Consensus statement immunonutrition and exercise

In this consensus statement on immunonutrition and exercise, a panel of knowledgeable contributors from across the globe provides a consensus of updated science, including the background, the aspects for which a consensus actually exists, the controversies and, when possible, suggested directions for future research

DataSheet_1_Time-restricted feeding reduces monocyte production by controlling hematopoietic stem and progenitor cells in the bone marrow during obesity.docx

Time-restricted feeding (TRF) has emerged as a promising dietary approach in improving metabolic parameters associated with obesity, but its effect on immune cells under obesogenic condition is poorly understood. We conducted this study to determine whether TRF exerts its therapeutic benefit over obesity-induced myeloid cell production by analyzing hematopoietic stem and progenitor cells in bone marrow (BM) and immune cell profile in circulation. Male C57BL/6 mice were fed a low-fat diet (LFD) or high-fat diet (HFD) ad libitum for 6 weeks and later a subgroup of HFD mice was switched to a daily 10 h-TRF schedule for another 6 weeks. Mice on HFD ad libitum for 12 weeks had prominent monocytosis and neutrophilia, associated with expansion of BM myeloid progenitors, such as multipotent progenitors, pre-granulocyte/macrophage progenitors, and granulocyte/macrophage progenitors. TRF intervention in overweight and obese mice diminished these changes to a level similar to those seen in mice fed LFD. While having no effect on BM progenitor cell proliferation, TRF reduced expression of Cebpa, a transcription factor required for myeloid differentiation. These results indicate that TRF intervention may help maintain immune cell homeostasis in BM and circulation during obesity, which may in part contribute to health benefits associated with TRF.</p

Nonionic Block Copolymers Assemble on the Surface of Protein Bionanoparticle

Efficient delivery of therapeutic proteins to a target site remains a challenge due to rapid clearance from the body. Here, we selected tobacco mosaic virus (TMV) as a model protein system to investigate the interactions between the protein and a nonionic block copolymer as a possible protecting agent for the protein. By varying the temperature, we were able to obtain core–shell structures based on hydrophobic interactions among PO blocks and noncovalent interactions between TMV and EO blocks. The protein–polymer interactions were characterized by dynamic light scattering and isothermal titration calorimetry. This study establishes principles for the possible design of clinically useful protein delivery systems

Model of LP and HE effects on macrophage activation and plasticity.

<p>A) Prenatal LP decreases the size of adipocytes, while increases adipose tissue catch-up growth. LP by itself also inhibited <i>IL-6</i> expression in ATMs, which is independent of the adipocyte size. Postnatal HE increases the size of adipocytes, which causes the recruitment of M1, especially m1b macrophages to the adipose tissue. These ATMs expressed more <i>IL-6</i> and <i>IL-1β</i>. B) When prenatal LP diets are combined with postnatal HE diets for 12 weeks, adipocyte is enlarged but is still smaller than NP+HE rats. There is induced adipose tissue inflammation in LP+HE rats; however, they have less ATM infiltration and decreased <i>IL-6</i> in ATMs comparing to that of NP+HE rats, which were correlated with smaller size of adipocytes. Considering that LP+HE rats have largest adipose tissue-catch up growth, it is predictable that prolonged HE diets on LP offspring for 20 weeks will eventually break up the temporary balance due to significantly enlarged adipocytes.</p

HE diets enhanced number of CD11c⁺ or CD206⁺ cells in visceral adipose tissue, while LP inhibited the increase of CD11c⁺ or CD206⁺ cells due to HE diets.

<p>A-H and R). Visceral adipose tissue was stained with anti-CD11c. Number of CD11c⁺ cells was counted per 1,000 adipocytes area. Three randomly selected areas were counted for each rat. Number of CD11c positive cells in each group is normalized to the number of CD11c⁺ macrophages in NP+NE group. Average number of the CD11c⁺ was used for further statistical analysis. Data are presented as mean ± SEM, n = 5.”#” P<0.05 compared to NE; “*” P<0.05 compared to NP. E, F, G, and H are enlargements of the framed fields of A, B, C, and D, respectively. I-P and S). Visceral adipose tissue was stained with anti-CD206. Number of CD206⁺ cells was counted per 1,000 adipocytes area. Three randomly selected areas were counted for each rat. Number of CD206 positive cells in each group is normalized to the number of CD206⁺ macrophages in NP+NE group. Average number of the CD206⁺ was used for further statistical analysis. Data are presented as mean ± SEM, n = 9–12. M, N, O, and P are enlargements of the framed fields of I, J, K, and L, respectively. Magnificence of A-D and I-L: 200X; E-H and M-P 400X.</p

Prenatal LP offspring had reduced adipose tissue mass but significantly increased adipose tissue gain.

<p>A and B). Body weight of the experimental rats was measured at week 0 (weaning weight) and week 12. Data are presented as mean ± SEM, n = 9–12. C). Body weight change was calculated by dividing the body weight (g) and then subtracted one at week 12 by the weaning body weight (g). Data are presented as mean ± SEM, n = 9–12. D-E) Body fat mass was measure by EchoMRI at week 0 (weaning weight) and week 12. Data are presented as mean ± SEM, n = 9–12. F) Body fat change was calculated by dividing the fat weight (g) at week 12 by the weaning fat weight (g). Data are presented as mean ± SEM, n = 9–12. Bars bearing different letters significantly differ at P<0.05. G and H) Visceral fat tissue was collected for tissue slide sectioning and H&E staining. Eight hundred adipocytes from each rat sectioning were randomly picked up and the size was measured by ImageJ. Five rats were counted in each group. Size of the adipocytes was normalized to that of the NP+NE rats. Data are presented as mean ± SEM, n = 5. Bars bearing different letters significantly differ at P<0.05. I). The feed efficiency was calculated by “body weight gain/energy intake x100”. Data are presented as mean ± SEM, n = 5. Bars bearing different letters significantly differ at P<0.05.</p

Prenatal LP prevented CD68⁺ ATM infiltration triggered by HE diets.

<p>A-I) ATMs were stained with anti-CD68 antibody. The number of ATMs was counted per 1,000 adipocytes area. Three randomly selected areas were counted for each rat. Average number of the ATMs was used for further statistical analysis. Number of CD68 positive cells in each group is normalized to the number of CD68⁺ macrophages in NP+NE group. Data are presented as mean ± SEM, n = 6–9.”#” P<0.05 compared to NE; “*” P<0.05 compared to NP. E, F, G, and H are enlargements of the framed fields of A, B, C, and D, respectively. Magnificence of A-D: 200X; E-H 400X.</p

Primers used for RT-PCR experiment.

<p>Primers used for RT-PCR experiment.</p

Model of LP and HE effects on macrophage activation and plasticity.

<p>A) Prenatal LP decreases the size of adipocytes, while increases adipose tissue catch-up growth. LP by itself also inhibited <i>IL-6</i> expression in ATMs, which is independent of the adipocyte size. Postnatal HE increases the size of adipocytes, which causes the recruitment of M1, especially m1b macrophages to the adipose tissue. These ATMs expressed more <i>IL-6</i> and <i>IL-1β</i>. B) When prenatal LP diets are combined with postnatal HE diets for 12 weeks, adipocyte is enlarged but is still smaller than NP+HE rats. There is induced adipose tissue inflammation in LP+HE rats; however, they have less ATM infiltration and decreased <i>IL-6</i> in ATMs comparing to that of NP+HE rats, which were correlated with smaller size of adipocytes. Considering that LP+HE rats have largest adipose tissue-catch up growth, it is predictable that prolonged HE diets on LP offspring for 20 weeks will eventually break up the temporary balance due to significantly enlarged adipocytes.</p

Prenatal low and normal protein diet composition.

<p>Prenatal low and normal protein diet composition.</p