11 research outputs found
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Cool, Pathogen-Free Refuge Lowers Pathogen-Associated Prespawn Mortality of Willamette River Chinook Salmon
Spring Chinook Salmon Oncorhynchus tshawytscha are transported above dams in the Willamette River to provide access to blocked spawning habitat. However, 30–95% of these transplants may die before spawning in some years. To varying degrees, salmon in other tributaries—both blocked and unblocked—have similar prespawn mortality (PSM) rates. Our study determined whether holding fish in constant temperature, pathogen-free conditions prior to spawning increased survival through spawning in 2010 through 2012. In addition, we evaluated pathogens as a potential cause of PSM. To monitor survival we captured adult Chinook Salmon early and late in the season from the lower Willamette River and upper tributaries and held them until spawning in 13°C, pathogen-free water. Samples were collected at the time of transport, from moribund or dead fish throughout the summer, and after spawning in the autumn. Prespawn mortalities and postspawned fish from river surveys on holding and spawning reaches above traps were also sampled. Necropsies were performed on all fish, and representative organs were processed for histopathological analysis. Using multiple logistic regression odds ratio analysis, fish that were held were up to 12.6 times less likely to experience PSM than fish that were outplanted to the river. However, Aeromonas salmonicida and Renibacterium salmoninarum were more prevalent in held fish that had PSM than in outplanted fish with PSM, suggesting that fish that were held were more susceptible to these bacteria. Spawned held fish were more likely to have Myxobolus sp. brain infections and less likely to be infected with the kidney myxozoan, Parvicapusla minibicornis, than were spawned outplanted fish. The equal likelihood of other pathogens for held fish and outplanted spawned fish suggests interactive effects determine survival and that holding Chinook Salmon at 13°C prevented expression of lethal pathogenesis. Overall, holding could be a viable method to reduce PSM, but issues of transport stress, proliferative disease, and antibiotics remain
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Innate and adaptive immune responses in migrating spring-run adult chinook salmon, Oncorhynchus tshawytscha
Adult Chinook salmon (Oncorhynchus tshawytscha) migrate from salt water to freshwater streams to spawn. Immune responses in migrating adult salmon are thought to diminish in the run up to spawning, though the exact mechanisms for diminished immune responses remain unknown. Here we examine both adaptive and innate immune responses as well as pathogen burdens in migrating adult Chinook salmon in the Upper Willamette River basin. Messenger RNA transcripts encoding antibody heavy chain molecules slightly diminish as a function of time, but are still present even after fish have successfully spawned. In contrast, the innate anti-bacterial effector proteins present in fish plasma rapidly decrease as spawning approaches. Fish also were examined for the presence and severity of eight different pathogens in different organs. While pathogen burden tended to increase during the migration, no specific pathogen signature was associated with diminished immune responses. Transcript levels of the immunosuppressive cytokines IL-10 and TGF beta were measured and did not change during the migration. These results suggest that loss of immune functions in adult migrating salmon are not due to pathogen infection or cytokine-mediated immune suppression, but is rather part of the life history of Chinook salmon likely induced by diminished energy reserves or hormonal changes which accompany spawning.Keywords: Parasite burden, Salmon, Immune respons
An Allograft Glioma Model Reveals the Dependence of Aquaporin-4 Expression on the Brain Microenvironment
Aquaporin-4 (AQP4), the main water channel of the brain, is highly expressed in animal glioma and human glioblastoma in situ. In contrast, most cultivated glioma cell lines don’t express AQP4, and primary cell cultures of human glioblastoma lose it during the first passages. Accordingly, in C6 cells and RG2 cells, two glioma cell lines of the rat, and in SMA mouse glioma cell lines, we found no AQP4 expression. We confirmed an AQP4 loss in primary human glioblastoma cell cultures after a few passages. RG-2 glioma cells if grafted into the brain developed AQP4 expression. This led us consider the possibility of AQP4 expression depends on brain microenvironment. In previous studies, we observed that the typical morphological conformation of AQP4 as orthogonal arrays of particles (OAP) depended on the extracellular matrix component agrin. In this study, we showed for the first time implanted AQP4 negative glioma cells in animal brain or flank to express AQP4 specifically in the intracerebral gliomas but neither in the extracranial nor in the flank gliomas. AQP4 expression in intracerebral gliomas went along with an OAP loss, compared to normal brain tissue. AQP4 staining in vivo normally is polarized in the astrocytic endfoot membranes at the glia limitans superficialis and perivascularis, but in C6 and RG2 tumors the AQP4 staining is redistributed over the whole glioma cell as in human glioblastoma. In contrast, primary rat or mouse astrocytes in culture did not lose their ability to express AQP4, and they were able to form few OAPs