Biomedical subjects

G F Erf

Publications and source records attributed to G F Erf.

At least 19 recordsLinked to original sources

PubMed2006

The influence of different management systems and age on intestinal morphology, immune cell numbers and mucin production from goblet cells in post-weaning pigs.

At time of weaning, the immune system in piglets is not fully mature resulting in reduced growth and increased mortality. Early-weaned pigs transported to a segregated early weaning (SEW) facility have enhanced performance and gut development compared to conventional (CONV) pigs which may be due, in part, to decreased pathogen challenge. To gain further insight into SEW enhanced performance and gut development, gut samples from pigs weaned at 19+/-2 days were assessed during the post-weaning (PW) period. The numbers of cells expressing CD2, CD4, CD8, and CD172 (the 74-22-15 (SWC3) antibody is now known to be specific for CD172), MHC class II, and CD25 were quantified using immunohistochemistry. Additionally, samples of duodenum, jejunum, and ileum were evaluated for the production of neutral, acidic, and sulfuric mucins from goblet cells and morphological measurements were also made. No effects due to the management systems alone were observed for any of the parameters. However, there were interactive effects of age/time post-weaning and management system on the immune cells as well as on the mucin secreting goblet cells. There were no differences in gut morphology between SEW and CONV reared pigs.

Age Factors↗

PubMed2006

Influence of aminoguanidine, an inhibitor of inducible nitric oxide synthase, on the pulmonary hypertensive response to microparticle injections in broilers.

The pulmonary hypertensive response to pulmonary vascular obstruction caused by intravenously injected microparticles is amplified by pretreatment with N(omega)nitro-L-arginine methyl ester (L-NAME). The L-NAME prevents the synthesis of the potent vasodilator nitric oxide (NO) by inhibiting both the constitutive [endothelial NO synthase (eNOS or NOS-3)] and inducible [inducible NO synthase (iNOS or NOS-2)] forms of NO synthase. In the present study we used the selective iNOS inhibitor aminoguanidine (AG) to evaluate the role of iNOS in modulating the pulmonary hypertension (PH) triggered by microparticle injections. Experiment 1 was conducted to confirm the ability of AG to inhibit NO synthesis by iNOS in broiler peripheral blood mononuclear cells exposed to bacterial lipopolysaccharide (LPS, endotoxin). Mononuclear leukocytes treated with LPS produced 10-fold more NO than untreated (control) cells. The LPS-stimulated production of NO was partially inhibited by L-NAME and was fully inhibited by AG, thereby confirming that AG inhibits LPS-mediated iNOS activation in broilers. In Experiment 2 we evaluated the responses of male progeny from a base population (MP Base) and from a derivative line selected for one generation from the survivors of an LD50 microparticle injection (MP Select). The pulmonary arterial pressure (PAP) was lower in MP Select than in MP Base broilers. Both lines exhibited similar percentage increases in PAP after microparticles were injected, and AG modestly amplified the PH triggered by microparticles in both lines. In Experiment 3 we evaluated the responses of male progeny from a second base population (PAC Base) and from a derivative line selected for 3 generations using the unilateral pulmonary artery clamp technique (PAC Select). The PAP was lower in PAC Select than in PAC Base broilers, and both lines exhibited similar percentage increases in PAP in response to the microparticles. The PH triggered by microparticles was not amplified by AG but was doubled by L-NAME. These experiments demonstrate that during the 30 min following pulmonary vascular entrapment of microparticles, iNOS modulated the PH elicited in broilers derived from the MP pedigree line, but not in broilers from the PAC pedigree line. Different NOS-mediated responses among broiler populations may affect pulmonary hemodynamic characteristics of broiler lines selected using i.v. microparticle injections.

Animals↗

PubMed2006

Pulmonary hypertension triggered by lipopolysaccharide in ascites-susceptible and -resistant broilers is not amplified by aminoguanidine, a specific inhibitor of inducible nitric oxide synthase.

Nitric oxide (NO) is a potent pulmonary vasodilator that modulates the pulmonary vasoconstriction and pulmonary hypertension (PH) triggered by bacterial lipopolysaccharide (LPS) in broilers. The amplitude and duration of the LPS-induced PH are markedly enhanced following pretreatment with N(omega)-nitro-L-arginine methyl ester (L-NAME), which inhibits NO synthesis by both the constitutive (endothelial) and inducible (inflammatory) forms of nitric oxide synthase (eNOS and iNOS, respectively). In the present study L-NAME and the selective iNOS inhibitor aminoguanidine (AG) were administered to differentiate between iNOS and eNOS as the primary source of NO that attenuates the pulmonary vascular response to LPS. Clinically healthy male progeny from ascites-susceptible and ascites-resistant lines were anesthetized, and their pulmonary artery was cannulated. The initial pulmonary arterial pressure (PAP) was recorded, then the broilers either remained untreated (control group) or were injected i.v. with AG. Ten minutes later all birds received an i.v. injection of LPS, followed 40 min later by an i.v. injection of L-NAME. When compared with untreated controls, AG neither increased the baseline PAP nor did it increase or prolong the PH response to LPS. The ascites-susceptible broilers maintained a higher PAP than the ascites-resistant broilers throughout the experiment, and the ascites-resistant broilers exhibited greater relative increases in PAP in response to LPS than did the ascites-susceptible broilers. Within 40 min after the LPS injection, PAP subsided to a level that did not differ from the respective preinjection value for each line. Injecting L-NAME reversed the decline in PAP, and within 5 min PAP returned to hypertensive levels approaching the maximum peak PH response to LPS. The absence of any impact of AG coupled with the profound response to L-NAME indicates that NO synthesized by eNOS rather than iNOS likely modulated the acute (within 1 h) PH elicited by LPS. Evidently eNOS is activated by the increased shear stress exerted on the endothelium during the PH response to LPS, whereas LPS-mediated up-regulation of iNOS expression may take longer than 1 h before biologically effective quantities of NO are produced.

Animals↗

PubMed2006

Variation in the pulmonary hypertensive responsiveness of broilers to lipopolysaccharide and innate variation in nitric oxide production by mononuclear cells.

Variability among broilers in their pulmonary hypertensive (PH) responsiveness to lipopolysaccharide (LPS) appears to reflect innate variation in the types or proportions of vasodilators and vasoconstrictors released by leukocytes and endothelial cells. Two experiments were designed to evaluate possible correlations between the PH responsiveness to LPS in vivo and the quantities of nitric oxide (NO; a potent pulmonary vasodilator) produced by mononuclear cells in vitro. In Experiment 1, blood samples were collected from male broilers from a base population (control group) and from survivors of a 60% lethal dose i.v. injection of cellulose microparticles (MP survivor group). In Experiment 2, blood samples were collected from male broilers from a relaxed line and from lines known to be susceptible or resistant to pulmonary hypertension syndrome. Peripheral mononuclear cells (PMNC) from each blood sample were cultured at 2 million cells per well, remained unstimulated, or were stimulated with LPS to elicit the expression of inducible NO synthase, and the 24-h production of NO was measured. In both experiments, unstimulated PMNC cultures did not produce consistently detectable levels of NO, whereas LPS-stimulated cultures produced quantities of NO that varied widely among individuals. Nitric oxide production by cultured PMNC also was evaluated by flow cytometry, demonstrating that LPS-stimulated PMNC produced substantially more NO than did unstimulated cells in all of the groups evaluated. Moreover, NO-producing PMNC were identified to be monocytes. The same broilers from which PMNC had been isolated were catheterized subsequently to record pulmonary arterial pressure, LPS was injected i.v. to assess the amplitudes of peak and postpeak PH responses, then N(omega)-nitro-L-arginine methyl ester was injected to inhibit ongoing NO production. In Experiment 1, the amplitude of the peak and postpeak PH responses to LPS were correlated with the quantity of NO produced by LPS-stimulated cultured PMNC from broilers in the control group but not for MP survivors. In Experiment 2, the postpeak PH response to LPS was correlated with the quantity of NO produced by LPS-stimulated PMNC from broilers in the relaxed line, but not in the susceptible or resistant lines. In all groups, N(omega)-nitro-L-arginine methyl ester injections triggered substantial increases in pulmonary arterial pressure (> or = 8 mm Hg), thereby revealing a significant ongoing modulation by NO of the PH response to LPS. We concluded that most of the modulatory NO generated in vivo during the acute PH response to LPS (within 60 min postinjection) likely is produced by constitutive NO synthase in the vascular endothelium. In addition, the NO produced by inducible NO synthase in PMNC appeared to have modulated the LPS-stimulated PH responses of unselected broilers having the broadest range of pulmonary vascular capacities (control broilers and relaxed line), but not in broilers whose pulmonary vascular capacities had been selected to represent the higher (MP survivors, resistant line) or lower (susceptible line) extremes of the population.

Animals↗

PubMed2006

Maternal antibody transfer from dams to their egg yolks, egg whites, and chicks in meat lines of chickens.

Maternal antibodies are transferred from hens to the chicks via the egg. To gain insight into maternal antibody transfer and endogenous production of antibodies in broiler chicks, total IgY, IgA, IgM, as well as anti-Newcastle disease virus (NDV) and anti-infectious bronchitis (IBV) antibody levels were examined in the dams' plasma, egg yolks, egg whites, and chicks' plasma on d 3, 7, 14, and 21. Blood was collected from 39-wk-old breeder hens (line 1, n = 17; line 2, n = 21). Fertile eggs were used for antibody extraction from the egg yolks and egg whites (4 to 5 eggs/dam) and for hatching. Unvaccinated chicks (4 to 5 chicks/dam) were reared in a HEPA-filtered room and were bled on d 3, 7, 14 and 21. Based on ELISA methods, plasma levels of IgY and IgM were higher (P < 0.0001), and those of IgA were similar (P = 0.31), in line 2 compared with line 1. Egg yolk IgY and IgA, as well as egg white IgY, IgA, and IgM levels were higher in line 2 compared with line 1 (P < 0.0001). Independent of line of chicken, the percentage dam-to-chick (3 d) plasma transfer of IgY was estimated to be approximately 30%, with that for IgM and IgA less than 1%. Chicks synthesized IgM first, followed by IgA and IgY. Anti-NDV and anti-IBV antibodies were detected in the dams' plasma, egg yolks, and in the chicks' plasma on d 3 and 7, with line 2 having higher anti-IBV and lower anti-NDV levels than line 1 in all samples (P < 0.0001). In summary, IgY levels, total or antigen-specific, in the dams' plasma or eggs were found to be a direct indicator of maternal antibody transfer to the chicks' circulation, with an expected percentage transfer of approximately 30%. This knowledge, together with the observed time course of endogenous antibody production in broiler chicks, may find direct application in formulating strategies for protecting chicks, especially during the first few weeks of age when their immune system is not yet fully functional.

Animals↗

PubMed2006

Ontogeny of T lymphocytes and intestinal morphological characteristics in neonatal pigs at different ages in the postnatal period.

To evaluate morphological characteristics and development of the immune system at different ages in neonatal pigs, 4 piglets were euthanized at 7, 14, and 18 d of age for collection of blood, bile, and intestinal tissue for morphological measurements. Blood was collected for differential cell counts, lymphocyte blastogenesis, immunoglobulin (Ig) concentrations, cytokine concentrations, and flow cytometric analysis. Bile was collected for quantification of Ig-A and Ig-M. Villus width and crypt depth from duodenum sections, as well as ileum crypt depth, were reduced (P < or = 0.08) in 18-d-old pigs compared with 7-d-old pigs. No age-related differences (P > or = 0.11) were observed in the number of goblet cells with neutral and acidic mucins, serum or enteric Ig concentrations, IL-2, IL-4, spontaneous lymphocyte proliferation, or leukocyte concentrations. When measured as counts per minute (cpm) and as a stimulation index (SI), lymphocyte proliferation responses to phytohaemagglutinin increased (P = 0.05) between 7 and 14 d of age; no changes (P = 0.10) occurred at 18 d of age. No age-related changes (P = 0.39) were observed in response to pokeweed mitogen (PWM) when measured as cpm; however, the SI from PWM-induced lymphocytes decreased (P = 0.04) 4-fold between 7 and 18 d of age. The CD4+:CD8+ and populations of lymphocytes expressing CD2+CD4+CD8- (T helper cells) and CD25+CD4+CD8- (activated T helper cells) were greater (P > or = 0.04) at 7 d of age than at 14 and 18 d. Populations of T lymphocytes, cytotoxic T cells (CD2+CD4-CD8+), activated lymphocytes (CD25+), and activated cytotoxic T cells (CD25+CD4-CD8+) were greater (P > or = 0.02) in 18-d-old pigs compared with 7-d-old pigs, whereas CD2+CD4-CD8- [double negative cells] were lower (P = 0.08) in 18-d-old pigs compared with 14-d-old pigs. The percentage of CD2+ T cells was 8.4% at 7 d of age, and by the time the pigs reached 18 d of age, the percentage of CD2+ T cells was 33.8%. Moreover, the percentage of gammadelta T cells was greater (P = 0.02) in 18-d-old pigs than in 7-d-old pigs (74.8 vs. 46.1%, respectively). Results indicate that the porcine immune system and gut are continuously changing as the young pig matures. Changes occurred in lymphocyte phenotypic expression and functional capabilities, as well as morphology and mucin production, and their role may be to further protect the neonate from antigenic challenge as protection from passive immunity declines.

Age Factors↗

PubMed2005

Pulmonary hypertensive responses of broilers to bacterial lipopolysaccharide (LPS): evaluation of LPS source and dose, and impact of pre-existing pulmonary hypertension and cellulose micro-particle selection.

Previous studies demonstrated that bacterial lipopolysaccharide (LPS, endotoxin) triggers pulmonary vasoconstriction leading to pulmonary hypertension (PHS, ascites) in broilers. The lungs of broilers are constantly challenged with LPS that can trigger pulmonary vasoconstriction. Among broilers from a single genetic line, some individuals respond to LPS with large increases in pulmonary arterial pressure (PAP), whereas others fail to exhibit any response to the same supramaximal dose of LPS. In the present study we evaluated the impact of a variety of factors on the magnitude of the PAP response of male broilers to LPS, including: (1) the role of the initial PAP (low vs. high initial PAP); (2) the source of the LPS (Salmonella typhimurium vs. Escherichia coli); (3) the dose of LPS (0.02, 0.1, and 0.5 mg/kg of BW); and (4) the role of micro-particle selection for improved pulmonary vascular capacity (cellulose survivors vs. saline-injected controls). Broilers in the low initial PAP group (21 +/- 0.34 mmHg, mean +/- SEM) did not differ in their pulmonary hypertensive response to LPS compared with broilers in the high initial PAP group (29 +/- 0.55 mmHg, mean +/- SEM). Lipopolysaccharide from S. typhimurium elicited pulmonary hypertensive responses qualitatively similar to those elicited by E. coli LPS. A detailed evaluation revealed that an LPS dose of 0.1 mg/kg of BW elicits a maximal pulmonary hypertensive response in male broilers, and broilers selected by micro-particle injection for a robust pulmonary vascular capacity did not differ in their pulmonary hypertensive response to LPS compared with unselected broilers. This research confirms that the variable pulmonary hypertensive responses among broilers cannot be attributed to the source or dosage of LPS, or to differences in the baseline pulmonary arterial pressure or micro-particle selection before injecting LPS. These findings are consistent with the hypothesis that innate rather than acquired variability may influence the profile of chemical mediators released during the inflammatory cascade.

Animals↗

PubMed2005

Pulmonary and systemic hemodynamic responses to intravenous prostacyclin in broilers.

The eicosanoid vasodilator prostacyclin (PGI2) reduces resistance to pulmonary blood flow and attenuates pulmonary hypertension in mammals. However, sparse information is available regarding the responsiveness of the avian pulmonary vasculature to PGI2. Accordingly, in 3 experiments we evaluated the pulmonary vascular responses to PGI2 in male broilers. In experiment 1, infusing PGI2 (10 microg/min) into clinically healthy broilers did not reduce their pulmonary vascular resistance (PVR) but did reduce their pulmonary arterial pressure (PAP) by lowering their cardiac output. Within 4 min after stopping the PGI2 infusion, the cardiac output and PAP returned to preinfusion levels. In experiment 2, the responses to PGI2 were evaluated after arachidonic acid (AA) had been infused to preconstrict the pulmonary vasculature. The AA infusion (400 microg/min) consistently triggered dramatic, sustained pulmonary vasoconstriction (increased PVR) and pulmonary hypertension (increased PAP). Concurrent PGI2 infusions did not reduce PVR but did reduce PAP by lowering cardiac output. Within 4 min after stopping the PGI2 infusion, PAP and cardiac output returned to their previous (hypertensive) levels attributable to the ongoing AA infusion. In experiment 3, PGI2 was infused (10 microg/min) into clinically healthy (PAP < or = 24 mmHg) or subclinically hypertensive (PAP > or = 27 mmHg) broilers. Throughout this experiment broilers in the hypertensive group had higher PAP values than broilers in the healthy group. The PGI2 infusion reduced PAP in both groups but did not reduce PVR. Instead, the pulmonary hypotensive response to PGI2 infusion was associated with a reduction in cardiac output in both groups. In all 3 experiments PGI2 reduced PAP by reducing cardiac output rather than by reducing PVR. There was no evidence that PGI2 acts as an effective pulmonary vasodilator in broilers regardless of whether their pulmonary vasculature was apparently normal (clinically healthy), had been pharmacologically preconstricted (AA infusion), or initially exhibited the vasoconstriction that is typical of the pathogenesis of pulmonary hypertension syndrome in broilers (PAP > or = 27 mmHg). The consistent failure of PGI2 to elicit pulmonary vasodilation in this study suggests fundamental differences in AA metabolism or the etiology of pulmonary hypertension may exist when broilers are compared with mammals.

Adenosine Diphosphate↗

PubMed2005

Nomega-nitro-L-arginine methyl ester (L-NAME) amplifies the pulmonary hypertensive response to microparticle injections in broilers.

We tested the hypothesis that microparticles entrapped within the pulmonary vasculature elicit the production of nitric oxide (NO) in quantities sufficient to modulate the combined impact of physical occlusion plus contemporaneously released vasoconstrictors. In experiment 1, male broilers were given an injection of the NO synthase (NOS) inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME), followed by an intravenous injection of cellulose microparticles while the pulmonary arterial pressure (PAP) and cardiac output (CO) were recorded. When L-NAME was used to block NO synthesis induced by the microparticles, an early peak of pulmonary hypertension was revealed that rarely developed in the absence of L-NAME. The subsequent more prolonged increases in PAP and pulmonary vascular resistance (PVR) were greater in amplitude and duration in broilers pretreated with L-NAME than in broilers in the control group. These amplified responses occurred in spite of a simultaneous reduction in CO, thereby conclusively demonstrating that inhibiting NOS permitted the development of a much more profound increase in the PVR. In experiment 2 the mortality triggered within 48 h after injecting microparticles was evaluated in the presence and absence of L-NAME. The 48 h postinjection mortality more than doubled when L-NAME was combined with microparticle injection doses that otherwise caused relatively low mortality in the absence of L-NAME. Experiment 3 was conducted to determine whether NO contributes to the systemic hypoxemia that develops after microparticles are injected. L-NAME administration had no impact on the magnitude and duration of the microparticle induced decline in the percentage saturation of hemoglobin with oxygen (%HbO2). Evidently hypoxemia per se contributes relatively little to the amplified pulmonary vasoconstriction and 48 h postinjection mortality triggered by microparticle injections in broilers pretreated with L-NAME. These observations indicate that NO modulates the responses to vasoconstrictors released when microparticles become entrapped in the pulmonary vasculature. Inhibition of NOS by L-NAME exposed a more dramatic increase in PVR and pulmonary hypertension leading to enhanced mortality in response to microparticle injections.

Animals↗

PubMed2004

Apoptosis in feathers of Smyth line chickens with autoimmune vitiligo.

Vitiligo is an acquired dermatological disorder characterized by a loss of epidermal melanocytes resulting in depigmentation of the skin. Mechanisms underlying the destruction of melanocytes in vitiligo remain unclear. An animal model to study spontaneously occurring autoimmune vitiligo is the mutant Smyth line (SL) of chickens. This investigation was designed to determine whether the pathogenesis of depigmentation in Smyth line chicken vitiligo (SLV) involves an apoptotic mechanism. Terminal deoxynucleotide transferase-mediated fluorescein-dUTP nick end labeling (TUNEL) was used to detect in situ cell apoptosis in cryostat sections of 2-week-old regenerating feathers. Two-week-old regenerating feathers were obtained from SL chickens and their normally pigmented controls including the parental Brown line (BL) and Light Brown Leghorn (LBL) chickens at 6, 8, 10 and 12 weeks of age. In feathers from vitiliginous SL chickens, the number of TUNEL+ cells was significantly (P<or=0.05) higher than that in the feathers of non-vitiliginous SL, BL or LBL chickens. These TUNEL+ cells were primarily located in the epithelial barb ridge where melanocyte cell bodies are located. The extent of this apoptosis in the feathers of SLV chickens varied with the severity of depigmentation of the feathers (i.e., highest in active depigmentation), suggesting a close association between apoptosis and the disappearance of melanocytes. In addition to TUNEL staining, most sections were double-stained with monoclonal antibodies specific to either CD8 or MHC class II molecules to further explore the relationship between CD8+ feather-infiltrating lymphocytes and this increase in apoptotic cells. Compared to normally pigmented controls, the number of CD8+ and MHC class II+ cells in the feather pulp and the barb ridge increased 2-4 weeks before the visible onset of SLV, and was directly related to the changes in the number of TUNEL+ cells prior to, at onset and during depigmentation. Moreover, some of these infiltrating CD8+ cells were localized next to or near the TUNEL+ cells. These observations suggest that enhanced apoptosis in the feather of SLV chickens is a pathogenic mechanism involved in the death of melanocytes and appears to be induced by infiltrating cytotoxic T lymphocytes (CD8+).

Animals↗

PubMed2004

Cell-mediated immunity in poultry.

In avian species, adaptive immunity involves both humoral and cell-mediated immune (CMI) responses. Although humoral or antibody-mediated immune responses are particularly effective against extracellular antigens, CMI responses are specialized in the elimination of intracellular antigens; the latter include those that have entered cells via the endocytic pathway (exogenous antigens; e.g., phagocytosed bacteria) or were produced within the cell such as viral proteins and proteins resulting from neoplastic transformation of the cell (endogenous antigens). CMI responses, like most humoral immune responses, are tightly regulated and require "help" from T helper cells, specifically the type 1 T helper cells (Th1, hence, the name Th1 responses). Th1 cells are characterized by their production of cytokines such as interferon-gamma (IFN-gamma), tumor-necrosis factor-alpha (TNF-alpha), and interleukin-2 that drive CMI responses. The functional effectors of CMI responses are various immune cells including cytotoxic lymphocytes (cytotoxic T cells and natural killer cells) and macrophages. Cytotoxic lymphocytes and macrophages are specialized in the elimination of endogenous and exogenous antigens, respectively. In the past decade, substantial progress has been made in defining the role and regulation of avian CMI responses. Other advances have addressed strategies that strengthen this arm of adaptive immunity to optimize defense as well as protection against neoplastic diseases and nonneoplastic diseases caused by intracellular pathogens.

Animals↗

PubMed2004

Immune modulation of the pulmonary hypertensive response to bacterial lipopolysaccharide (endotoxin) in broilers.

The lungs of broilers are constantly challenged with lipopolysaccharide (LPS, endotoxin) that can activate leukocytes and trigger thromboxane A2 (TxA2)- and serotonin (5HT)-mediated pulmonary vasoconstriction leading to pulmonary hypertension. Among broilers from a single genetic line, some individuals respond to LPS with large increases in pulmonary arterial pressure, whereas others fail to exhibit any response to the same supramaximal dose of LPS. This extreme variability in the pulmonary hypertensive response to LPS appears to reflect variability in the types or proportions of chemical mediators released by leukocytes. Our research has confirmed that TxA2 and 5HT are potent pulmonary vasoconstrictors in broilers and that broilers hatched and reared together consistently exhibit pulmonary hypertension after i.v. injections of TxA2 or 5HT. Previous in vitro studies conducted using macrophages from different lines of chickens demonstrated innate variability in the LPS-stimulated induction of nitric oxide synthase (iNOS) followed by the onset of an LPS-refractory state. The NOS enzyme converts arginine to citrulline and nitric oxide (NO). It is known that NO produced by endothelial NOS serves as a key modulator of flow-dependent pulmonary vasodilation, and it is likely that NO generated by iNOS also contributes to the pulmonary vasodilator response. Accordingly, it is our hypothesis that the pulmonary hypertensive response to LPS in broilers is minimal when more vasodilators (NO, prostacyclin) than vasoconstrictors (TxA2, 5HT) are generated during an LPS challenge. Indeed, inhibiting NO production through pharmacological blockade of NOS with the inhibitor Nomega-nitro-L-arginine methyl ester modestly increased the baseline pulmonary arterial pressure and dramatically increased the pulmonary hypertensive response to LPS in all broilers evaluated. Innate differences in the effect of LPS on the pulmonary vasculature may contribute to differences in susceptibility of broilers to pulmonary hypertension syndrome (ascites).

Animals↗

PubMed2004

Influence of dietary vitamin E on phagocytic functions of macrophages in broilers.

Vitamin E (VE) is known for its antioxidant properties and has been shown to modulate immune system functions in various species. This study examined the influence of different levels of dietary VE (alpha-tocopherol acetate) on phagocytic functions of macrophages (abdominal exudate cells) in broiler chickens at 3, 5, and 7 wk. Birds were fed commercial diets containing 16 (control), 110, or 220 mg of VE/kg of feed. Macrophages were elicited into the abdominal cavity by injecting a 3% Sephadex solution prepared in PBS (G50-50, 1 mL/100 g of BW) 42 h prior to harvest. The percentage of phagocytically active macrophages and the number of SRBC phagocytosed per macrophage for unopsonized and antibody-opsonized SRBC were determined. These aspects of macrophage function were assessed based on 900 macrophages per sample. When unopsonized SRBC were used, dietary VE supplementation above control level did not affect phagocytic function of macrophages at wk 3, 5, or 7. With antibody-opsonized SRBC, the percentage of phagocytically active macrophages and the number of SRBC phagocytosed per macrophage were higher (P = 0.08 and P = 0.01, respectively) in 3-wk-old birds fed 110 and 220 mg of VE/kg of feed compared with age-matched controls. This enhancing effect of VE supplementation on macrophage function was not observed in 5- and 7-wk-old broilers. It appears from this study that supplemental VE enhances Fc-receptor-mediated macrophage phagocytic activity at early stages of broiler growth.

Abdominal Cavity↗

PubMed2004

Dietary supplementation with phosphorylated mannans improves growth response and modulates immune function of weanling pigs.

Phosphorylated mannans derived from the yeast cell wall of Saccharomyces cerevisiae may beneficially modulate immune function in the weanling pig, possibly providing an alternative to the use of dietary growth-promoting antibiotics. Therefore, in this study, 32 pigs averaging 19 d of age and 5.7 +/- 0.2 kg initial BW were randomly assigned to 16 pens in an environmentally controlled nursery to determine the effects of dietary supplementation with phosphorylated mannans on growth and immune function. Average daily gain and G:F ratio increased (P < 0.05) when pigs were fed diets supplemented with mannans from d 0 to 14 after weaning and in the overall experiment. Percentage of neutrophils was lower (P < 0.08) and percentage of lymphocytes was higher (P < 0.05) in blood from pigs fed mannans than when pigs were fed the basal diet. Lamina propria macrophages isolated from pigs fed diets containing mannans phagocytosed a greater (P < 0.05) number of sheep red blood cells (2.63 +/- 0.11) than did lamina propria macrophages isolated from pigs fed the basal diet (2.31 +/- 0.11). On d 19 after weaning, pigs fed diets supplemented with mannans tended to have a greater (P < 0.10) percentage of CD14+ lamina propria leukocytes than did pigs fed the basal diet. On d 21 following weaning, the percentage of CD14+MHCII+ leukocytes isolated from lamina propria tissue tended (P < 0.10) to be lower when pigs were fed mannans than when pigs were fed the basal diet. Pigs fed diets containing mannans had a lower (P < 0.05) ratio of CD3+CD4+:CD3+CD8+ T lymphocytes isolated from jejunal lamina propria tissue only on d 21 after weaning compared with pigs fed the basal diet. Supplementation of mannans in the diets of weanling pigs improved gain and efficiency, and intermittently affected selected components of the young pigs' immune function both systemically and enterically.

Animal Feed↗

PubMed2003

Melanocyte-specific cell mediated immune response in vitiliginous Smyth line chickens.

Smyth line chickens (SL) are an animal model to study human autoimmune vitiligo. Vitiligo in SL chickens is characterized by a post-hatch loss of feather melanocytes (MC) resulting in feather depigmentation. The etiopathology of this disease remains unclear, however, a hypothesis that cell-mediated immunity (CMI) plays an important role in the destruction of melanocytes has been proposed based on previous studies. To support this hypothesis, the delayed wattle response (DWR) to MC lysates was examined in SL chickens and normally pigmented, MHC-matched controls (Brown line, BL; Light Brown Leghorn, LBL) to determine whether vitiliginous SL chickens have MC-specific CMI. Chickens were challenged in one wattle with a lysate of either embryo- or feather-derived cultured MC. Lysates of chick-embryo-fibroblasts (CEF) associated turkey herpesvirus (HVT) vaccine and syngeneic CEF were used as positive and negative control, respectively. Vitiliginous SL chickens exhibited a significantly greater DWR to feather-MC but not to embryo-MC and CEF than nonvitiliginous SL chickens and normally pigmented controls. The DWR to feather-MC peaked at 3 to 5 days post feather-MC lysate injection. Immunohistochemical staining of DWR-positive wattle tissue revealed extensive lymphocyte infiltration at the site of feather-MC injection consisting primarily of T cells (TCR2+, CD4+ or CD8+ T cells). These observations support the presence of MC-specific CMI in SL chickens with vitiligo. The anti-MC CMI activity appears to be specific to MC derived from feathers. SDS-PAGE analysis of different sources of MC lysates revealed a 43 kDa missing band in the lysate of feather-MC established from SL chickens. No other obvious protein pattern differences that could account for the feather MC-specific CMI response in vitiliginous SL chickens were observed among the MC lysates.

Animals↗

PubMed2003

Effect of intravenous endotoxin on blood cell profiles of broilers housed in cages and floor litter environments.

Commercial broilers are constantly exposed to airborne microorganisms and endotoxin (lipopolysaccharide, LPS). It has been shown that microbial contamination of the air was higher in broiler houses using floor litter than in broiler houses using netting-type floors. The current study evaluated the effect of housing conditions on blood leukocyte profiles and tested the hypothesis that, when compared to broilers reared in clean stainless steel cages (Cage group), broilers raised on floor litter (Floor group) should experience a higher environmental challenge and have a desensitized immune system that may exhibit better tolerance/resistance to subsequent intravenous LPS challenge. Hematological parameters were evaluated prior to and following i.v. administration of 1 mg/kg BW Salmonella typhimurium LPS (dissolved at 1 mg/0.25 mL in PBS) or i.v. injection of 0.25 mL/kg BW PBS alone. The results showed that prior to LPS/PBS injection, broilers in the cage group had higher heterophil and monocyte concentrations, a higher B cell percentage within the lymphocyte population, and a higher heterophil to lymphocyte (H:L) ratio in the blood. The i.v. LPS injection resulted in 25% mortality in the cage group and 42% mortality in the floor group within 8 h post-injection. LPS reduced the concentrations of total white blood cells (WBC) and all differential WBC except eosinophils and increased thrombocyte concentrations within 1 h post-injection in both groups. All of these values returned to their respective pre-injection levels within 48 h post-injection in the surviving birds. The two groups exhibited similar overall hematological changes after LPS injection except that the cage group showed a higher H:L ratio at 8 h post-injection and a lower B-cell percentage within the lymphocyte population at 48 h post-injection when compared with the floor group. We concluded that the immune systems of broilers reared on floor litter were desensitized and exhibited less pronounced leukocyte responses to i.v. LPS when compared with those of broilers reared in clean stainless steel cages. However, such desensitization of the immune system did not help broilers survive subsequent i.v. LPS challenge.

Air Microbiology↗

PubMed2003

Broiler survivors of intravenous micro-particle injections: evaluation of growth, livability, meat quality, and arterial blood gas values during a cyclic heat challenge.

When broilers are exposed to high ambient temperatures, their cardiac output can increase by 20 to 50%. Previously, we developed an intravenous micro-particle injection technique to select broilers having a cardiopulmonary capacity capable of accommodating increases in cardiac output associated with fast growth and cool temperatures. In the present study, male broilers were injected at 18 to 20 d of age with cellulose micro-particles sufficient to trigger >50% mortality by 35 d of age. The survivors of micro-particle injections (cellulose survivors) and saline-injected flock mates (control group) were exposed to a moderate cyclic heat challenge (peak temperature of 35 to 37 degrees C) beginning on d 36 and continuing through d 57. We tested the hypothesis that if the cellulose survivors represent the population cohort having the most robust cardiopulmonary capacity, then during a subsequent heat challenge these survivorspotentially may perform better than their unselected flock mates. Based on data combined from two independent experiments, the cellulose survivors exhibited improved livability and body weight gain when compared with their unselected flock mates during the cyclic heat challenge. Meat quality characteristics did not differ between the groups. In a third experiment, cellulose survivors and saline-injected male broilers were reared at thermoneutral temperatures or were exposed to a cyclic heat challenge beginning on d 36. Arterial blood samples were collected from unanesthetized birds at 47 to 49 d of age and were analyzed for pH, partial pressure of CO2, bicarbonate, partial pressure of O2, and saturation of hemoglobin with O2. The blood gas values for the cellulose survivors and saline-injected broilers did not differ within a temperature regimen, regardless of whether the broilers were chronically acclimated to heat or were exposed to an acute heat challenge at the end of the experiment. The cellulose survivors did not differ in susceptibility to panting-induced respiratory alkalosis or hypoxemia when compared with their saline-injected flock mates. Overall, these observations indicate that selection for a robust cardiopulmonary capacity can confer advantages in growth and livability without affecting meat quality when broilers are exposed to a moderate heat challenge.

Animals↗

PubMed2003

Pulmonary and hematological inflammatory responses to intravenous cellulose micro-particles in broilers.

When injected intravenously, cellulose micro-particles become lodged in pulmonary arterioles. The current study investigated the systemic and pulmonary inflammatory responses triggered by cellulose micro-particles at 3, 24, and 48 h postinjection in 6-wk-old broilers. Proportions and concentrations of circulating white blood cells were assessed in saline-injected (control group) and cellulose-injected (particle group) birds. Hematoxylin-eosin (HE)-stained cross-sections of the lungs were used to count the number of granuloma/lymphocyte aggregates, which is indicative of the severity of the inflammatory response to the trapped particles. The cellular components of the aggregates were identified by immunohistochemical staining of frozen cross sections of the lungs. Results showed that cellulose micro-particles trapped in the pulmonary vasculature initiated a dynamic, localized inflammatory response within the surrounding lung parenchyma. Monocytes and basophilic granulocytes closely surrounded the particles. CD4, CD8, TCR1, TCR2, and TCR3 subsets of T cells and B cells were present in the outer rim of the granuloma/lymphocyte aggregates. Circulating total white blood cell (WBC, leukocytes) concentrations were similar in both groups at all times postinjection, whereas at 48 h post-injection the percentages of eosinophils and basophils among circulating WBC were higher in the particle group than in the control group (P < or = 0.05). The circulating monocyte concentration also increased within 24 h postinjection (P < or = 0.05). These observations demonstrate that cellulose micro-particles trapped in the pulmonary vasculature initiated acute focal inflammatory responses in the lungs and that the proportions of WBCs in the blood are modulated within 48 h postinjection.

Animals↗