Some fish populations are able to adapt and thrive in contaminated habitats. Survival of populations depends on the ability of the organism to elicit resistance, either due to genetic adaptation or physiological acclimations. Brown Bullheads (Ameiurus nebulosus) are able to survive in very contaminated areas and their benthic and philopatric characteristics make them a model organism to study chronic exposure. This research assesses the immune function of brown bullhead collected at four pre-determined sites along the Detroit River, which are characterized by high or low concentrations of environmental toxicants. Clean and contaminated sediment used for contaminant exposure was collected by ponar at designated sites of the river. The bullheads were vaccinated with heat-killed V. anguillarum in order to induce an immune response, before the vaccinated bullheads were randomly divided into corresponding contaminant exposure tanks. Respiratory burst assays to assess innate oxygen radical production 24hrs post vaccination and sediment exposure identified an inhibition of neutrophil oxidative activity in adult 6 month cleared of contaminant bullheads collected from a clean (Peche Island) site exposed to contaminated sediment, and of F1 raised populations from a contaminated (Trenton Channel) site. Results also showed overall inhibition on contaminated sediment in both PI and TC recently captured fish. Enzyme linked immunosorbant assay (ELISA) to assess antibody production revealed no difference between those fish exposed to either sediment. Results did show a lower expression of total antibody in chronically contaminant exposed bullheads (acute adults). Real time PCR to assess immune gene expression was conducted using cloned Major Histocompatibility Class II Beta (MHIIB), Interleukin-8 (IL-8) and Interleukin-1 Beta (IL-1B) 24hr post vaccination and sediment exposure. No contaminant induced immunosuppression of MHIIB was observed, while a reduction in IL-8 and IL-1B in acute adults may signify a delayed response due to chronic sediment exposure or of a normal functioning delayed response in wild bullheads. Results of the present study indicate negative environmental impacts on the innate immune response, leading to physiological adaptations in the brown bullhead, which can be reversed upon removal of the contaminants.

Some fish populations are able to adapt and thrive in contaminated habitats. Survival of populations depends on the ability of the organism to elicit resistance, either due to genetic adaptation or physiological acclimations. Brown Bullheads (Ameiurus nebulosus) are able to survive in very contaminated areas and their benthic and philopatric characteristics make them a model organism to study chronic exposure. This research assesses the immune function of brown bullhead collected at four pre-determined sites along the Detroit River, which are characterized by high or low concentrations of environmental toxicants. Clean and contaminated sediment used for contaminant exposure was collected by ponar at designated sites of the river. The bullheads were vaccinated with heat-killed V. anguillarum in order to induce an immune response, before the vaccinated bullheads were randomly divided into corresponding contaminant exposure tanks. Respiratory burst assays to assess innate oxygen radical production 24hrs post vaccination and sediment exposure identified an inhibition of neutrophil oxidative activity in adult 6 month cleared of contaminant bullheads collected from a clean (Peche Island) site exposed to contaminated sediment, and of F1 raised populations from a contaminated (Trenton Channel) site. Results also showed overall inhibition on contaminated sediment in both PI and TC recently captured fish. Enzyme linked immunosorbant assay (ELISA) to assess antibody production revealed no difference between those fish exposed to either sediment. Results did show a lower expression of total antibody in chronically contaminant exposed bullheads (acute adults). Real time PCR to assess immune gene expression was conducted using cloned Major Histocompatibility Class II Beta (MHIIB), Interleukin-8 (IL-8) and Interleukin-1 Beta (IL-1B) 24hr post vaccination and sediment exposure. No contaminant induced immunosuppression of MHIIB was observed, while a reduction in IL-8 and IL-1B in acute adults may signify a delayed response due to chronic sediment exposure or of a normal functioning delayed response in wild bullheads. Results of the present study indicate negative environmental impacts on the innate immune response, leading to physiological adaptations in the brown bullhead, which can be reversed upon removal of the contaminants.

No description available.

No description available.

The studies described herein were designed to determine the influence of temperament on stress hormones and the immune system in response to various stressors. These stressors included transportation, lipopolysaccharide (LPS) challenge, and adrenocorticotropin (ACTH) challenge. In the first transportation study, bulls (8 Calm, 8 Intermediate, and 8 Temperamental) were loaded into a trailer and transported for 9 hr. Rectal temperature (monitored via indwelling recorders) increased within 0.5 hr of transportation, with greater peak rectal temperature in Temperamental than Calm bulls. Pre- and post-transport concentrations of cortisol and epinephrine were not affected by transportation, but were greater in Temperamental than Calm bulls. A second transportation study utilized 2 automatic sampling devices to allow the recording of rectal temperature and collection of blood samples, respectively. Rectal temperature was not affected by transportation or temperament in response to 4-hr of transport. Average heart rate oscillated between 60 and 130 bpm in Temperamental bulls, but remained around 100 bpm in Calm bulls. Transportation did not affect concentrations of epinephrine, although concentrations were greater in Temperamental bulls than Calm bulls. Cortisol concentrations increased in Calm bulls but not in Temperamental bulls in response to transportation. Additionally, there were limited effects of transportation on peripheral blood mononuclear cell proliferation, IgM production, and cytokine gene expression. Specifically, proliferation tended to be greater post-transport. Expression of the glucocorticoid receptor was, and the expression of toll-like receptor 4 tended to be, reduced post-transport, as analyzed by quantitative real-time RT-PCR. In a study utilizing a LPS challenge, basal stress hormone concentrations during the pre-challenge period were greater in Temperamental bulls than Calm bulls. However, in response to the LPS challenge, only the epinephrine response was influenced by temperament. Additionally, Temperamental bulls exhibited a smaller increase in rectal temperature and sickness behavior than Calm bulls. In the last study, change in gene expression in peripheral blood mononuclear cells in response to acute increases in cortisol was assessed. Plasma cortisol and gene expression of cytokines and the glucocorticoid receptor tended to increase in response to placement of jugular cannula. Additionally, administration of ACTH significantly increased plasma concentrations of cortisol and the gene expression of some cytokines (interleukin-4 and interleukin-10). This suggests that acute increases in cortisol may have positive effects on immune function in Brahman calves. Through an increased understanding of the interaction between the stress response and animal temperament, as well as how stress hormones and temperament influence immune function, animal management practices can be modified to reduce negative impacts on growth and productivity.

No description available.

There are eight described human herpesviruses. All share the ability to achieve latency in their host following primary infection and may subsequently reactivate later in life. In immunocompetent individuals herpesvirus infections, especially those caused by reactivating virus, are usually mild however in patients with impaired cellular immune function they may cause significant morbidity and mortality. In this thesis molecular and serological techniques were used to define the prevalence of the human herpesviruses in a variety of immunocompromised groups as these individuals are at greatest risk of severe herpesviral disease. Human herpesvirus 8 (HHV8) is the most recently discovered of the human herpesviruses. A nested polymerase chain reaction (PCR) for detecting HHV8 genome was designed and used to examine the association between infection with HHV8 and FIIV-associated Kaposi's sarcoma (KS). The prevalence of HHV8 genome carriage in the general UK population was defined, as were potential routes of HHV8 transmission. Novel treatments for HIV-KS were investigated. The value of herpesviral genome detection in predicting associated disease was evaluated, together with the genome load response of cytomegalovirus (CMV), a significant herpesviral pathogen, to a novel chemotherapeutic protocol for immunosuppressed patients receiving allogenic bone marrow transplantation. The prevalence and epidemiology of HHV8 were found to be compatible with that predicted for a causal agent of KS, but not the haematological malignancy multiple myeloma. Apart from 1-IHV8, Epstein-Barr virus and CMV were found to be the most significant herpesvirus pathogens in the immunocompromised host. The use of molecular detection techniques, such as PCR, were shown to be of great value in the diagnostic and epidemiological determination of herpesviral infection in immunocompromised patients.

No description available.

Early during an immune response, dendritic cells (DC) interact closely with CD4+ T cells, and cross-talk between these cells can come in the form of tumour necrosis factor (TNF) superfamily ligand-receptor interactions. These signals are critical for the maturation, function and survival of DC, and thereby dictate the capacity of DC to prime a robust T cell response. Among these cues, helper T cell-expressed CD40L interaction with DC-expressed CD40 is required to fully mature DC for cross-priming of help-dependent CD8+ T cell responses. The lymphotoxin-beta receptor (LTβR) is another TNF family receptor on DC, and it’s ligands LTα1β2 and LIGHT are expressed on activated T cells. Since abrogated LTβR signaling impairs T cell immunity, we have examined whether LTαβ represents another possible helper T cell-derived cue for full DC maturation. However the LT pathway controls lymphoid tissue organization and DC homeostasis, a second possible mechanism explaining the necessity of LTβR signaling for T cell immunity. Here we dissect the role of helper T cell-expressed LTβR ligands and DC-intrinsic LTβR signaling, independent of DC homeostasis or lymphoid organization, in DC function and T cell immunity. Absence of LTα1β2 and not LIGHT on helper T cells results in compromised T cell priming by DC ex vivo, and LTβ-/- CD4+ T cell responses are impaired in vivo. Ag-specific CD4+ T cell-expressed LTα1β2 and DC-intrinsic LTβR signaling are required for an optimal cytotoxic T lymphocyte (CTL) response in vivo. While CD40 induces IL-12 and is required for CTL function, DC-intrinsic LTβR signaling is necessary for CTL activation and expansion, early up-regulation of CD86 and IFNα/β production. Our results reveal non-redundant roles for distinct TNF family receptors in enabling DC to program different features in Ag-specific CD8+ T cells.

abstract: Environmental changes are occurring at an unprecedented rate, and these changes will undoubtedly lead to alterations in resource availability for many organisms. To effectively predict the implications of such changes, it is critical to better understand how organisms have adapted to coping with seasonally limited resources. The vast majority of previous work has focused on energy balance as the driver of changes in organismal physiology. While energy is clearly a vital currency, other resources can also be limited and impact physiological functions. Water is essential for life as it is the main constituent of cells, tissues, and organs. Yet, water has received little consideration for its role as a currency that impacts physiological functions. Given the importance of water to most major physiological systems, I investigated how water limitations interact with immune function, metabolism, and reproductive investment, an almost entirely unexplored area. Using multiple species and life stages, I demonstrated that dehydrated animals typically have enhanced innate immunity, regardless of whether the dehydration is a result of seasonal water constraints, water deprivation in the lab, or high physiological demand for water. My work contributed greatly to the understanding of immune function dynamics and lays a foundation for the study of hydration immunology as a component of the burgeoning field of ecoimmunology. While a large portion of my dissertation focused on the interaction between water balance and immune function, there are many other physiological processes that may be impacted by water restrictions. Accordingly, I recently expanded the understanding of how reproductive females can alter metabolic substrates to reallocate internal water during times of water scarcity, an important development in our knowledge of reproductive investments. Overall, by thoroughly evaluating implications and responses to water limitations, my dissertation, when combined previous acquired knowledge on food limitation, will enable scientists to better predict the impacts of future climate change, where, in many regions, rainfall events are forecasted to be less reliable, resulting in more frequent drought. / Dissertation/Thesis / Doctoral Dissertation Biology 2019