Functional Characterization of the Avian Inflammatory Mediators Nod1, MIF and IL-22

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dc.contributor.authorKim, Sungwonen
dc.contributor.committeechairDalloul, Rami A.en
dc.contributor.committeememberMcElroy, Audrey P.en
dc.contributor.committeememberMiska, Kate B.en
dc.contributor.committeememberWong, Eric A.en
dc.contributor.committeememberLi, Liwuen
dc.contributor.committeememberKeeler, Calvin L.en
dc.contributor.departmentAnimal and Poultry Sciencesen
dc.date.accessioned2017-04-06T15:44:00Zen
dc.date.adate2011-10-31en
dc.date.available2017-04-06T15:44:00Zen
dc.date.issued2011-09-16en
dc.date.rdate2016-10-04en
dc.date.sdate2011-09-30en
dc.description.abstractInflammation can be initiated by an innate immune sensor, followed by activation of a signal mediator, resulting in control of immune response by a signal regulator. Mammalian nucleotide-binding oligomerization domain protein 1 (Nod1) and Nod2 initiate host innate immune response by recognition of specific bacterial molecules, resulting in the production of pro-inflammatory cytokines, chemokines, and anti-microbial peptides. A candidate sequence of chicken Nod1 (ChNod1) was identified with no current evidence of ChNod2. Stimulation of transiently overexpressed ChNod1 and its mutants with mammalian Nod-specific ligands was not conclusive of the function of ChNod1 most likely due to self-activation of ChNod1. In vitro studies showed no significant difference in expression of Nod1, its signaling molecules and pro-inflammatory cytokines in stimulated chicken mononuclear cells with synthetic ligands for mammalian Nod1 or Nod2. A signal mediator, macrophage migration inhibitory factor (MIF) inhibits the random migration of macrophages. Chemotaxis assay using recombinant ChMIF (rChMIF) revealed a substantial decrease in migration of macrophages. qRT-PCR analysis revealed that the presence of rChMIF enhanced levels of IL-1β and iNOS during monocytes stimulation with LPS. Additionally, Con A-stimulated lymphocytes exhibited enhanced IFN-γ and IL-2 transcripts in the presence of rChMIF. IL-22, which may act as a signal regulator, is an important effector of activated Th1 and Th17 as well as natural killer cells during inflammation. Recombinant ChIL-22 alone did not have an impact on chicken embryo kidney epithelial cells (CKECs); however, co-stimulation of CKECs with LPS and rChIL-22 enhanced the production of pro-inflammatory cytokines and anti-microbial peptides. Furthermore, rChIL-22 alone stimulated acute phase reactants in chicken embryo liver cells. These effects of rChIL-22 were abolished by addition of rChIL22 binding protein. Taken together, these results indicate an important role of ChIL-22 on epithelial cells and hepatocytes during inflammation. In this project, we identified and characterized the avian inflammatory mediators ChNod1, ChMIF, and ChIL-22. Studying each of their biological function in avian inflammation, especially under pathogenic challenges in epithelial tissues will provide a foundation for understanding the role of these inflammatory mediators in mucosal immunity.en
dc.description.degreePh. D.en
dc.identifier.otheretd-09302011-113316en
dc.identifier.sourceurlhttp://scholar.lib.vt.edu/theses/available/etd-09302011-113316/en
dc.identifier.urihttp://hdl.handle.net/10919/77232en
dc.language.isoen_USen
dc.publisherVirginia Techen
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subjectNod1en
dc.subjectMIFen
dc.subjectIL-22en
dc.subjectinflammationen
dc.subjectcytokinesen
dc.titleFunctional Characterization of the Avian Inflammatory Mediators Nod1, MIF and IL-22en
dc.typeDissertationen
dc.type.dcmitypeTexten
thesis.degree.disciplineAnimal and Poultry Sciencesen
thesis.degree.grantorVirginia Polytechnic Institute and State Universityen
thesis.degree.leveldoctoralen
thesis.degree.namePh. D.en

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