT spleen. Indicated are means and standard deviation (n = 4–11, * = p < 0.05, ** = p < 0.01). (B) LTβR^-/- recipients without prior splenectomy were either sham operated or received WT or LTβR^-/- splenic implants. Eight weeks later weight (left side) and cell number (right side) of the endogenous spleen was determined. Only WT splenic regenerates significantly reduced weight and cell number of the endogenous LTβR^-/- deficient spleen. Indicated are means and standard deviation (n = 5–8, ** = p < 0.01). These experiments were 2 times independently performed.</p

Offspring data.

<p>Offspring data.</p

The splenic transplantation model.

<p>After removal of the endogenous spleen the recipient (WT or LTβR^-/-) receives a splenic implant which is composed of two pieces representing 50% of a WT or LTβR deficient spleen. The implanted splenic tissue first becomes necrotic because the blood supply is lacking. Then, formation of splenic tissue starts and within eight weeks splenic regeneration is completed.</p