Thesis (M. Phil.)--University of Hong Kong, 2006. / Title proper from title frame. Also available in printed format.

Objectives of this study were to examine effects of dietary pyrrolizidine alkaloids (PA) on copper and vitamin A metabolism in the chicken which are very susceptible to the hepatoxic effects of PA and Japanese quail which are highly resistant to PA. Also, the possible interaction between copper and vitamin A in the two species and effect of PA on retention of previously stored vitamin A in the chicken were investigated. Three experiments were designed. Experiment 1 was to examine the effect of feeding the PA-containing plant tansy ragwort (TR)(Senecio jacobaea) on tissue levels of copper and vitamin A in the chicken. Experiment 2 was to investigate if dietary PA affected the retention of previously stored vitamin A in the chicken. Experiment 3 was to determine if hepatoxic effects of PA are necessary to influence copper and vitamin A metabolism in Japanese quail. In experiment 1, a 2x2x2 factorial design with dietary 0 and 5% TR, 0 and 250 ppm copper, and 0 and 25,000 IU/kg diet vitamin A was used. The results showed that body weight gain was reduced (P < 0.01) in birds fed TR. Both serum and liver copper concentrations were markedly increased (P <0.01) in the TR-fed group with 250 ppm copper supplement. Zinc concentrations in the serum and liver were significantly decreased (P <0.05) in the TR-fed groups compared to TR-free groups. Liver iron was increased (P <0.05) in the TR-fed birds. The serum vitamin A levels were significantly decreased (P < 0.01) in all TR-fed groups. The ranges of decrease were from 62 to 72 % in four TR -fed groups. The liver vitamin A concentrations were also significantly decreased (P <0.05) in TR-fed groups without vitamin A supplement. The effects of PA on liver and blood vitamin A concentration may reflect PA inhibition of synthesis of retinol-binding proteins, or impaired vitamin A absorption from reduced biliary excretion. There was no interaction between dietary copper and vitamin A levels and tissue concentrations of these nutrients. In experiment 2, a two period experiment was carried out. In the first period, two groups of chicks were fed a diet containing 25,000 IU vitamin A/kg diet for two weeks followed by a control or TR-containing diet for four weeks. Blood samples were taken at 4 day intervals for 24 days. It was found that by day 8, serum vitamin A levels were significantly depressed (P <0.05). After 24 days of PA exposure, serum vitamin A levels were reduced by 55 % and 8.5% in the TR-fed group and the control group, respectively. Liver concentration of vitamin A was increased (P < 0.05) at day 24 of TR feeding, while liver vitamin A concentration in birds fed the control diet was decreased by 13% over the same period. The results indicate that PA inhibit the mobilization of previously stored vitamin A from the liver, probably by inhibiting hepatic synthesis of retinol-binding proteins. Experiment 3 was a 2x2x2 factorial design with added 0 and 5% tansy ragwort, 0 and 250 ppm copper, and 0 and 25,000 IU/kg diet vitamin A. The results showed that consumption of TR did not affect the growth rate of Japanese quail. There were no significant differences in the serum copper concentrations among all treatment groups. Liver copper levels were decreased with TR feeding (P <0.05). The concentrations of zinc and iron in the serum and liver were normal in TR-fed groups compared to the controls. There was no significant effect (P >0.05) on the serum vitamin A concentration. The liver vitamin A concentrations were also not significantly different with the exception of the basal TR group. Copper supplementation of the diet increased serum vitamin A levels (P <0.05). The results suggest that hepatotoxicity is necessary to induce the changes in tissue levels of copper and vitamin A seen in PA-susceptible species. / Graduation date: 1991

The pathogenesis of <i>C. jejuni</i> in broiler chickens is still poorly understood despite the importance of poultry meat as a source of infection in humans. The overall objective of this project was to understand the role of flagella and Campylobacter invasion antigens in mucosal and systemic colonization, and to evaluate the vaccine potential of <i>C. jejuni</i> paralyzed flagella mutants. As a first step to track <i>C. jejuni in vivo</i>, a Green Fluorescent Protein (GFP) reporter system that is constitutively expressed was constructed. The system was transformed into different <i>C. jejuni</i> strains and isolates, and their mucosal and systemic spreading was studied over the period of 7 days. <i>C. jejuni</i> NCTC11168V1 and V26 share the same background but differ in their ability to colonize chickens. <i>C. jejuni</i> 81-176 and K2-55 share the same genetic background but K2-55 has an insertion mutation in <i>pflA</i> gene that produced paralyzed flagella. Although the K2-55 flagella remained intact structurally, it did not secret <i>Campylobacter</i> invasion antigens (Cia). The reporter system was stable in all of these strains both <i>in vitro</i> and <i>in vivo</i>. Fluorescent bacteria were visualized successfully using fluorescent and confocal microscopes. C. jejuni NCTC11168V1 and 81-176 were detected in the intestinal tract and in the liver and spleen of more than 30% of the challenged birds, while V26 and K2-55 were only detected in the intestinal tract. <i>C. jejuni</i> 81-176 and K2-55 did not spread systemically to the spleen and liver of BALB/c mice challenged using the same approach, although they colonized the ceca.<p> A live attenuated vaccine based on <i>C. jejuni</i> K2-55 protected broiler chickens from <i>C. jejuni</i> 81-176 challenge in chickens following streptomycin treatment of drinking water. The same vaccine had no significant protection against a heterolgous <i>C. jejuni</i> NCTC11168V1 strain challenge. The vaccine was a poor stimulator of secretory IgA.<p> Macrophage-like HD11 cells inflammatory response to the presence of <i>C. jejuni</i> K2-55 was not significantly different from their response to wild-type 81-176 when measured by qRT-PCR. The lack of Cia secretion and motility had no effect on expression of IL-1â, IL-2, IL-6, IL-8, IL, IL-10, IL-12â, or TLR5. A <i>flgK</i> mutant expressing the flagella up to the hook had a significantly lower expression of these genes.

The pathogenesis of <i>C. jejuni</i> in broiler chickens is still poorly understood despite the importance of poultry meat as a source of infection in humans. The overall objective of this project was to understand the role of flagella and Campylobacter invasion antigens in mucosal and systemic colonization, and to evaluate the vaccine potential of <i>C. jejuni</i> paralyzed flagella mutants. As a first step to track <i>C. jejuni in vivo</i>, a Green Fluorescent Protein (GFP) reporter system that is constitutively expressed was constructed. The system was transformed into different <i>C. jejuni</i> strains and isolates, and their mucosal and systemic spreading was studied over the period of 7 days. <i>C. jejuni</i> NCTC11168V1 and V26 share the same background but differ in their ability to colonize chickens. <i>C. jejuni</i> 81-176 and K2-55 share the same genetic background but K2-55 has an insertion mutation in <i>pflA</i> gene that produced paralyzed flagella. Although the K2-55 flagella remained intact structurally, it did not secret <i>Campylobacter</i> invasion antigens (Cia). The reporter system was stable in all of these strains both <i>in vitro</i> and <i>in vivo</i>. Fluorescent bacteria were visualized successfully using fluorescent and confocal microscopes. C. jejuni NCTC11168V1 and 81-176 were detected in the intestinal tract and in the liver and spleen of more than 30% of the challenged birds, while V26 and K2-55 were only detected in the intestinal tract. <i>C. jejuni</i> 81-176 and K2-55 did not spread systemically to the spleen and liver of BALB/c mice challenged using the same approach, although they colonized the ceca.<p> A live attenuated vaccine based on <i>C. jejuni</i> K2-55 protected broiler chickens from <i>C. jejuni</i> 81-176 challenge in chickens following streptomycin treatment of drinking water. The same vaccine had no significant protection against a heterolgous <i>C. jejuni</i> NCTC11168V1 strain challenge. The vaccine was a poor stimulator of secretory IgA.<p> Macrophage-like HD11 cells inflammatory response to the presence of <i>C. jejuni</i> K2-55 was not significantly different from their response to wild-type 81-176 when measured by qRT-PCR. The lack of Cia secretion and motility had no effect on expression of IL-1â, IL-2, IL-6, IL-8, IL, IL-10, IL-12â, or TLR5. A <i>flgK</i> mutant expressing the flagella up to the hook had a significantly lower expression of these genes.

Thesis (Ph. D.)--University of Texas at Austin, 2001. / Vita. Includes bibliographical references. Available also from UMI/Dissertation Abstracts International.

Includes bibliographical references (p. 89-101).

Thesis (Ph. D.)--Swedish University of Agricultural Sciences, 2001. / Includes bibliographical references.

Thesis (Ph. D.)--University of North Texas, Aug., , 2009. / Title from title page display. Includes bibliographical references.

Thesis (M. Phil.)--University of Hong Kong, 2002. / Includes bibliographical references (leaves 88-110).

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