Colostrum-fed Pigs Research Articles

Feeding Colostrum Rapidly Alters Enzymatic Activity and the Relative Isoform Abundance of Jejunal Lactase in Neonatal Pigs ,

Our objective was to determine the short-term effects of feeding colostrum and mature milk on the enzyme activity and relative isoform abundance of lactase in neonatal pigs. We studied newborn pigs that were fed colostrum, mature milk and water for 6 h (Study 1). We also studied unfed pigs shortly after birth, and newborn pigs fed either colostrum or mature milk for 24 h (Study 2). The specific activity (micromol x min(-1) x g protein(-1)) of lactase in ajejunal mucosal homogenate and a purified membrane fraction was lower in pigs fed colostrum than in unfed newborns or those fed either milk or water. However, after 24 h, total jejunal lactase activity (micromol x mol(-1)), jejunal mass and protein content were higher in the colostrum- and milk-fed pigs than in the unfed newborns. In colostrum-fed pigs, the reduction in lactase specific activity after 6 h was associated with 1) a marked increase in the relative abundance of a 180-kDa protein, which was shown to be one of three pro-lactase isoforms, and 2) a lower relative abundance of the 160-kDa isoform, considered to be the mature form of the enzyme. Our evidence suggests that feeding either colostrum or mature milk increases total jejunal lactase activity. The reduction in both the specific activity and abundance of the mature isoform in conjunction with an increased relative abundance of the 180-kDa pro-lactase isoform suggests that feeding colostrum alters the post-translational processing of intestinal lactase in neonatal pigs.

Effect of feeding colostrum versus exogenous immunoglobulin G on gastrointestinal structure and enteric nervous system in newborn pigs1

Colostrum is an indispensable source of antibodies (IgG) protecting the newborn pig against infection. We studied the effect of feeding colostrum and purified IgG on early structure and development of the gastrointestinal tract (GIT). Newborn littermate pigs were fed either colostrum, an elemental diet (ED), or an ED supplemented with purified serum IgG (ED + IgG) for 24 h or then only ED up to 72 h. Afterwards, pigs were slaughtered. Colostrum-fed pigs or ED supplemented with IgG (ED + IgG) increased thickness (P < 0.001) of stomach mucosa and muscularis (P < 0.05) compared to the ED group not receiving IgG. Feeding an ED supplemented with IgG improved morphology of the GIT towards that of colostrum-fed piglets and indicates a beneficial effect of IgG on GIT development in neonatal pigs. Immunohistochemical studies indicate that ED feeding may influence the expression of nitric oxide synthase in jejunal myenteric (but not submucous) neurons of newborn pigs.

Formula Induces Intestinal Apoptosis in Preterm Pigs Within a Few Hours of Feeding

Nutrition regimens influence postnatal small intestinal development, which shows prominent changes after 6 hours of suckling. Such influences are particularly important in preterm neonates as inappropriate feeding responses may predispose to gastrointestinal disorders such as necrotizing enterocolitis (NEC). The authors investigated the early morphological responses to enteral feeding, prior to the time period when a large proportion of preterm pigs normally develop clinical NEC symptoms. Preterm piglets (106-107 days of gestation) were fed parenteral nutrition (PN) for 2 days with or without a subsequent 8-hour or 17-hour period of enteral nutrition (EN) with sow's colostrum or formula. Another group of piglets was delivered at 108-109 days of gestation and used for comparison to PN pigs before enteral feeding. Stereological measurements of the mucosal surface density and the volume densities of the tunica mucosa, tunica muscularis, proliferative, and apoptotic cells were made and related to microscopical NEC-lesion score. In addition, villus length and crypt depth were measured. PN-fed piglets showed minimal PN-induced mucosal atrophy, although their crypts were deeper, together with lower cell proliferation and higher apoptotic indices, than newborn (NB) unfed piglets. After PN, enteral feeding with colostrum, for just 8 hours, induced a rapid increase in the mucosal volume density while formula feeding was associated with an elevated number of both proliferating and apoptotic cells and a higher NEC lesion score than PN- or colostrum-fed pigs. Enteral feeding of formula, for only a few hours, induces rapid enterocyte turnover and mucosal structural changes that may predispose to later development of NEC.

Formula-feeding reduces lactose digestive capacity in neonatal pigs

The intestine of newborn pigs develops rapidly during the first days postpartum. We investigated if feeding milk replacer (infant formula) as an alternative to colostrum has compromising effects on nutrient digestive function in the neonatal period. Nineteen piglets born at term were assigned to one of four treatments: (1) newborn controls; (2) natural suckling for 24 h; (3) tube-fed formula for 24 h; (4) tube-fed porcine colostrum for 24 h. All three fed groups showed significant increases in small-intestinal and colonic weights, villous heights and widths, maltase and aminopeptidase A activities, and decreases in dipeptidylpeptidase IV activity, relative to newborn pigs. Following oral boluses of mannitol, lactose or galactose, formula-fed pigs showed significantly reduced plasma levels of mannitol and galactose compared with colostrum-fed pigs. Activity of intestinal inducible NO synthase and plasma levels of cortisol were significantly increased, whereas intestinal constitutive NO synthase and alpha-tocopherol were decreased in formula-fed pigs compared with colostrum-fed pigs. Although formula-fed pigs only showed minor clinical signs of intestinal dysfunction and showed similar intestinal trophic responses just after birth, as those fed colostrum, lactose digestive capacity was markedly reduced. We conclude that formula-feeding may exert detrimental effects on intestinal function in neonates. Formula-induced subclinical malfunction of the gut in pigs born at term was associated with altered NO synthase activity and antioxidative capacity.

Preterm birth makes the immature intestine sensitive to feeding-induced intestinal atrophy

Preterm birth and formula feeding predispose to small intestinal dysfunction, which may lead to necrotizing enterocolitis (NEC). In piglets, we tested whether the physiological and environmental transitions occurring at birth affect the response of the immature intestine to enteral feeding. Pig fetuses (106 days gestation, term = 115 days) were prepared with esophageal feeding tubes and fed either sow's colostrum (n = 8) or infant formula (n = 7) in utero. After 24 h of oral feeding, the pig fetuses were delivered by cesarean section and their gastrointestinal morphology and function were compared with those of preterm newborn (NB) littermates that were not fed (n = 8) or fed colostrum (n = 7) or formula (n = 13) for 24 h after birth. Before birth, both colostrum and formula feeding resulted in marked increases in intestinal mass, brush-border enzyme activities, and plasma glucagon-like peptide 2 concentrations, to levels similar to those in NB colostrum-fed piglets. In contrast, NB formula-fed piglets showed reduced intestinal growth, decreased brush-border enzyme activities, and intestinal lesions, reflecting NEC. NB formula-fed pigs also showed impaired enterocyte endocytotic function and decreased antioxidative capacity, whereas brush-border enzyme mRNA levels were unaltered, relative to NB colostrum-fed pigs. Our results indicate that the feeding-induced growth and enzyme maturation of the immature intestine are not birth dependent. However, with a suboptimal diet (milk formula), factors related to preterm birth (e.g., microbial colonization and metabolic and endocrine changes) make the immature intestine sensitive to atrophy and development of NEC.

Experimental infection of 3-week-old conventional colostrum-fed pigs with porcine circovirus type 2 and porcine parvovirus

This report describes an experimental infection with porcine circovirus type 2 (PCV2) in combination with porcine parvovirus (PPV) in 3-week-old conventional colostrum-fed pigs with maternal antibodies to both viruses. Two groups of four pigs each were inoculated with PCV2 and PPV. One of the groups received also a commercial inactivated vaccine against porcine pleuropneumonia to evaluate possible effects of the stimulation of the immune system of pigs on the infection. Another group of four pigs was kept as uninfected control. Clinical signs, rectal temperatures and body weights were recorded. Serum antibody titers to PCV2 and PPV were determined at weekly intervals. Pigs were killed 42 days after inoculation and tissue samples were examined for the presence of gross and microscopic lesions. Tissues were also analyzed for the presence of PCV2 and PPV DNA by PCR, and for the presence of PCV2 antigen by immunohistochemistry (IHC). All the pigs had serum antibodies to PCV2 and PPV at the beginning of the trial. None of them developed clinical symptoms or pathological lesions typical of post-weaning multisystemic wasting syndrome (PMWS), a disease associated to PCV2 infection. However, IHC and/or PCR analyses showed that clinically silent PCV2 infection developed in five of the eight inoculated pigs, regardless of the administration of the vaccine. In particular, PCV2 DNA and/or antigen were detected in most of the tissues examined in the two pigs with the lowest titer of maternal PCV2 antibodies at the beginning of the trial. PPV DNA was not detected in any of the samples examined. The five pigs with PCR and/or IHC evidence of PCV2 infection had a mean weight gain during the experiment lower than that of the inoculated PCR-negative pigs considered together and that of the control pigs. In conclusion, it would appear that passive immunity against PCV2 can play a role in preventing the development of PMWS, but is not able to prevent the establishing of clinically silent PCV2 infections. The dissemination and persistence of the virus in the tissues may depend on the level of PCV2 antibodies at the time of inoculation.

Nonnutritive factors in colostrum enhance myofibrillar protein synthesis in the newborn Pig.

Colostrum is a complex source of nutrients, immune factors, and bioactive substances consumed by newborn mammals. In previous work, we observed that protein synthesis in the skeletal muscle of newborn piglets is enhanced when they are fed colostrum rather than a nutrient-matched formula devoid of growth factors. To elucidate the mechanisms responsible for this response, we contrasted the fractional rates of sarcoplasmic and myofibrillar protein synthesis of newborn piglets that received only water with those fed for 24 h with colostrum, a nutrient-matched formula, or mature sow's milk. Compared with water, feeding resulted in a 2.5- to 3-fold increase in total skeletal muscle protein synthesis, and this increase was 28% greater in the colostrum-fed than either the formula- or mature milk-fed piglets. Feeding also stimulated muscle ribosome and total polyadenylated RNA accretion. Ribosomal translational efficiency, however, was similar across all fed groups. The greater stimulation of protein synthesis in colostrum-fed pigs was restricted entirely to the myofibrillar protein compartment and was associated with higher ribosome and myosin heavy chain mRNA abundance. Taken together, these data suggest that nonnutritive factors in colostrum enhance ribosomal accretion and muscle-specific gene transcription that, in turn, stimulate specifically the synthesis of myofibrillar proteins in the skeletal musculature of the newborn.

Feeding colostrum increases circulating insulin-like growth factor I in newborn pigs independent of endogenous growth hormone secretion.

Our objective was to examine the influence of feeding and endogenous GH secretion on circulating IGF-I in colostrum-deprived newborn pigs fed colostrum (n = 4), formula (control, n = 4), or water (n = 4). In another four formula-fed pigs, GH was ablated (GRF-A) with two intravenous injections of a GH releasing-factor antagonist (N-Ac-Tyr1,D-Arg2)-GRF(1-29)-NH2. Blood was serially sampled in all pigs to measure plasma IGF-I and GH profiles. Feeding increased plasma IGF-I concentration two- to fourfold and decreased GH secretion. Despite a more than 80% decrease in the plasma GH in GRF-A pigs, the circulating IGF-I concentration was similar to that in control pigs. In colostrum-fed pigs, plasma IGF-I was higher than that in control pigs, despite equal nutrient intake and lower circulating GH. There were no differences in plasma IGF binding protein (IGFBP)-3 levels among the treatment groups. However, the relative abundance of plasma IGFBP-4 was lower, and that of IGFBP-1 higher, in unfed pigs than in any of the three fed groups. The plasma insulin concentration was not different among fed pigs, but it was lower in unfed pigs. Our results indicate that the circulating IGF-I concentration is more dependent on nutrient intake than on GH in newborn pigs, despite relatively high GH concentrations. However, because the nutrient content in the formula was designed to match that of colostrum, a factor other than nutrient intake and GH was responsible for the maximal increase in circulating IGF-I concentration observed in colostrum-fed pigs.

Colostrum Enhances the Nutritional Stimulation of Vital Organ Protein Synthesis in Neonatal Pigs , ,

Our objective was to determine the relative importance of the macronutrient components of colostrum in the stimulation of vital organ protein synthesis in neonatal pigs. We studied colostrum-deprived newborn pigs within 4–6 h after birth (unfed) and three groups fed for 24 h mature milk, colostrum, or a formula containing a macronutrient composition comparable to that of colostrum. We measured protein synthesis in vivo using a flooding dose of 3H-phenylalanine. The fractional rates of protein synthesis (Ks) in the brain, heart, lung, kidney and spleen were significantly higher in all fed groups than in the unfed newborns. Among the three fed groups, brain and heart protein synthesis rates were greater in colostrum-fed than in either milk- or formula-fed pigs. Kidney and spleen protein synthesis rates in colostrum- and formula-fed pigs were not significantly different, but both were higher than in milk-fed pigs. The stimulation of kidney protein synthesis in response to feeding was primarily a consequence of greater protein synthetic efficiency; however, protein synthetic capacity in the heart, lung and spleen was generally greater in colostrum- and formula-fed pigs than in unfed newborns. Our results suggest that the predominant stimulus for vital organ protein synthesis in colostrum-fed neonatal pigs is nutrient intake. However, there was a specific stimulation of both brain and heart protein synthesis in colostrum-fed pigs that cannot be attributed to macronutrients.

Nutrient-Independent and Nutrient-Dependent Factors Stimulate Protein Synthesis in Colostrum-Fed Newborn Pigs

We hypothesized that nonnutrient components, including growth factors, present in colostrum contribute to the stimulation of protein synthesis in colostrum-fed neonatal pigs. We studied neonatal pigs fed mature milk, colostrum, or a formula containing a macronutrient composition comparable to that of colostrum for 24 h. We measured the circulating concentrations of insulin, insulin-like growth factor I, glucose, and amino acids at intervals throughout the 24-h period, after which we measured in vivo protein synthesis using a flooding dose of [3H]phenylalanine. The rates of protein synthesis in several tissues measured after 24 h of feeding were greater than those we reported previously after 6 h of feeding. The acute (within 6 h) stimulation of protein synthesis in visceral and skeletal muscle tissues of neonatal pigs fed milk, colostrum, or formula was primarily influenced by nutrient intake and associated with rapid secretion of insulin. Indirect evidence suggests that intestinal absorption of ingested colostral insulin was minimal. However, the sustained increase in tissue protein synthesis between 6 and 24 h coincided with an increase in circulating insulin-like growth factor I. We found a novel, specific stimulation of skeletal muscle and jejunal protein synthesis in colostrum-fed pigs that can be attributed to some nonnutrient component of colostrum.

Feeding Colostrum Rapidly Alters Enzymatic Activity and the Relative Isoform Abundance of Jejunal Lactase in Neonatal Pigs ,

Our objective was to determine the short-term effects of feeding colostrum and mature milk on the enzyme activity and relative isoform abundance of lactase in neonatal pigs. We studied newborn pigs that were fed colostrum, mature milk and water for 6 h (Study 1). We also studied unfed pigs shortly after birth, and newborn pigs fed either colostrum or mature milk for 24 h (Study 2). The specific activity (µmol·min-1·g protein-1) of lactase in a jejunal mucosal homogenate and a purified membrane fraction was lower in pigs fed colostrum than in unfed newborns or those fed either milk or water. However, after 24 h, total jejunal lactase activity (µmol·mol-1), jejunal mass and protein content were higher in the colostrum- and milk-fed pigs than in the unfed newborns. In colostrum-fed pigs, the reduction in lactase specific activity after 6 h was associated with 1) a marked increase in the relative abundance of a 180-kDa protein, which was shown to be one of three pro-lactase isoforms, and 2) a lower relative abundance of the 160-kDa isoform, considered to be the mature form of the enzyme. Our evidence suggests that feeding either colostrum or mature milk increases total jejunal lactase activity. The reduction in both the specific activity and abundance of the mature isoform in conjunction with an increased relative abundance of the 180-kDa pro-lactase isoform suggests that feeding colostrum alters the post-translational processing of intestinal lactase in neonatal pigs.

Antibody response of swine to outer membrane components of Haemophilus pleuropneumoniae during infection.

Sera from pigs infected with Haemophilus (Actinobacillus) pleuropneumoniae were tested for antibodies to outer membrane proteins (OMPs) of the organism by immunoblotting. Convalescent sera were produced in naturally born, colostrum-fed pigs and in cesarean-derived, colostrum-deprived pigs given H. pleuropneumoniae serotype 5 intranasally twice at 5-week intervals. Sera, collected at weekly intervals, were reacted with Sarkosyl-insoluble, OMP-enriched preparations of H. pleuropneumoniae which had been separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and electrophoretically transferred to nitrocellulose. Antibodies were detected to OMPs with an apparent molecular weight of 16,500 (16.5K OMP); to 29K, 38.5K, 43.5K, 45K, 49.5K, and 66.5K OMPs; and to several high-molecular-weight (greater than or equal to 94,000) OMPs, but not to the major 42K OMP. Antibodies to the heat-modifiable OMP (29K/43.5K) and the 38.5K OMP were detected in sera from noninfected pigs. Antibodies were also detected to two broad 54,000- and 95,000-molecular-weight bands which did not stain with Coomassie blue, stained with silver nitrate, resisted proteinase K digestion, and were eliminated by oxidation with sodium metaperiodate. This indicates that the 54,000- and 95,000-molecular-weight bands represent polysaccharide, possibly capsular or lipopolysaccharide immunogens. Adsorption of sera with cells from the homologous serotype 5 strain removed antibodies to the 45K, 49.5K, 66.5K, and greater than or equal to 94K OMPs and to the two polysaccharide bands, indicating that these antibodies were directed primarily to surface-exposed epitopes. When tested with OMP preparations from other serotype 5 strains, heterogeneity was apparent, both in the reactions with OMPs and with the polysaccharide bands. Silver staining of proteinase K-treated, whole-cell lysates from serotype 5 strains also indicated variable expression of the polysaccharide bands. Sera also reacted with OMPs from H. pleuropneumoniae serotypes 1 and 7; however, several OMPs and the lipopolysaccharide or polysaccharide determinants of these serotypes appeared to be type specific.

IgA Immunoglobulin Levels in Porcine Sera and Mammary Secretions

IgA immunoglobulin levels were measured in the sera of 29 pigs from birth to maturity and in their dams. Adult levels were reached by 18-21 weeks of age. The serum IgA concentration at 6 weeks of age was double that of the concentration at 3 weeks and it appears that the IgA synthesis in young colostrum-fed pigs already has reached a significant level by 6 weeks of age. IgA immunoglobulin levels were estimated in porcine mammary secretions during the first 35 days of lactation and in secretions of individual mammary glands of vaccinated and non-vaccinated sows during the first 7 days of lactation. It appears that a 3-week-old pig receives 1.6 g of IgA per day via the milk of the dam and that IgA quantitatively is a major immunoglobulin in sows’ milk. There are significant differences in the IgA concentrations in secretions from individual glands of a SOW and in the IgA concentrations from different SOWS. Intramammary vaccination with an E. coli vaccine had no apparent influence on the quantity of IgA in secretions from the vaccinated gland when compared to the concentrations in non-vaccinated glands from the same sow or to the concentration in secretions from non-vaccinated sows. The significance of mammary secretion IgA in relation to enteric diseases in suckling pigs is discussed.

Crystals in the intestinal epithelium of neonatal pigs.

Laminated crystalline structures occurred within vacuoles of absorptive intestinal cells in colostrum-fed pigs. They are believed to be bilirubin crystals formed by breakdown of ingested red blood cells, but this could not be substantiated histochemically, and they could not be produced experimentally.

The Immunologic Behavior of Baby Pigs

Summary Colostrum-deprived pigs formed tetanus, but not diphtheria antibodies following intraperitoneal inoculation of tetanus and diphtheria toxoids at birth. Colostrum-fed pigs formed diphtheria antibodies after intraperitoneal inoculation of the toxoid at birth, but their antibody response to tetanus toxoid was depressed. The interpretation of these results is discussed in the light of the assumption that a degree of transplacental transfer of maternal antibody took place and that antibodies against tetanus, but not against diphtheria are present in the sow's blood. γ-Globulin was found in the serum of newborn, colostrum-deprived pigs.