College of Agriculture & Natural Resources

Permanent URI for this communityhttp://hdl.handle.net/1903/1598

The collections in this community comprise faculty research works, as well as graduate theses and dissertations.

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Subject: search.filters.subject.immune response

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    Marek’s Disease Virus Infection Induced Mitochondria Changes in Chickens
    (MDPI, 2019-06-27) Chu, Qin; Ding, Yi; Cai, Wentao; Liu, Lei; Zhang, Huanmin; Song, Jiuzhou
    Mitochondria are crucial cellular organelles in eukaryotes and participate in many cell processes including immune response, growth development, and tumorigenesis. Marek’s disease (MD), caused by an avian alpha-herpesvirus Marek’s disease virus (MDV), is characterized with lymphomas and immunosuppression. In this research, we hypothesize that mitochondria may play roles in response to MDV infection. To test it, mitochondrial DNA (mtDNA) abundance and gene expression in immune organs were examined in two well-defined and highly inbred lines of chickens, the MD-susceptible line 72 and the MD-resistant line 63. We found that mitochondrial DNA contents decreased significantly at the transformation phase in spleen of the MD-susceptible line 72 birds in contrast to the MD-resistant line 63. The mtDNA-genes and the nucleus-genes relevant to mtDNA maintenance and transcription, however, were significantly up-regulated. Interestingly, we found that POLG2 might play a potential role that led to the imbalance of mtDNA copy number and gene expression alteration. MDV infection induced imbalance of mitochondrial contents and gene expression, demonstrating the indispensability of mitochondria in virus-induced cell transformation and subsequent lymphoma formation, such as MD development in chicken. This is the first report on relationship between virus infection and mitochondria in chicken, which provides important insights into the understanding on pathogenesis and tumorigenesis due to viral infection.
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    EVALUATING DIFFERENCES IN BODY WEIGHT, GUT MORPHOLOGY, IMMUNE RESPONSE, AND SICKNESS BEHAVIOR IN FAST- AND SLOW- GROWING BROILER CHICKENS WHEN INFECTED WITH SALMONELLA ENTERICA SEROVAR TYPHIMURIUM
    (2021) Snyder, Ashlyn Marie; Weimer, Shawna; Animal Sciences; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    Fast growth rate in broilers comes with welfare concerns and research is needed to determine if fast- and slow-growing broilers differ in pathogen resistance. The objective of this study was to evaluate differences in fast- (FG) and slow-growing (SG) broilers when challenged with Salmonella Typhimurium or broth (control) 14 days post-hatch. Plasma IgA and IgG, jejunum and ileum histomorphology, and behaviors were measured. FG had greater d12 and d24 body weight and d7 jejunum measures, indicating better absorption, and earlier increases in plasma IgA and IgG, indicating earlier immune development. SG had greater d7 IgG, indicating stronger maternal immunity. Post-challenge, FG gut morphology was more impaired, and SG had greater IgA and reduced sham foraging, indicating a stronger immune response to challenge. The results illustrate fast- and slow-growing broilers differ in Salmonella resistance, which can help breeders make selection decisions to prevent Salmonella transmission into the human food supply.
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    Antagonizing JAK-STAT signaling by porcine reproductive and respiratory syndrome virus
    (2018) Yang, Liping; Zhang, Yanjin; Veterinary Medical Science; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    The Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway is activated by numerous cytokines. JAK-STAT pathways involve in regulation of cell growth, proliferation, differentiation, apoptosis, angiogenesis, immunity and inflammatory response. Because of their significance in immune response, they are often targeted by pathogens, including porcine reproductive and respiratory syndrome virus (PRRSV). PRRSV causes reproductive failure in sows and severe respiratory disease in pigs of all ages. A typical feature of the immune response to PRRSV infection in pigs is delayed production and low titer of virus neutralizing antibodies, and weak cell-mediated immune response. One possible reason for the weak protective immune response is that PRRSV interferes with innate immunity and modulates cytokine signaling, including JAK-STAT pathways. The objective of this project was to elucidate the mechanisms of PRRSV interference with JAK-STAT2 and JAK-STAT3 signaling. This study demonstrates that PRRSV antagonizes interferon (IFN)-activated JAK-STAT2 signaling and oncostatin M (OSM)-activated JAK-STAT3 pathway via inducing STAT2 and STAT3 degradation. Mechanistically, PRRSV non-structural protein 11 (nsp11) and nsp5 induce the degradation of STAT2 and STAT3, respectively, via the ubiquitin-proteasome pathway. Notably, PRRSV manipulates karyopherin alpha 6 (KPNA6), an importin that is responsible for STAT3 nuclear translocation in the JAK-STAT signaling, to facilitate viral replication. Knockdown of KPNA6 expression led to significant reduction in PRRSV replication. These data demonstrate that PRRSV interferes with different JAK-STAT pathways to evade host antiviral response while harnessing cellular factors for its own replication. These findings provide new insights into PRRSV-cell interactions and its molecular pathogenesis in interference with the host immune response, and facilitate the development of novel antiviral therapeutics.