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1.
Supplemental parenteral nutrition improves immunity with unchanged carbohydrate and protein metabolism in critically ill patients: The SPN2 randomized tracer study.
Berger, MM, Pantet, O, Jacquelin-Ravel, N, Charrière, M, Schmidt, S, Becce, F, Audran, R, Spertini, F, Tappy, L, Pichard, C
Clinical nutrition (Edinburgh, Scotland). 2019;(5):2408-2416
Abstract
BACKGROUND & AIMS Individualized supplemental parenteral nutrition (SPN) providing measured energy expenditure from day 4 reduced infectious complications in a previous study including 305 intensive care (ICU) patients. The study aimed at investigating the metabolic, and immune responses underlying the clinical response of the previous trial. METHODS Randomized controlled trial enrolling 23 critically ill patients on day 3 (D3) of admission to the ICU who were fed less than 60% of their energy target by the enteral nutrition (EN) alone: allocation to either continued EN or to SPN to a target validated by indirect calorimetry. Protein and glucose metabolism (primary endpoint) were investigated with tracer isotopes on D4 and D9. Secondary endpoints: 1) immune response, investigated in serum and in stimulated peripheral blood mononuclear cells (PMBC), by dosing a panel of cytokines (infectious complications were recorded), and 2) Muscle mass was assessed by ultrasound of the thigh. RESULTS Comparable at baseline, the SPN group (n = 11) received more energy (median 24.3 versus 17.8 kcal/kg/day: p < 0.001) and proteins (1.11 versus 0.69 g/kg/day: p < 0.001) than the control group during the five days' intervention, resulting in a less negative energy balance by D9 (p = 0.0027). Net protein breakdown and Glucose kinetics on D9 did not differ, within or between groups. In agreement with a decrease in infection rate, immune response in the SPN group showed decreased serum IL-6 (p = 0.024), IL-1β, IL-10 levels and TNF-α secretion by PBMC (p = 0.018) at D9. Muscle mass loss from D4 to D15 tended to be less in the SPN group (-16% versus -23%: p = 0.06). Clinical course by D28 did not differ. CONCLUSIONS Feeding patients to cover an individualised measured energy target with SPN from D4 to cover needs, was associated with improved immunity, less systemic inflammation and a trend to less muscle mass loss. CLINICAL TRIAL REGISTRY NCT02022813 at https://clinicaltrials.gov/.
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2.
The effect of ginger supplementation on some immunity and inflammation intermediate genes expression in patients with active Rheumatoid Arthritis.
Aryaeian, N, Shahram, F, Mahmoudi, M, Tavakoli, H, Yousefi, B, Arablou, T, Jafari Karegar, S
Gene. 2019;:179-185
Abstract
OBJECTIVE Rheumatoid Arthritis (RA) is an autoimmune disease. The aim of this study was to investigate the effect of ginger supplementation on the expression of some immunity and inflammation intermediate genes in patients who suffer from RA. METHODS In this randomized double-blind placebo-controlled clinical trial, seventy active RA patients were allocated randomly into two groups who either received 1500 mg ginger powder or placebo daily for 12 weeks. Disease activity score and gene expression of NF-κB, PPAR-γ, FoxP3, T-bet, GATA-3, and RORγt as immunity and inflammation intermediate factors were measured using quantitative real-time PCR before and after the intervention. RESULTS After the intervention, FoxP3 genes expression increased significantly within ginger group and between the two groups (P-value = 0.02). Besides, T-bet and RORγt genes expression decreased significantly between the two groups (P-value < 0.05). In ginger group, PPAR-γ genes expression increased significantly (P-value = 0.047) but the difference between the two groups wasn't statistically significant (P-value = 0.12). The reduction in disease activity score was statistically significant within ginger group and between the two groups after the intervention. CONCLUSION It seems that ginger can improve RA by decreasing disease manifestations via increasing FoxP3 genes expression and by decreasing RORγt and T-bet genes expression.
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3.
Protein intake and amino acid supplementation regulate exercise recovery and performance through the modulation of mTOR, AMPK, FGF21, and immunity.
Torre-Villalvazo, I, Alemán-Escondrillas, G, Valle-Ríos, R, Noriega, LG
Nutrition research (New York, N.Y.). 2019;:1-17
Abstract
Exercise is considered to be the best approach to improve quality of life, and together with a healthy and adequate dietary pattern, exercise represents the best strategy to reduce the risk of chronic metabolic and inflammatory diseases, such as those related to obesity. The regularity and intensity of exercise is modulated at the molecular level in the skeletal muscle by two protein kinases, the mechanistic target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK), which act as sensors of external stimuli, showing the energy status of muscular fibers. The mTOR pathway is activated by insulin and amino acid availability, and its metabolic actions culminate in increased protein synthesis and reduced autophagy, leading to an increase in muscle mass. In contrast, AMPK activation induces a transcriptional program aimed to increase the mitochondrial content in skeletal muscle, transforming fast-twitch glycolytic fibers to slow-twitch oxidative fibers and increasing resistance to fatigue. In addition, inadequate exercise training induces imbalance in the immune response, generating excessive inflammation and/or immunosuppression. The purpose of this review is to summarize recent studies that provide insight into dietary protein interventions and/or amino acid supplementation that may improve outcomes after exercise by modulating 1) mTOR and AMPK activation during early exercise recovery, leading to increased muscle protein synthesis or increased oxidative capacity; 2) undesirable inflammatory responses; and 3) fibroblast growth factor 21 (FGF21) levels that may have relevant implications in skeletal muscle metabolism, particularly during the exercise recovery and performance of obese subjects.
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4.
Immune Function and Micronutrient Requirements Change over the Life Course.
Maggini, S, Pierre, A, Calder, PC
Nutrients. 2018;(10)
Abstract
As humans age, the risk and severity of infections vary in line with immune competence according to how the immune system develops, matures, and declines. Several factors influence the immune system and its competence, including nutrition. A bidirectional relationship among nutrition, infection and immunity exists: changes in one component affect the others. For example, distinct immune features present during each life stage may affect the type, prevalence, and severity of infections, while poor nutrition can compromise immune function and increase infection risk. Various micronutrients are essential for immunocompetence, particularly vitamins A, C, D, E, B2, B6, and B12, folic acid, iron, selenium, and zinc. Micronutrient deficiencies are a recognized global public health issue, and poor nutritional status predisposes to certain infections. Immune function may be improved by restoring deficient micronutrients to recommended levels, thereby increasing resistance to infection and supporting faster recovery when infected. Diet alone may be insufficient and tailored micronutrient supplementation based on specific age-related needs necessary. This review looks at immune considerations specific to each life stage, the consequent risk of infection, micronutrient requirements and deficiencies exhibited over the life course, and the available evidence regarding the effects of micronutrient supplementation on immune function and infection.
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5.
The developing gut microbiota and its consequences for health.
Butel, MJ, Waligora-Dupriet, AJ, Wydau-Dematteis, S
Journal of developmental origins of health and disease. 2018;(6):590-597
Abstract
The developmental origin of health and disease highlights the importance of the period of the first 1000 days (from the conception to the 2 years of life). The process of the gut microbiota establishment is included in this time window. Various perinatal determinants, such as cesarean section delivery, type of feeding, antibiotics treatment, gestational age or environment, can affect the pattern of bacterial colonization and result in dysbiosis. The alteration of the early bacterial gut pattern can persist over several months and may have long-lasting functional effects with an impact on disease risk later in life. As for example, early gut dysbiosis has been involved in allergic diseases and obesity occurrence. Besides, while it was thought that the fetus developed under sterile conditions, recent data suggested the presence of a microbiota in utero, particularly in the placenta. Even if the origin of this microbiota and its eventual transfer to the infant are nowadays unknown, this placental microbiota could trigger immune responses in the fetus and would program the infant's immune development during fetal life, earlier than previously considered. Moreover, several studies demonstrated a link between the composition of placental microbiota and some pathological conditions of the pregnancy. All these data show the evidence of relationships between the neonatal gut establishment and future health outcomes. Hence, the use of pre- and/or probiotics to prevent or repair any early dysbiosis is increasingly attractive to avoid long-term health consequences.
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6.
From Infections to Anthropogenic Inflicted Pathologies: Involvement of Immune Balance.
Lee, F, Lawrence, DA
Journal of toxicology and environmental health. Part B, Critical reviews. 2018;(1):24-46
Abstract
A temporal trend can be seen in recent human history where the dominant causes of death have shifted from infectious to chronic diseases in industrialized societies. Human influences in the current "Anthropocene" epoch are exponentially impacting the environment and consequentially health. Changing ecological niches are suggested to have created health transitions expressed as modifications of immune balance from infections inflicting pathologies in the Holocene epoch (12,000 years ago) to human behaviors inflicting pathologies beginning in the Anthropocene epoch (300 years ago). A review of human immune health and adaptations responding to environmental (biological, chemical, physical, and psychological) stresses, which are influenced by social conditions, emphasize the involvement of fluctuations in immune cell subsets affecting influential gene-environment interactions. The literature from a variety of fields (anthropological, immunological, and environmental) is incorporated to present an expanded perspective on shifts in diseases within the context of immune balance and function and environmental immunology. The influences between historical and contemporary human ecology are examined in relation to human immunity. Several examples of shifts in human physiology and immunity support the premise that increased incidences of chronic diseases are a consequence of human modification of environment and lifestyle. Although the development of better health care and a broader understanding of human health have helped with better life quality and expectancy, the transition of morbidity and mortality rates from infections to chronic diseases is a cause for concern. Combinations of environmental stressors/pollutants and human behaviors and conditions are modulating the immune-neuroendocrine network, which compromises health benefits.
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7.
The Microbiotic Highway to Health-New Perspective on Food Structure, Gut Microbiota, and Host Inflammation.
Hansen, NW, Sams, A
Nutrients. 2018;(11)
Abstract
This review provides evidence that not only the content of nutrients but indeed the structural organization of nutrients is a major determinant of human health. The gut microbiota provides nutrients for the host by digesting food structures otherwise indigestible by human enzymes, thereby simultaneously harvesting energy and delivering nutrients and metabolites for the nutritional and biological benefit of the host. Microbiota-derived nutrients, metabolites, and antigens promote the development and function of the host immune system both directly by activating cells of the adaptive and innate immune system and indirectly by sustaining release of monosaccharides, stimulating intestinal receptors and secreting gut hormones. Multiple indirect microbiota-dependent biological responses contribute to glucose homeostasis, which prevents hyperglycemia-induced inflammatory conditions. The composition and function of the gut microbiota vary between individuals and whereas dietary habits influence the gut microbiota, the gut microbiota influences both the nutritional and biological homeostasis of the host. A healthy gut microbiota requires the presence of beneficial microbiotic species as well as vital food structures to ensure appropriate feeding of the microbiota. This review focuses on the impact of plant-based food structures, the "fiber-encapsulated nutrient formulation", and on the direct and indirect mechanisms by which the gut microbiota participate in host immune function.
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8.
Modulatory effect of three probiotic strains on infants' gut microbial composition and immunological parameters on a placebo-controlled, double-blind, randomised study.
De Andrés, J, Manzano, S, García, C, Rodríguez, JM, Espinosa-Martos, I, Jiménez, E
Beneficial microbes. 2018;(4):573-584
Abstract
The gut microbiota plays a crucial role in gastrointestinal health. Current use of probiotics is aimed at modulating the bacterial gut composition to alleviate specific diseases. The safety and tolerance of three probiotic strains (Bifidobacterium longum subsp. infantis R0033, Lactobacillus helveticus R0052 and Bifidobacterium bifidum R0071) has recently been described. The objective of the present study was to analyse the microbiological composition and immunological parameters of faecal samples obtained from healthy infants from 3 to 12 months of age after receiving either one of the three probiotic strains or placebo for 8 weeks. 16S ribosomal RNA gene sequencing and multiplexing technology was used for analysis. Faecal sample analysis showed that the most abundant genus in all four groups of infants pre- and post-intervention was Bifidobacterium, representing approximately 50% of the sequences. After the intervention period the microbial composition of faecal samples in the probiotic groups did not display notable changes. In contrast, a decrease in different Bifidobacterium species, such as B. bifidum and Bifidobacterium breve and an increase in Bacteroides, Blautia, Clostridium, Coprococcus and Faecalibacterium genera was observed in the placebo group. The analysis of a wide range of immune factors in faecal samples suggests a modulatory effect by these three probiotic strains during the intervention period. The anti-inflammatory ratio interleukin (IL)-10/IL-12 increased at the end of the intervention period in the B. infantis R0033 group while the TNF-α/IL-10 ratio increased in the L. helveticus R0052 group. The decrease of the IL-10/IL-12 ratio together with the increase of the tumour necrosis factor alpha (TNF-α)/IL-10 ratio demonstrated a pro-inflammatory profile in the placebo group. In conclusion, the species profile of the microbiome observed in all three probiotic groups resembled that of a younger infant, similar to an unweaned infant, when compared to the placebo group which may also be related with an anti-inflammatory effect.
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9.
Supplementation of fermented Maillard-reactive whey protein enhances immunity by increasing NK cell activity.
Kang, M, Oh, NS, Kim, M, Ahn, HY, Yoo, HJ, Sun, M, Kang, SH, Yang, HJ, Kwon, DY, Lee, JH
Food & function. 2017;(4):1718-1725
Abstract
OBJECTIVE The objective of this study was to investigate the impact of supplementation with fermented Maillard-reactive whey protein (F-MRP) on natural killer (NK) cell activity, circulating cytokines, and serum protein levels. METHODS A randomized, double-blind, placebo-controlled study was conducted on a sample of 80 participants without diabetes or obesity. Over an 8-week study period, the F-MRP group consumed 6 g of powder containing 4.2 g of F-MRP each day, whereas the placebo group consumed the same amount of maltodextrin. For each participant, NK cell activity was evaluated based on the ratio of effector cells (E; peripheral blood mononuclear cells, PBMCs) to target cells (T; K562 cells) at E : T ratios of 10 : 1, 5 : 1, 2.5 : 1, and 1.25 : 1. RESULTS Body mass index (BMI) and NK cell activity under all assay conditions were significantly increased in the F-MRP group at the 8-week follow-up visit compared with the values at the baseline, whereas the placebo group showed significant reductions in NK cell activity (at an E : T ratio of 5 : 1), serum albumin, and pre-albumin at the 8-week follow-up visit compared with the values at the baseline. When comparing the changes between the placebo and F-MRP groups, the increases in NK cell activity under all assay conditions and serum interleukin (IL)-12 in the F-MRP group were greater than those in the placebo group after adjusting for baseline values. There were also significant differences in pre-albumin and insulin-like growth factor (IGF)-1 between the two groups; the change in (Δ) IL-12 was positively correlated with both Δpre-albumin (r = 0.435, P = 0.006) and ΔNK cell activity at an E : T ratio of 10 : 1 (r = 0.571, P < 0.001) in the F-MRP group. CONCLUSION Daily consumption of F-MRP enhanced NK cell function, which was positively associated with ΔIL-12. Moreover, ΔIL-12 was positively correlated with Δpre-albumin.
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10.
The Transcription Factor EB Links Cellular Stress to the Immune Response
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Nabar, NR, Kehrl, JH
The Yale journal of biology and medicine. 2017;(2):301-315
Abstract
The transcription factor EB (TFEB) is the master transcriptional regulator of autophagy and lysosome biogenesis. Recent advances have led to a paradigm shift in our understanding of lysosomes from a housekeeping cellular waste bin to a dynamically regulated pathway that is efficiently turned up or down based on cellular needs. TFEB coordinates the cellular response to nutrient deprivation and other forms of cell stress through the lysosome system, and regulates a myriad of cellular processes associated with this system including endocytosis, phagocytosis, autophagy, and lysosomal exocytosis. Autophagy and the endolysosomal system are critical to both the innate and adaptive arms of the immune system, with functions in effector cell priming and direct pathogen clearance. Recent studies have linked TFEB to the regulation of the immune response through the endolysosmal pathway and by direct transcriptional activation of immune related genes. In this review, we discuss the current understanding of TFEB's function and the molecular mechanisms behind TFEB activation. Finally, we discuss recent advances linking TFEB to the immune response that positions lysosomal signaling as a potential target for immune modulation.