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Fe supplementation is a common strategy to correct Fe-deficiency anaemia in children; however, it may modify the gut microbiota and increase the risk for enteropathogenic infection. In the present study, we studied the impact of Fe supplementation on the abundance of dominant bacterial groups in the gut, faecal SCFA concentration and gut inflammation in children living in rural South Africa. In a randomised, placebo-controlled intervention trial of 38 weeks, 6- to 11-year-old children with Fe deficiency received orally either tablets containing 50 mg Fe as FeSO4 (n 22) for 4 d/week or identical placebo (n 27). In addition, Fe-sufficient children (n 24) were included as a non-treated reference group. Faecal samples were analysed at baseline and at 2, 12 and 38 weeks to determine the effects of Fe supplementation on ten bacterial groups in the gut (quantitative PCR), faecal SCFA concentration (HPLC) and gut inflammation (faecal calprotectin concentration). At baseline, concentrations of bacterial groups in the gut, faecal SCFA and faecal calprotectin did not differ between Fe-deficient and Fe-sufficient children. Fe supplementation significantly improved Fe status in Fe-deficient children and did not significantly increase faecal calprotectin concentration. Moreover, no significant effect of Fe treatment or time × treatment interaction on the concentrations of bacterial groups in the gut or faecal SCFA was observed compared with the placebo treatment. Also, there were no significant differences observed in the concentrations of any of the bacterial target groups or faecal SCFA at 2, 12 or 38 weeks between the three groups of children when correcting for baseline values. The present study suggests that in African children with a low enteropathogen burden, Fe status and dietary Fe supplementation did not significantly affect the dominant bacterial groups in the gut, faecal SCFA concentration or gut inflammation.

Iron deficiency may impair adaptive immunity and is common among African infants at time of vaccination. Whether iron deficiency impairs vaccine response and whether iron supplementation improves humoral vaccine response is uncertain. We performed two studies in southern coastal Kenya. In a birth cohort study, we followed infants to age 18 mo and assessed whether anemia or iron deficiency at time of vaccination predicted vaccine response to three-valent oral polio, diphtheria-tetanus-whole cell pertussis- type b vaccine, ten-valent pneumococcal-conjugate vaccine and measles vaccine. Primary outcomes were anti-vaccine-IgG and seroconversion at age 24 wk and 18 mo. In a randomized trial cohort follow-up, children received a micronutrient powder (MNP) with 5 mg iron daily or a MNP without iron for 4 mo starting at age 7.5 mo and received measles vaccine at 9 and 18 mo; primary outcomes were anti-measles IgG, seroconversion and avidity at age 11.5 mo and 4.5 y. In the birth cohort study, 573 infants were enrolled and 303 completed the study. Controlling for sex, birthweight, anthropometric indices and maternal antibodies, hemoglobin at time of vaccination was the strongest positive predictor of: (A) anti-diphtheria and anti-pertussis-IgG at 24 wk ( = 0.0071, = 0.0339) and 18 mo ( = 0.0182, = 0.0360); (B) anti-pertussis filamentous hemagglutinin-IgG at 24 wk ( = 0.0423); and (C) anti-pneumococcus 19 IgG at 18 mo ( = 0.0129). Anemia and serum transferrin receptor at time of vaccination were the strongest predictors of seroconversion against diphtheria ( = 0.0484, = 0.0439) and pneumococcus 19 at 18 mo ( = 0.0199, = 0.0327). In the randomized trial, 155 infants were recruited, 127 and 88 were assessed at age 11.5 mo and 4.5 y. Compared to infants that did not receive iron, those who received iron at time of vaccination had higher anti-measles-IgG ( = 0.0415), seroconversion ( = 0.0531) and IgG avidity ( = 0.0425) at 11.5 mo. In Kenyan infants, anemia and iron deficiency at time of vaccination predict decreased response to diphtheria, pertussis and pneumococcal vaccines. Primary response to measles vaccine may be increased by iron supplementation at time of vaccination. These findings argue that correction of iron deficiency during early infancy may improve vaccine response.

The systemic immune-inflammation index (SII) is widely used in monitoring disease progression, evaluating treatment efficacy, and predicting outcomes across diverse diseases. Yet, its roles in iron deficiency (ID) remains unclear. This investigation aims to explore the association between SII and ID in 20–80 years old individuals which can accurately represent the people’s health status in the United States. This cross-sectional study analyzed data from 4,075 National Health and Nutrition Examination Survey(NHANES) participants. The relationship between SII (SII = platelet counts × neutrophil counts/ lymphocyte counts) and C-reactive protein (CRP) with iron metabolism indicators including total body iron (TBI), serum ferritin (SF), soluble transferrin receptor (sTfR), total iron binding capacity (TIBC), transferrin saturation (TS), mean corpuscular volume (MCV), and hemoglobin (Hb) and ID, anemia and iron deficiency anemia (IDA) were assessed using multiple linear regression or logistic regression, respectively. Interaction tests were performed to explore whether these relationships between SII and iron metabolism indicators varied by sex, age, and race. Among 9,254 screened participants, 4,075 U.S. adults aged 20-80 years met inclusion criteria. Compared to individuals with low SII, high SII people have lower family income-to poverty ratio (PIR), higher proportion of females, lower level of SF, TBI, TS and Hb, higher level of sTfR, TIBC and the odd of ID and IDA. In the fully adjusted model, SII exhibited significant correlations with sTfR (β = 0.62, 95% CI 0.45－0.78), TIBC (β = 13.19, 95% CI 8.90－17.49), SF (β = -16.07, 95% CI -30.51－-1.64), TBI (β = -1.23, 95% CI -1.56 － -0.90), TS (β = -1.55, 95% CI -2.53－-0.57), Hb (β = -0.18, 95% CI -0.30－-0.05), ID (OR = 2.22, 95% CI 1.69－2.85) and IDA (OR = 1.96, 95% CI 1.35－2.85) and CRP exhibited significant correlations with SII (β = 010.62, 95% CI 9.55－11.70), sTfR (β = 0.02, 95% CI 0.01－0.03), SF (β = 1.62, 95% CI 1.05－2.19), TBI (β = 0.02, 95% CI 0.01－0.03). Smooth curves in all participants indicated correlations between SII and various iron indicators. Independent correlations between the SII and various iron markers, as well as the occurrence of ID and IDA, were observed in the interaction tests stratified by age, sex, and race. An association was identified between SII representing systemic inflammation and a tendency towards ID, along with heightened odds of experiencing both ID and IDA. SII exhibited a more comprehensive association with ID than CRP.

The metabolism of nutritional iron, required by viruses to replicate and proliferate, is regulated by hepcidin, a peptide hormone of 25 amino acids. Overexpression of hepcidin results in iron deficiency anemia (IDA), while its downregulation can lead to an iron overload. Recently, IDA has been highlighted for its role in the impairment of adaptive immunity and poor vaccine effectiveness. Here, we assessed the possible role of IDA in oral rotavirus (RV) vaccine take among South African infants. Paired stool and unstimulated saliva were collected from oral RV vaccinated infants, who attended a routine immunization program at Oukasie Healthcare clinic, north of Pretoria, South Africa, to decide vaccine shedders (n = 20) and non-shedders (n = 18). IDA was determined by assaying the salivary hepcidin levels using an ELISA kit, while expression of hepcidin, hepcidin inducer IL-6, Interferon I (IFN I) and IFN-γ were determined by qPCR. There were no significant differences in the average hepcidin levels between vaccine shedders and non-shedders ( = 0.83). Hepcidin levels were decreased 0.43-fold a week after vaccination versus pre-vaccination, = 0.0001. Unlike the concentration, the expression of hepcidin increased 5-5-fold in non-shedders compared to vaccine shedders. Similarly, the expression of IL-6 and IFN I were increased 5.2- and 4.9-fold, respectively, in non-shedders compared to shedders. In contrast, the expression of IFN-γ was increased 3.2-fold in shedders compared to non-shedders. Collectively, our observations suggest a possible role for IDA in impediment of oral RV vaccine take among South African infants.

Background Iron plays an important role in body defense and essential for normal immune system development where its deficiency may result in an inadequate immune response. We aimed to assess the lymphocyte subsets in childhood iron deficiency anemia (IDA) with their laboratory correlations. Methods Fifty IDA (< 18 years) and 25 age and sex-matched healthy children were enrolled and a complete history was obtained and clinical examination was performed. Complete blood count, serum iron, total iron binding capacity and serum ferritin, were performed. Flow cytometric determination of peripheral blood CD3+, CD4+, CD8+ T-lymphocytes and CD19+ B-lymphocytes and CD4/CD8 ratio were done. Results Patients had significantly lower hemoglobin, Serum iron, ferritin levels and higher lymphocytic count in patients compared with controls ( p  = 0.001, 0.03, 0.001, 0.001 respectively). CD3 count and percentage were significantly lower in IDA patients compared to controls ( p  = 0.007 and 0.005 respectively). There was a Significant reduction in the CD4 count, percentage and CD4/CD8 ratio in patients compared with controls ( p  = 0.001, 0.001 and 0.005 respectively) while there was no significant difference regarding CD8 count and percentage. No significant difference between the two studied groups regarding either CD19 count or percentage ( p  = 0.28 and 0.18 respectively) were found. Conclusions IDA is associated with impaired cell-mediated immune response specifically T-cell mediated immunity.

Background: Iron deficiency anemia (IDA) is the most prevalent micronutrient deficiency in preschool children in developing countries including India. IDA is associated with immune perturbation, which is reflected in greater frequency of infections in these children. Recent research has shown three distinct monocyte subsets with distinct functions linked to infectious, inflammatory, and autoimmune diseases. These subsets have not been studied in chil-dren with IDA. Objective: The aim of the study was to assess the percentage of monocyte population and the three subset populations in children with IDA and to compare the data with age-matched healthy controls. Methods: Venous blood samples (5 mL) from 40 IDA children and 20 controls were collected after taking informed consent. Monocyte subpopulations were compared across the two groups. The outcome variables were calculated using Students Independent t-test or Mann– Whitney U test. P value of <0.05 was taken as significant. Results: No significant difference was found in the absolute numbers as well as percentages of total monocytes between the control and case (study) group. Children in the IDA group showed a significant (p = 0.03) decrease in the nonclassical subset population when compared to the control group. Conclusion: This is the first study done on monocyte subsets in iron-deficient children. Decrease in nonclassical monocytes observed may be associated with a pro-inflammatory state and increased risk of inflammatory and auto immune diseases. Follow-up studies are needed to confirm these findings.

Early nutrition is key to promoting gut growth and education of the immune system. Although iron deficiency anemia has long been recognized as a serious iron disorder, the effects of iron supplementation on gut development are less clear. Therefore, using suckling piglets as the model for iron deficiency, we assessed the impacts of iron supplementation on hematological status, gut development, and immunity improvement. Piglets were parenterally supplied with iron dextran (FeDex, 60 mg Fe/kg) by intramuscular administration on the third day after birth and slaughtered at the age of two days, five days, 10 days, and 20 days. It was expected that iron supplementation with FeDex improved the iron status with higher levels of serum iron, ferritin, transferrin, and iron loading in the liver by regulating the interaction of hepcidin and ferroportin (FPN). FeDex supplementation increased villus length and crypt depth, attenuated the pathological status of the duodenum, and was beneficial to intestinal mucosa. FeDex also influenced the intestinal immune development by stimulating the cytokines’ production of the intestine and enhancing the phagocytotic capacity of monocytes. Overall, the present study suggested that iron supplementation helped promote the development of the intestine by improving its morphology, which maintains its mucosal integrity and enhances the expression of immuno-associated factors.

Prebiotics may increase intestinal Fe absorption in anaemic growing rats. The present study evaluated the effects of high-performance (HP) inulin and oligofructose on factors that regulate Fe absorption in anaemic rats during the growth phase. Male Wistar rats aged 21 d of age were fed AIN-93G ration without Fe for 2 weeks to induce Fe-deficiency anaemia. The rats were fed on day 35 a control diet, or a diet with 10 % HP inulin, or a diet with 10 % oligofructose, without Fe supplementation. The animals were euthanised after 2 weeks, and segments of the duodenum, caecum, colon and liver were removed. The expression levels of proteins in the intestinal segments were assessed using Western blotting. The levels of serum, urine and liver hepcidin and the concentrations of IL-10, IL-6 and TNF-α in the caecum, colon and liver were measured using the ELISA test. HP inulin increased the expression of the divalent metal transporter 1 protein in the caecum by 162 % (P= 0·04), and the expression of duodenal cytochrome b reductase in the colon by 136 % (P= 0·02). Oligofructose decreased the expression of the protein ferroportin in the duodenum (P= 0·02), the concentrations of IL-10 (P= 0·044), IL-6 (P= 0·036) and TNF-α (P= 0·004) in the caecum, as well as the level of urinary hepcidin (P< 0·001). These results indicate that prebiotics may interfere with the expression of various intestinal proteins and systemic factors involved in the regulation of intestinal Fe absorption in anaemic rats during the growth phase.

The present study was to evaluate the consequences of iron status across oral and parenteral iron administrations in prevention of iron deficiency anemia. A total of 24 one-day-old male neonatal piglets were allocated into three groups given non-iron supplementation (NON), intramuscular iron dextran injection (FeDex), and oral administration of ferrous glycine chelate (FeGly), respectively. At day 8, no significant differences in final body weight, average weight gain, and tissue coefficients were observed among three groups (P > 0.05). Both oral FeGly and FeDex injection significantly increased serum iron, ferritin, hemoglobin, and tissue iron deposition (P < 0.05). However, FeDex-injected supplementation resulted in rapidly rising hepcidin levels and hepatic iron deposition (P < 0.05). In addition, compared to parenteral iron supplementation, greater serum IgA level, SOD, and GSH-Px activities, lower expressions of IL-1β and TNF-α in the liver, and lower expressions of IL-6 and TNF-α in the spleen were found in oral iron piglets (P < 0.05). According to our results, oral administration of ferrous glycine chelate improved iron homeostasis, and oxidative and immune status in anemic neonatal pigs.

Iron is utilised by the body for oxygen transport and energy production, and is therefore essential to athletic performance. Commonly, athletes are diagnosed as iron deficient, however, contrasting evidence exists as to the severity of deficiency and the effect on performance. Iron losses can result from a host of mechanisms during exercise such as hemolysis, hematuria, sweating and gastrointestinal bleeding. Additionally, recent research investigating the anemia of inflammation during states of chronic disease has allowed us to draw some comparisons between unhealthy populations and athletes. The acute-phase response is a well-recognised reaction to both exercise and disease. Elevated cytokine levels from such a response have been shown to increase the liver production of the hormone Hepcidin. Hepcidin up-regulation has a negative impact on the iron transport and absorption channels within the body, and may explain a potential new mechanism behind iron deficiency in athletes. This review will attempt to explore the current literature that exits in this new area of iron metabolism and exercise.