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Macrophage activation plays a crucial role in regulating adipose tissue inflammation and is a major contributor to the pathogenesis of obesity-associated cardiovascular diseases. On various types of stimuli, macrophages respond with either classic (M1) or alternative (M2) activation. M1- and M2-mediated signaling pathways and corresponding cytokine production profiles are not completely understood. The discovery of microRNAs provides a new opportunity to understand this complicated but crucial network for macrophage activation and adipose tissue function. We have examined the activity of microRNA-223 (miR-223) and its role in controlling macrophage functions in adipose tissue inflammation and systemic insulinresistance. miR-223-/- mice on a high-fat diet exhibited an increased severity of systemic insulin resistance compared with wild-type mice that was accompanied by a marked increase in adipose tissue inflammation. The specific regulatory effects of miR-223 in myeloid cell-mediated regulation of adipose tissue inflammation and insulin resistance were then confirmed by transplantation analysis. Moreover, using bone marrow-derived macrophages, we demonstrated that miR-223 is a novel regulator of macrophage polarization, which suppresses classic pro-inflammatory pathways and enhances the alternative anti-inflammatory responses. In addition, we identified Pknox1 as a genuine miR-223 target gene and an essential regulator for macrophage polarization. For the first time, this study demonstrates that miR-223 acts to inhibit Pknox 1,suppressing pro-inflammatory activation of macrophages; thus, it is a crucial regulator of macrophage polarization and protects against diet-induced adipose tissue inflammatory response and systemic insulin resistance.

Some mounted ill. / Bibliography: leaves 197-226 / xiv, 226, [137] leaves : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Clinical and Experimental Pharmacology, 1987

Research Doctorate - Doctor of Philosophy (PhD) / In Western society, increased asthma prevalence over recent years has coincided with changes in dietary patterns, leading to the hypothesis that a Western diet increases susceptibility to asthma. Components of the diet that may be important are antioxidants (e.g. lycopene) and fatty acids. Lycopene and long chain n-3 polyunsaturated fatty acids (LCn-3PUFA) including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have anti-inflammatory effects. As asthma is a disease linked to oxidative stress and inflammation, it was hypothesised that these nutrients may have a beneficial effect individually, and may have a synergistic anti-inflammatory effect when used in combination. The aim was to examine the ability of lycopene and/or LCn-3PUFAs to protect against virus-induced inflammation, as rhinovirus infection is the primary cause of asthma exacerbation. The results presented demonstrate that both lycopene and DHA (but not EPA) individually decreased the inflammatory response of airway epithelial cells infected with rhinovirus. The results also showed that DHA supplementation increased the utilization of lycopene by cells. Furthermore, lycopene reduced rhinovirus replication. A combination of lycopene and DHA also reduced the inflammatory response of cells to rhinovirus infection, however, no synergistic anti-inflammatory effect was apparent. It is concluded that consumption of foods containing lycopene and DHA may exhibit a beneficial effect on the inflammatory response to rhinovirus infection. This may have important clinical implications, as increased dietary intake of foods rich in these nutrients may lead to a reduction in the frequency and severity of asthma exacerbations.

Diss. (sammanfattning) Göteborg : Göteborgs universitet, 2007. / Härtill 3 uppsatser.

Thesis (Ph. D.)--Dept. of Medicine, University of Adelaide, 1990. / Typescript (Photocopy). Includes bibliographical references (leaves 202-281).

Diss. (sammanfattning) Göteborg : Univ. , 2007. / Härtill 4 uppsatser.

Thesis (M.Sc.). / Written for the Dept. of Neurology and Neurosurgery. Title from title page of PDF (viewed 2008/12/07). Includes bibliographical references.

Thesis (Ph.D.) - University of Glasgow, 2008. / Ph.D. thesis submitted to the Division of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, University of Glasgow, 2008. Includes bibliographical references. Print version also available.

Thesis (M.S.)--Cleveland State University, 2008. / Abstracts. Title from PDF t.p. (viewed on Jan. 29, 2009). Includes bibliographical references (p. 33-36). Available online via the OhioLINK ETD Center. Also available in print.