SEARCH · PubMed Health

Results for “zinc”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources

PubMed2003

A sodium zinc exchange mechanism is mediating extrusion of zinc in mammalian cells.

Zinc influx, driven by a steep inward electrochemical gradient, plays a fundamental role in zinc signaling and in pathophysiologies linked to intracellular accumulation of toxic zinc. Yet, the cellular transport mechanisms that actively generate or maintain the transmembrane gradients are not well understood. We monitored Na+-dependent Zn2+ transport in HEK293 cells and cortical neurons, using fluorescent imaging. Treatment of the HEK293 cells with CaPO4 precipitates induced Na+-dependent Zn2+ extrusion, against a 500-fold transmembrane zinc gradient, or zinc influx upon reversal of Na+ gradient, thus indicating that Na+/Zn2+ exchange is catalyzing active Zn2+ transport. Depletion of intracellular ATP did not inhibit the Na+-dependent Zn2+ extrusion, consistent with a mechanism involving a secondary active transporter. Inhibitors of the Na+/Ca2+ exchanger failed to inhibit Na+-dependent Zn2+ efflux. In addition, zinc transport was unchanged in HEK293 cells heterologously expressing functional cardiac or neuronal Na+/Ca2+ exchangers, thus indicating that the Na+/Zn2+ exchange activity is not mediated by the Na+/Ca2+ exchanger. Sodium-dependent zinc exchange, facilitating the removal of intracellular zinc, was also monitored in neurons. To our knowledge, the Na+/Zn2+ exchanger described here is the first example of a mammalian transport mechanism capable of Na+-dependent active extrusion of zinc. Such mechanism is likely to play an important role, not only in generating the transmembrane zinc gradients, but also in protecting cells from the potentially toxic effects of permeation of this ion.

Animals↗

PubMed2004

Extracellular zinc triggers ERK-dependent activation of Na+/H+ exchange in colonocytes mediated by the zinc-sensing receptor.

Extracellular zinc promotes cell proliferation and its deficiency leads to impairment of this process, which is particularly important in epithelial cells. We have recently characterized a zinc-sensing receptor (ZnR) linking extracellular zinc to intracellular release of calcium. In the present study, we addressed the role of extracellular zinc, acting via the ZnR, in regulating the MAP kinase pathway and Na+/H+ exchange in colonocytes. We demonstrate that Ca2+ release, mediated by the ZnR, induces phosphorylation of ERK1/2, which is highly metal-specific, mediated by physiological concentrations of extracellular Zn2+ but not by Cd2+, Fe2+, Ni2+, or Mn2+. Desensitization of the ZnR by Zn2+, is followed by approximately 90% inhibition of the Zn2+ -dependent ERK1/2 phosphorylation, indicating that the ZnR is a principal link between extracellular Zn2+ and ERK1/2 activation. Application of both the IP3 pathway and PI 3-kinase antagonists largely inhibited Zn2+ -dependent ERK1/2 phosphorylation. The physiological significance of the Zn2+ -dependent activation of ERK1/2 was addressed by monitoring Na+/H+ exchanger activity in HT29 cells and in native colon epithelium. Preincubation of the cells with zinc was followed by robust activation of Na+/H+ exchange, which was eliminated by cariporide (0.5 microm); indicating that zinc enhances the activity of NHE1. Activation of NHE1 by zinc was totally blocked by the ERK1/2 inhibitor, U0126. Prolonged acidification, in contrast, stimulates NHE1 by a distinct pathway that is not affected by extracellular Zn2+ or inhibitors of the MAP kinase pathway. Desensitization of ZnR activity eliminates the Zn2+ -dependent, but not the prolonged acidification-dependent activation of NHE1, indicating that Zn2+ -dependent activation of H+ extrusion is specifically mediated by the ZnR. Our results support a role for extracellular zinc, acting through the ZnR, in regulating multiple signaling pathways that affect pH homeostasis in colonocytes. Furthermore activation of both, ERK and NHE1, by extracellular zinc may provide the mechanism linking zinc to enhanced cell proliferation.

Animals↗

PubMed1993

[Estimation of the zinc requirement for broilers using their ability for selective zinc absorption and by dose-response relations].

Broiler chicks are able to select an adequate dietary Zn-concentration in choice-feeding. The zinc requirement should be ascertained by this method of self-selection. 72 day-old chicks were divided into 9 groups and were kept over 5 weeks in individual cages. By gradually supplementing ZnSO4.7H2O to a semisynthetic basal diet with isolated soybean protein 5 diets were made with Zn-concentrations of 14, 22, 30, 38 and 50 ppm, which respectively were fed to one group. The four other groups had to choose between two rations: 14/38; 14/50; 22/38; 22/50. Selective zinc intake was represented by a significant increase of dietary zinc concentration compared to random selection (mean of both diets). Feed intake, zinc intake and weight gain were measured daily and the end total feed consumption, live weight, feed conversion rate, plasma-zinc concentration and plasma-zinc binding capacity at the end of the experiment. In comparison optimal dietary zinc levels were estimated by dose-response relations, both by sigmoid growth curves and by broken-line model. With 30 ppm Zn chickens reached a high fattening level with daily weight gains of 60 g. Feed intake and growth rate were markedly reduced at a dosage of 14 and 22 ppm Zn, feed conversion rate was tendentially decreased below a level of about 34 ppm, whereas above zinc binding capacity reached a plateau. Birds self-selected a dietary zinc level of 32 ppm, which were adequate for the criteria feed intake and weight gains. Zinc requirements of about 40 ppm were assessed by conventional methods.

Absorption↗

PubMed1979

Saliva zinc levels: potential indicators of zinc status.

Mixed saliva was collected from eight adolescent females participating in a metabolic study and from 59 adolescent females participating in a nutrition survey. Zinc concentrations, protein concentrations, and zinc:protein ratios of whole mixed saliva samples and of supernatant samples, which were prepared from the mixed saliva, were determined. Zinc analyses were performed with an atomic absorption spectrophotometer equipped with a graphite furnace. Significantly (P less than 0.05) lower levels of zinc were found in the supernant samples, but not in the whole saliva samples, when the same subjects were fed 11.5 mg zinc daily rather than 14.7 mg zinc daily during the metabolic study. The mean zinc concentrations of the whole saliva and the supernatant samples collected during the survey were 173 +/- 94 (SD) and 30.5 +/- 14.8 ng/ml, respectively. The levels of zinc and protein in the whole mixed saliva (r = 0.460, P less than 0.001) and the supernatant samples (4 = 0.486, P less than 0.001) were correlated. The levels of zinc in both types of saliva samples were not correlated to serum or hair zinc levels of girls in the survey.

Adolescent↗

PubMed1980

Zinc-binding properties of bovine and human milk in vitro: influence of changes in zinc content.

The total zinc content of samples of fat-free human and bovine milk was 3.5 and 3.6 micrograms/ml, respectively. The total protein content was 5.3 and 29.0 mg/ml, respectively, Sephadex G-75 gel filtration chromatography of bovine milk revealed no evidence of zinc associated with low molecular weight fractions (less than 2000 daltons). However, chromatography revealed that 10% of the zinc in human milk was associated with these fractions. When the zinc content of these milks was raised by adding Zn2+ in vitro, chromatography of milk from both species revealed the presence of zinc with the low molecular weight fractions. More zinc was associated with these fractions from human milk than from bovine milk. Recovery of zinc was nearly 100% for all columns. It is proposed, based upon these binding data, that the association of zinc with low molecular weight components of milk is related in part to both protein content and composition and the relative zinc concentrations. These binding differences might influence the bioavailability of zinc from milk.

Animals↗

PubMed1983

Zinc supplementation during pregnancy: zinc concentration of serum and hair from low-income women of Mexican descent.

The effect of zinc supplementation on concentrations of zinc in hair and serum of 213 pregnant Hispanic women attending a clinic in Los Angeles was assessed using a random, double-blind experiment. Both the treatment (T) and control (C) groups received similar vitamin and mineral supplements except that 20 mg zinc was added to the supplements for the treatment group. Nutrient intakes were calculated from 24-h recalls. The initial mean dietary zinc intake of both groups was about 50% of the Recommended Dietary Allowance (9 +/- 5 mg). Initially there were no significant differences between the two groups in mean zinc levels in serum (66 +/- 11 micrograms/dl, C, and 65 +/- 12 micrograms/dl, T) or in hair (184 +/- 41 micrograms/g, C, and 175 +/- 38 micrograms/g, T). Zinc supplementation did not alter mean zinc levels in serum or hair but significantly (p less than 0.05) reduced the number of low serum zinc values (less than or equal to 53.3 micrograms/dl) toward the end of pregnancy. Although serum zinc levels do decline in pregnancy, our results suggest that severely depressed levels (less than or equal to 50 to 55 micrograms/dl) indicate inadequate zinc status.

Adolescent↗

PubMed1987

Bioavailability of zinc from zinc-histidine complexes. II. Studies on patients with liver cirrhosis and the influence of the time of application.

Supplementation may benefit patients with liver cirrhosis. Zinc uptake from zinc-histidine complex 1:2 was assessed in eight patients with liver cirrhosis. Influence of the time of application was also studied. Compared with healthy controls, patients showed a 40% lower uptake of zinc after 20 mg zinc from zinc histidine. Bioavailability was identical when zinc was taken 6 h or 1 h before a meal but an order of magnitude greater than with or 1 h after a meal. No significant increase of serum zinc was found when zinc was given with a meal or 1 h after. Lower doses of zinc-histidine complexes than of zinc sulfate may be used to supplement patients with liver cirrhosis. Time of application is of great importance if this substitution is to be successful.

Adult↗

PubMed2003

A community-based randomized controlled trial of iron and zinc supplementation in Indonesian infants: interactions between iron and zinc.

BACKGROUND: Combined supplementation with iron and zinc during infancy may be effective in preventing deficiencies of these micronutrients, but knowledge of their potential interactions when given together is insufficient. OBJECTIVE: The goal was to compare the effect in infants of combined supplementation with iron and zinc and of supplementation with single micronutrients on iron and zinc status. DESIGN: Indonesian infants (n = 680) were randomly assigned to daily supplementation with 10 mg Fe (Fe group), 10 mg Zn (Zn group), 10 mg Fe + 10 mg Zn (Fe+Zn group), or placebo from 6 to 12 mo of age. Venous blood samples were collected at the start and end of the study. Five hundred forty-nine infants completed the supplementation and had both baseline and follow-up blood samples available for analysis. RESULTS: Baseline prevalences of anemia, iron deficiency anemia (anemia and low serum ferritin), and low serum zinc (< 10.7 micromol/L) were 41%, 8%, and 78%, respectively. After supplementation, the Fe group had higher hemoglobin (119.4 compared with 115.3 g/L; P < 0.05) and serum ferritin (46.5 compared with 32.3 microg/L; P < 0.05) values than did the Fe+Zn group, indicating an effect of zinc on iron absorption. The Zn group had higher serum zinc (11.58 compared with 9.06 micromol/L; P < 0.05) than did the placebo group. There was a dose effect on serum ferritin in the Fe and Fe+Zn groups, but at different levels. There was a significant dose effect on serum zinc in the Zn group, whereas no dose effect was found in the Fe+Zn group beyond 7 mg Zn/d. CONCLUSION: Supplementation with iron and zinc was less efficacious than were single supplements in improving iron and zinc status, with evidence of an interaction between iron and zinc when the combined supplement was given.

Anemia, Iron-Deficiency↗

PubMed1998

Zinc replenishment reduces esophageal cell proliferation and N-nitrosomethylbenzylamine (NMBA)-induced esophageal tumor incidence in zinc-deficient rats.

Previous work has shown that sustained increased and decreased cell proliferation, induced by dietary zinc deficiency and caloric restriction respectively, influence the course of N-nitrosomethylbenzylamine (NMBA)-induced esophageal carcinogenesis in rats. The present study considered whether the increased cell proliferation and esophageal tumor incidence induced by zinc deficiency are reversed upon zinc replenishment. Weanling rats were maintained initially on a deficient diet containing 4 p.p.m. zinc. After 5 weeks, carcinogen-treated animals were given six intragastric doses of NMBA (2 mg/kg twice weekly). Controls were untreated. After the second NMBA dose, the rats were divided into three dietary groups. One group was continued on the deficient diet, while the other two groups were switched to diets containing either 75 or 200 p.p.m. zinc, with half of the members in each group fed ad libitum and half pair-fed with deficient rats. NMBA-untreated controls were similarly replenished. At various time points, esophageal cell proliferation was assessed in five animals from each group by immunohistochemical detection of cells in S phase, with in vivo 5-bromo-2'deoxyuridine labeling. At 11 weeks after the first dose, esophageal tumor incidence was greatly reduced, from 100% in the deficient group to 26 and 14% respectively in the replenished groups fed ad libitum 75 and 200 p.p.m. zinc and to 14 and 11% respectively in the replenished groups pair-fed 75 and 200 p.p.m. zinc. In addition, the number of tumors per esophagus was reduced from 9.93 +/- 4.25 in deficient rats, to a range of 0.11 +/- 0.31-0.30 +/- 0.54 in replenished animals. Following zinc replenishment, esophageal cell proliferation, as measured by labeling index (LI), the number of labeled cells and the total number of cells, was markedly decreased in NMBA-untreated and -treated esophagi as compared with those in corresponding deficient esophagi. Thus, the esophageal cell proliferation induced by zinc deficiency is reversed by zinc replenishment and replenished animals have a markedly lower incidence of esophageal tumors.

Animals↗

PubMed1998

Low seminal zinc bound to high molecular weight proteins in asthenozoospermic patients: evidence of increased sperm zinc content in oligoasthenozoospermic patients.

Total seminal zinc concentration, seminal zinc fraction bound to high molecular weight proteins (HMW-Zn%) and zinc content in spermatozoa were assayed in the ejaculates of 90 asthenozoospermic patients subdivided into two study groups: normoasthenozoospermics (group I: n = 50) and oligoasthenozoospermics (group II: n = 40). The zinc concentrations of patients were compared with those of a control group of donors showing normal semen parameters. All samples were also investigated for their sperm membrane functional integrity by the hypo-osmotic swelling test (HOS). The results showed normal total zinc concentrations but very low HMW-Zn% values (P < 0.001) in seminal plasma of the two groups of asthenozoospermic patients compared to the controls. Furthermore higher zinc amounts (P < 0.001) were measured in spermatozoa of oligoasthenozoospermic patients compared to group I and to the control group. Oligoasthenozoospermics also displayed a lower HOS score (P < 0.001) compared to the other two groups. These data suggest that the increased unbound seminal zinc could contribute to the decrease of sperm motility in normoasthenozoospermic and oligoasthenozoospermic patients. A further impairment in sperm motility could occur in the oligoasthenozoospermic patients where the increase of seminal free zinc was followed by a major zinc uptake by spermatozoa. The higher intrasperm zinc content in these patients could be a reflection of their low sperm membrane functionality.

Adult↗

PubMed1980

Total true efficiency of zinc utilization: determination and homeostatic dependence upon the zinc supply status in young rats.

Total true efficiency of zinc utilization and its component factors, true absorption and metabolic efficiency, were studied in relation to dietary zinc supply in a 15-day experiment with 36 weanling rats in six groups. After day 3, the initial supply of 18.2 ppm zinc in the diet for all groups was changed to 5.6, 10.6, 18.2, 39, 70 and 141 ppm in groups 1 to 6, respectively. During the 6-day balance period after day 9, zinc intake was proportional to dietary zinc concentration. Mean daily rates of weight gain and apparent zinc retention increased from a near zero level in group 1 to a high plateau from group 4 to 6. True absorption rate steadily rose and reached about twice that of apparent absorption in group 6. This difference in rates was due to endogenous zinc excretion. Percent total utilization and percent true absorption steadily declined from a mean of about 100 in groups 1 and 2 to nearly 15 and 30, respectively, in group 6. Metabolic efficiency, reflecting true retention of absorbed zinc, similarly declined as percent true absorption did. The major conclusion was that not only the absorptive but also the metabolic efficiency greatly contributed to zinc homeostasis and total true efficiency of zinc utilization.

Absorption↗

PubMed1984

Measurement of plasma metallothionein-I in the assessment of the zinc status of zinc-deficient and stressed rats.

These studies were designed to investigate the effects of stress and of changes in zinc status on plasma and liver concentrations of metallothionein-I (MT-I) in rats and to assess the value of plasma MT-I assays in the diagnosis of zinc deficiency. No MT-I was detected by radioimmunoassay in the plasma or liver of rats made hypozincaemic by feeding diets with less than 1 or 3 mg Zn/kg. Injection of normal rats with endotoxin or CCl4 also decreased plasma zinc levels, but these treatments greatly increased MT-I concentrations in both liver and plasma. Moreover plasma MT-I levels in zinc-deprived rats given endotoxin were only slightly greater than those in untreated rats of normal zinc status. Neither plasma zinc nor MT-I levels were altered in starved rats despite increased levels of the protein in the liver, although a slight increase in plasma MT-I was found in rats pair-fed with zinc-deficient animals. It appears therefore that reduced plasma levels of both zinc and MT-I are indicative of a zinc deficiency state and that assay of plasma MT should be of value in the diagnosis of zinc deficiency.

Animals↗

PubMed2002

Zinc status influences zinc transport by porcine brain capillary endothelial cells.

Brain capillary endothelial cells (BCEC) were cultured as an in vitro model of the blood-brain barrier (BBB) and manipulated to investigate how the BBB responds to changes in zinc status. BCEC were grown in minimum essential medium (MEM) with 2% fetal bovine serum and 13% platelet-poor horse serum. A moderate zinc deficiency was imposed by growing the cells in medium containing serums that had previously been dialyzed against EDTA to remove endogenous labile zinc. The control treatment was MEM with undialyzed serums (3 micro mol Zn/L); low-Zn was MEM with dialyzed serums (1.5 micro mol Zn/L); Zn-back was MEM with dialyzed serums, plus ZnCl(2) added back (3 micro mol Zn/L); high-Zn was MEM with undialyzed serums, plus ZnCl(2) (50 micro mol Zn/L). Low-Zn treatment increased (P < 0.02) the rate of zinc uptake into BCEC, relative to control and Zn-back; low-Zn treatment also increased (P < 0.05) the rate of zinc transport across the BCEC into the abluminal chamber (analogous to the brain), relative to control and Zn-back. High-Zn decreased (P < 0.02) the rate of zinc transport across BCEC into the brain, while increasing (P < 0.001) the rate of zinc uptake into BCEC, relative to controls. We conclude that BCEC responded to changes in zinc status by altering the rate of zinc transport in a manner consistent with the BBB actively working to sustain brain zinc homeostasis.

Animals↗

PubMed1993

Giant GABAB-mediated synaptic potentials induced by zinc in the rat hippocampus: paradoxical effects of zinc on the GABAB receptor.

The interaction of zinc with pre- and postsynaptic GABAB receptors was studied in adult rat hippocampal slices using intracellular recording in CA1 and CA3 pyramidal neurons. Zinc (50-300 microM) antagonized baclofen responses with a variable potency, whereas CGP-35348 (100 microM) or barium (300 microM) produced a more substantial and consistent inhibition. Zinc also induced giant GABAA-mediated depolarizing potentials (GDP) in these neurons. After blocking GABAA and excitatory synaptic transmission, monosynaptic hyperpolarizing inhibitory postsynaptic potentials (IPSP) mediated by GABAB receptors (IPSPB) were inhibited by CGP-35348 or barium; however, zinc increased the latency and prolonged the duration of the IPSPB and also induced the appearance of spontaneous giant GABAB-mediated hyperpolarizing potentials (GHP). In some cells, IPSPBs in zinc exhibited a multiphasic appearance. The early component was partially inhibited by 300 microM zinc and was followed by a late GHP. CGP-35348 at 100 microM inhibited the early monosynaptic IPSPB but not the GHP; however, at 300 microM both components were blocked. Paired-pulse inhibition of the IPSPB was used to assess the effect of zinc on presynaptic GABAB receptors. Neither the zinc-chelating agent CP94 (400 microM) nor zinc affected this phenomenon. CGP-35348, barium and polyvalent cations, such as cadmium, copper, cobalt, manganese, iron and aluminum, failed to induce giant potentials in hippocampal neurons. It is concluded that zinc is apparently unique in synchronizing the release of GABA to produce GDPs and GHPs.

Animals↗

PubMed1994

Zinc intake, zinc status and growth in a longitudinal study of healthy Danish infants.

Mild, growth-limiting zinc deficiency might be prevalent in otherwise healthy infants according to recent studies. We examined zinc intake and status in 91 healthy term infants from birth to 12 months, as part of the Copenhagen Cohort Study on Infant Nutrition and Growth. Zinc intake was recorded monthly and the amount of zinc absorbed was estimated. These estimates were below recently published FAO/WHO/IAEA values for basal requirements in 68%, 62% and 14% of the infants at 2, 4 and 9 months of age, respectively. Serum zinc decreased significantly (p < 0.01) from 10.6 mumol/l at 6 months to 8.4 mumol/l at 9 months of age (normal range 10-18 mumol/l). Erythrocyte metallothionein values, a tentative indicator of long-term zinc status, decreased significantly from 2 to 6 months (p < 0.001) and from 6 to 9 months (p < 0.01). Serum zinc at 9 months was positively associated with growth velocity during the period from 6 to 9 months (weight: p = 0.05; knee-heel length: p = 0.002). The results provide descriptive data on zinc intake and zinc status in healthy Danish infants. Although some of our data suggest suboptimal zinc status during late infancy, evidence for this can only be obtained through a randomized intervention study.

Deficiency Diseases↗

PubMed1993

Zinc status in pregnancy: the effect of zinc therapy on perinatal mortality, prematurity, and placental ablation.

Zinc is present in and indispensable to all forms of life. Zinc is essential for the normal growth of human beings, and zinc proteins have been shown to be involved in the transcription and translation of the genetic material. Zinc deficiency has been incriminated in infertility, abortions, malformations, fetal intrauterine growth retardation, premature and postmature births, perinatal death, and abnormal deliveries with dystocia and placental ablation. Risk groups for developing zinc deficiency, which in turn might modify the expression of the underlying disease, are found among those with insufficient food intake, especially in protein malnutrition; abnormal mucosal uptake, as in celiac disease; abnormal intestinal losses, as in steatorrhea and inflammatory bowel disease; abnormal renal excretion, as in diabetes with insufficient metabolic control; alcoholism; and treatment with diuretic drugs. Zinc deficiency could be identified by means of fasting serum or plasma samples or the more laborious estimation of zinc in leucocytes or monocytes if sampling and handling is carefully performed and if stressful situations and acute-phase reactions as fever, delivery, or abortion are avoided. Zinc therapy in identified low-zinc groups has given favorable results and has reduced the frequencies of premature birth, placental ablation, perinatal death, and postmaturity. It is suggested, as we did in 1980, that these data are compatible with the presence of a zinc-deficiency syndrome in pregnancy, which includes increased maternal morbidity, abnormal taste sensations, abnormally short or prolonged gestations, inefficient labor, atonic bleeding, and increased risks to the fetus such as malformations, growth retardation, prematurity, postmaturity, and perinatal death.

Female↗

PubMed1980

Prevention of ovine lupinosis by the oral administration of zinc sulphate and the effect of such therapy on liver and pancreas zinc and liver copper.

Three experiments were carried out using Merino wethers to investigate if oral administration of zinc sulphate would provide protection against the liver damage that occurs in lupinosis. At the same time, the effect of this zinc therapy on liver and pancreas zinc, and liver copper concentrations, was studied. The zinc therapy caused increases in liver and pancreas zinc concentrations, and a drop in the liver copper concentration. Administration of the toxins of Phomopsis leptostromiformis with the zinc increased the magnitude of these changes. Administration of 0.5 g zinc or greater per day, as zinc sulphate, reduced the liver damage caused by the toxins of P. leptostromiformis. The degree of liver protection provided by the zinc therapy varied both between animals within treatments and between treatments in different experiments. Zinc toxicity was encountered.

Administration, Oral↗

PubMed2003

Effects of zinc deficiency and pneumococcal surface protein a immunization on zinc status and the risk of severe infection in mice.

Streptococcus pneumoniae is a major cause of illness and death in children in developing countries. In these children, zinc deficiency is associated with an increased risk of acute respiratory tract infections, which can be reduced by daily zinc administration. Severe infections decrease zinc levels in plasma and may thereby move individuals with preexisting low zinc stores into a vicious cycle of infection and unavailable zinc. Pneumococcal surface protein A (PspA) has emerged as a promising vaccine candidate, and immunization with this antigen protects animals from pneumococcal infection. In an animal experiment, we measured the effect of zinc depletion on the immune response to parenterally administrated PspA and assessed the effect of this PspA vaccination and zinc depletion on the severity of pneumococcal infection and on zinc status. Mice were kept on different diets for 5 weeks, immunized twice 14 days apart, and challenged intranasally with S. pneumoniae. Mice on the zinc-deficient diet showed substantially reduced immune responses to PspA, more extensive pneumococcal colonization in the nasal mucosa, more severe infections, and an increased risk of death. PspA immunization reduced the risk of severe disease, and the reduction in severity was reflected in substantially reduced zinc depletion from bones.

Animals↗