Thermal status for different breeds of dairy cattle exposed to summer heat stress in a grazing environment [abstract]

Abstract only availableA study was conducted to investigate thermal balance of lactating dairy cattle managed in an intensive managed rotational grazing system. The farm was located at the University of Missouri Southwest Research Center in Vernon County, MO. Thirty six lactating dairy cows were blocked by parity, days in milk, milk production and breed. Cows were grouped by breed with 100% Holstein (H, n=8), 75%H:25% Jersey (J) (75H, n=5), 50%H:50%J (50H, n=8), 25%H:75%J (75J, n=7), and 100% J (J, n=8), and maintained on the same pastures from June 15 through August 1, 2006. Cows were rotated to paddocks to maintain ad libitum access to pasture. Ambient variables, including air temperature (Ta) and relative humidity, were measured continuously. Ranges of Ta and calculated THI were 12 to 38C and 55 to 87, respectively. Thermal balance was evaluated prior to morning (0500) and afternoon (1600) milkings by measuring rectal temperature (Tre) and respiration rate (RR) on 16 days throughout the study during periods of maximum and minimum heat stress. Breed groups had different body weights (p < 0.0001) ranging from 530 kg (H) to 378 (J). However, body weight was similar for 75J and 75H (460 kg versus 501 kg, respectively). Although body weights were different across breed, combined change in rectal temperature with Ta (r = 0.89) and THI (r = 0.92) was predictable (p < 0.0001). Change in Tre with increasing Ta and THI was slowest for J and 75J, and highest for H and 75H. Change in Tre was influenced more by breed more than body weight. Respiration rate was correlated with Ta (r = 0.88) and THI (r = 0.89) (p < 0.0001), with 75J being more responsive than 75H. These results suggest that breed selection can be used to improve thermal balance of cows in intensively managed rotational grazing systems.CAFNR On Campus Research Internshi

MCP-1 and its role in macrophage recruitment in Lyme carditis [abstract]

Abstract only availableLyme disease is caused by infection with the bacteria Borrelia burgdorferi, causing arthritis and carditis in infected animals. The presence of spirochetes in the heart tissue induces recruitment of leukocytes to the area of infection and leads to the production of proinflammatory cytokines which are thought to play a role in the development of pathology. MCP-1 (macrophage chemoattractant protein-1) is responsible for the recruitment of macrophages, the main leukocyte found in carditis, to the infected tissue and has been related to increased severity of Lyme carditis. Based on these observations, the importance and role of MCP-1 in the development of Lyme carditis was investigated. It was hypothesized that carditis severity and pro-inflammatory cytokine production would be decreased in MCP-1 knock out (KO) mice, while the number of the number of B. burgdorferi organisms found in the heart of MCP-1 KO mice would be increased due the lack of recruited macrophages. MCP-1 KO and wild type mice were infected with B. burgdorferi in the hind paws and at 21 days post infection, the peak of Lyme disease pathogenesis, the heart of each mouse was harvested. After staining, heart sections were scored for the development of carditis. The severity of inflammation was scored on a scale from 0 to 3 according to the number of infiltration foci. There appeared to be no difference in the development of carditis between the wild type and the MCP-1 KO mice. Similarly, there was no difference between the number of B. burgdorferi organisms found in the hearts of MCP-1 KO and wild type mice. Studies are underway to determine the cellular makeup of immune cells in the heart tissue.McNair Scholars Progra

Role of Cyclooxygenase-1 during the immunological response in lyme arthritis [abstract]

Abstract only availablePreviously, pharmacological inhibition of COX-1 in wild-type C3H mice resulted in changes in antibody production in response to infection with the causative agent of Lyme Disease, the spirochete Borrelia burgdorferi (Bb). These results suggests that the changes seen in the progression of Lyme Disease, including joint inflammatory arthritis and clearance of Bb maybe due to the COX-1 enzyme. A murine model of Lyme Disease using C3H/HeJ strain was used. Progression of Lyme Disease inflammation was followed from the day of infection through day 21 post-infection by correlating histology of ankle inflammation, quantitative PCR determination of Bb load in inflamed ankle and in ear, and quantitation of the production of cytokines, chemokines and eicosanoids in inflamed knee joints. The response to Bb infection in wild type C3H mice was compared to development of inflammation in C3H mice made genetically deficient for the COX-1 gene. In both wild type and COX-1 knockout mice, experiments are being conducted to observe histological changes post infection, including changes in cellularity and tissue organization. Currently, the ability of each mouse strain to clear the infecting Bb is being determined by using quantitative PCR to compare the incidence of Bb genomes to a mouse reference gene. Finally, experiments are being conducted to compare the cytokine and chemokine secretion responses and patterns of eicosanoid production of the wild type mice to their COX-1 knockout counterparts determine if changes in inflammatory mediators result from loss of COX-1 function. The data produced in this study will analyzed in order to define differences of wild type mice and COX-1 mice in the induction and resolution of inflammatory processes in response to Bb infection in a mouse model of Lyme Disease. This experiment provide valuable insight into the causes of Lyme arthritis and help to explain the differences in antibody responses observed after COX-1 pharmacological inhibition or genetic deletion.McNair Scholars Progra

MCP-1 and its role in lyme arthritis [abstract]

Abstract only availableLyme disease is caused by infection with the bacteria Borrelia burgdorferi, causing arthritis and carditis in infected animal models. The presence of spirochetes in the joint and other soft tissues induce recruitment of leukocytes to the area of infection and leads to the production of proinflammatory cytokines which are thought to play a role in the development of pathology. MCP-1 (macrophage chemoattractant protein-1) is one of the cytokines responsible for the recruitment of macrophages to infected tissue during normal disease pathogenesis. It was previously found that MCP-1 does not play a significant role in the pathogenesis of Lyme carditis, therefore the importance and role of MCP-1 in the development of Lyme arthritis was investigated. It was hypothesized that arthritis severity and pro-inflammatory cytokine production would be decreased in MCP-1 knock out (KO) mice, while the number of the number of B. burgdorferi organisms found in joint tissue of MCP-1 KO mice would be increased due the lack of recruited macrophages. MCP-1 KO and wild type (WT) C3H and B6 mice were infected with B. burgdorferi in the hind paws and they were sacrificed at 21 days post infection, the peak of Lyme disease pathogenesis. Ankle diameter was measured weekly throughout the infection and histological ankle sections were scored for the severity of inflammation on a scale from 0 to 3, according to the number of infiltration foci. Ankle diameter of C3H WT mice was on average greater than C3H MCP-1 KO mice, while the pro-inflammatory and anti-inflammatory cytokine levels were on average lower than KO mice. In B6 mice, WT mice had decreased ankle diameter and higher cytokine levels compared to B6 MCP-1 KO mice. These data suggest that MCP-1 may play more of a role in Lyme arthritis than Lyme carditis pathology.Life Sciences Undergraduate Research Opportunity Progra