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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    Interferon Independent Non-Canonical STAT Activation and Virus Induced Inflammation
    (MDPI, 2018-04-14) Nan, Yuchen; Wu, Chunyan; Zhang, Yan-Jin
    Interferons (IFNs) are a group of secreted proteins that play critical roles in antiviral immunity, antitumor activity, activation of cytotoxic T cells, and modulation of host immune responses. IFNs are cytokines, and bind receptors on cell surfaces to trigger signal transduction. The major signaling pathway activated by IFNs is the JAK/STAT (Janus kinase/signal transducer and activator of transcription) pathway, a complex pathway involved in both viral and host survival strategies. On the one hand, viruses have evolved strategies to escape from antiviral host defenses evoked by IFN-activated JAK/STAT signaling. On the other hand, viruses have also evolved to exploit the JAK/STAT pathway to evoke activation of certain STATs that somehow promote viral pathogenesis. In this review, recent progress in our understanding of the virus-induced IFN-independent STAT signaling and its potential roles in viral induced inflammation and pathogenesis are summarized in detail, and perspectives are provided.
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    Kale Attenuates Inflammation and Modulates Gut Microbial Composition and Function in C57BL/6J Mice with Diet-Induced Obesity
    (MDPI, 2021-01-24) Shahinozzaman, Md; Raychaudhuri, Samnhita; Fan, Si; Obanda, Diana N.
    Kale (Brassica oleracea var. acephala) is a vegetable common in most cultures but is less studied as a functional food compared to other cruciferous vegetables, such as broccoli. We investigated the effect of supplementing a high-fat diet (HFD) with kale (HFKV) in C57BL/6J mice. We particularly explored its role in metabolic parameters, gut bacterial composition and diversity using 16S rRNA sequencing, systematically compared changes under each phylum and predicted the functional potential of the altered bacterial community using PICRUSt2. Like other cruciferous vegetables, kale attenuated HFD-induced inflammation. In addition, kale modulated HFD-induced changes in cecal microbiota composition. The HFD lowered bacterial diversity, increased the Firmicutes: Bacteroidetes (F/B) ratio and altered composition. Specifically, it lowered Actinobacteria and Bacteroidetes (Bacteroidia, Rikenellaceae and Prevotellaceae) but increased Firmicutes (mainly class Bacilli). Kale supplementation lowered the F/B ratio, increased both alpha and beta diversity and reduced class Bacilli and Erysipelotrichi but had no effect on Clostridia. Within Actinobacteria, HFKV particularly increased Coriobacteriales/Coriobacteriaceae about four-fold compared to the HFD (p < 0.05). Among Bacteroidia, HFKV increased the species Bacteroides thetaiotaomicron by over two-fold (p = 0.05) compared to the HFD. This species produces plant polysaccharide digesting enzymes. Compared to the HFD, kale supplementation enhanced several bacterial metabolic functions, including glycan degradation, thiamine metabolism and xenobiotic metabolism. Our findings provide evidence that kale is a functional food that modulates the microbiota and changes in inflammation phenotype.
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    Investigating genetic and health factors related to AA amyloidosis prevalence in captive cheetahs (Acinonyx jubatus): implications for population management
    (2014) Franklin, Ashley Danielle; Porter, Tom E; Crosier, Adrienne E; Animal Sciences; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    Systemic amyloid A (AA) amyloidosis is an increasingly important cause of morbidity and mortality among captive cheetahs, yet wild cheetahs are virtually unaffected, suggesting the phenomenon is a result of the captive condition. The self-aggregating AA protein responsible for this disease, is a byproduct of serum amyloid A (SAA) protein degradation, an acute phase protein highly upregulated during inflammation. The objective of this study was to identify the relationship between genetics, stress, and inflammation with serum concentrations of the SAA protein and the incidence of AA amyloidosis in captive cheetahs. Fecal and serum samples collected from cheetahs held at the Smithsonian (NZP-SCBI) and Cheetah Conservation Fund (CCF) facilities, as well as wild, free-ranging cheetahs, were examined. Enzyme-linked immunosorbent assays were used to measure SAA protein and proinflammatory cytokine concentrations in serum samples and cortisol concentrations in feces. Additionally, cheetahs were genotyped for the SAA1A-97delG single nucleotide polymorphism (SNP) in the promoter region of the SAA1 gene. This study was the first to demonstrate that serum concentrations of the SAA protein in cheetahs are affected by the SAA1A-97delG SNP (P=0.0453). However, the high prevalence of AA amyloidosis observed among captive cheetahs is not attributable to genetic differences at this locus, but rather appears to be related to stress and/or inflammation, as captive cheetahs at NZP-SCBI have significantly higher SAA protein concentrations in serum compared to captive cheetahs at CCF, regardless of genotype (P=0.0003). Captive cheetahs at NZP-SCBI show levels of stress (fecal cortisol concentrations) greater than their captive counterparts at CCF in Namibia. Interestingly, wild cheetahs and captive cheetahs at CCF in Namibia had significantly higher proinflammatory cytokine concentrations (TNF-α and IL-1β) in serum compared to cheetahs at NZP-SCBI (P<0.0001). It is possible that chronic stress may be suppressing the production of proinflammatory cytokines in the NZP-SCBI cheetah population. Controlling the currently high SAA protein concentrations associated with AA amyloidosis is the best strategy to decreasing the diseases prevalence among captive cheetahs. Promoting management practices that reduce stress could help re-establish proper immune system homeostasis and mitigate the overproduction of SAA protein, decreasing the probability of developing AA amyloidosis.
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    CD23 MEDIATED IGE TRANSCYTOSIS IN AIRWAY INFLAMMATION
    (2012) Palaniyandi, Senthilkumar; Zhu, Xiaoping; Veterinary Medical Science; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    CD23 (FceRII), a C-type lectin type II membrane glycoprotein, plays an important role in IgE homeostasis and development of allergic inflammation. I showed that CD23 was constitutively expressed in the established or primary human airway epithelial cells and its expression was significantly up-regulated by IL-4 stimulation. In a transcytosis assay, human IgE or IgE derived immune complex was transported and enhanced by IL-4 stimulation across a polarized Calu-3 monolayer. A CD23 specific antibody or soluble CD23 significantly reduced the transcytosis, suggesting a specific receptor-mediated transport by CD23. Transcytosis of both IgE and the immune complex was further verified in primary human airway epithelial cell monolayers. Furthermore, the transcytosed antigen-IgE complexes were competent in inducing degranulation of the cultured human mast cells. This study implies CD23-mediated IgE transcytosis in human airway epithelial cells may play a critical role in initiating and contributing to the perpetuation of airway allergic inflammation. To verify the above results in a mouse model, CD23 expression was detected in epithelial cells lining mouse airway and enhanced by IL-4 exposure as well as in ovalbumin (OVA) sensitized mouse. I showed that CD23 transported IgE and OVA-IgE derived immune complex across airway epithelial cells in wild-type, but not CD23 knockout (KO), mice. The chimeric CD23KO mice repopulated with wild-type myeloid cells, sensitized and challenged with OVA showed significant reduction in siglec-F+ cells, eosinophils, macrophages and IL-4 in bronchoalveolar lavage fluid recovered 24 hours later compared to the wild-type mice. Our finding of CD23-mediated IgE transport in airway epithelial cells suggest a possibility of CD23 transporting an IgE Fc-fused protein for immunotherapy. CTLA-4 (Cytotoxic T-Lymphocyte Antigen 4) which competitively binds CD80 and CD86 expressed on antigen presenting cells and inhibits CD28 mediated co-stimulation of T cell activation. A CTLA4-Fc (IgE) fusion protein produced in Chinese hamster ovary cells was intranasally administrated into mouse airway for assessing its specific transport by CD23. The effect of this fusion protein on the development of allergic inflammation is being fully investigated in wild-type, CD23-KO, and chimeric mouse model.
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    Effects of Diet and Weight Gain on Subcutaneous Body Fat Accretion Patterns and Adipocytokine Production in Thoroughbred Geldings
    (2007-05-08) Suagee, Jessica K; Burk, Amy O; Animal Sciences; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    Fifteen Thoroughbred geldings on an eight month weight gain study were used to evaluate 1) the effects of weight gain and diet on body area (neck, withers, shoulders, ribs, loin, tailhead) condition scores, and 2) the effects of weight gain, diet, and exercise on serum concentrations of tumor necrosis factor-α. The body condition scoring system developed in Quarter horse was slightly modified for use Thoroughbred geldings and involved developing prediction equations that utilized a smaller subset of the body areas. Horses at a BCS of 4 were found to be at a higher risk of inflammation that horses at a BCS of 7. The degree of inflammation was similar between horses fed either a high starch and sugar diet or high fiber and fat diet, indicated by similar TNF concentrations. Restricting daily exercise for two weeks was associated with increased inflammation.