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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

ROLE OF ACTIVATED MACROPHAGES AND PRO-INFLAMMATORY CYTOKINES IN PLACENTAL TROPHOBLAST INVASION AND FETAL OUTCOME

Renaud, STEPHEN 30 September 2008 (has links)
The invasion of trophoblast cells into the uterine wall is an essential component of normal human pregnancy. These trophoblast cells transform the uterine spiral arterioles into high-flow, low-resistance vessels that supply the placenta to support fetal growth and development. Inadequate trophoblast invasion and spiral arteriole remodelling may result in excessive placental pathology leading to pre-eclampsia and intra-uterine growth restriction (IUGR), which are major causes of maternal and fetal morbidity and mortality. These pregnancy complications have also been linked to an increased presence of pro-inflammatory cytokine-secreting (activated) macrophages at the fetal-maternal interface. In particular, increased production of tumour necrosis factor-alpha (TNF) by activated macrophages has been implicated as a causative factor mediating various pregnancy complications. Results from this thesis showed that macrophage-derived TNF decreased the invasiveness of trophoblast cells, primarily by affecting the urokinase system of plasminogen activators, a network of proteases that promotes cellular invasion. TNF also stimulated the production of macrophage chemoattractants by trophoblast cells, providing a putative mechanism for the aberrant recruitment and localization of macrophages in complicated pregnancies. Administration of lipopolysaccharide (LPS), a potent stimulator of macrophage activation and TNF production, to pregnant rats resulted in IUGR and fetal death correlating with significant placental pathology, including displaced endovascular trophoblast cells and increased fibrinoid and macrophage accumulation at the fetal-maternal interface. The immunoregulatory cytokine interleukin-10, which inhibited TNF production from macrophages after LPS-exposure, completely prevented the adverse effects of TNF in vitro and in vivo. Collectively, these findings show that the aberrant presence and localization of TNF-secreting macrophages may be involved in the etiology and pathophysiology of various pregnancy-related complications. / Thesis (Ph.D, Anatomy & Cell Biology) -- Queen's University, 2008-09-29 16:32:00.845
2

The Role of cIAP2 in Early and Late Atherosclerosis Lesion Development

Sleiman, Lyne 22 September 2011 (has links)
Cellular Inhibitor of Apoptosis 2 (cIAP2) belongs to the IAP family, a group of endogenous proteins that inhibit apoptosis. However, the physiological role of cIAP2 remains poorly defined. Knock-out (KO) and wild type (WT) mice were used to examine the effect of cIAP2 protein on the progression of atherosclerosis in apoE -/- mice. Following the high-fat diet period of 4 and 12 wks, tissues were harvested and analysis focused on the aortic root, the aortic arch, the descending aorta, and the blood. Ex vivo results show a significant decrease in aortic arch lesion area in KO vs. WT in both study groups. Results also show a decrease in aortic root lesion size in KO vs. WT in both study groups. These results support that cIAP2 is an important survival factor for lesion-associated macrophages, since loss of cIAP2 expression in this mouse model reduced atherosclerotic lesion development.
3

Melano-macrophage characterization and their possible role in the goldfish (Carassius auratus) antibody affinity maturation

Diaz Satizabal, Laura P Unknown Date
No description available.
4

Transcriptional control of macrophage function in the pig and its relationship to infectious disease susceptibility

Fairbairn, Lynsey January 2012 (has links)
The biology of cells of the mononuclear phagocyte system has been studied extensively in the mouse. Studies of the pig as an experimental model have commonly been consigned to specialist animal science journals. This thesis considered some of the many ways that pigs may address the shortcomings of mice as models for the study of macrophage differentiation and activation in vitro, and the biology of sepsis and other pathologies in the living animal. Flow cytometry was used initially to phenotype cells from the porcine lung, peritoneal cavity, blood and bone marrow using the LPS receptor CD14 and the FC receptor CD16, markers frequently employed to differentiate human monocytes into subsets. The expression of SIRP-alpha (SWC3a, CD172a), which is present on all cells of myeloid origin, and the haemoglobin scavenger receptor, CD163 which has previously been used to study monocyte differentiation in the pig was also studied. The findings validated previous work where blood monocytes were divided into subsets on the expression of CD14 and CD163. Furthermore, like human and mouse, pig monocytes also exhibited variation in CD16 expression, having a subset which was CD14hiCD16lo and another which was CD14loCD16hi. A whole genome approach was then used to study the differences between the monocyte subsets in the pig, using monocytes sorted into two populations based on the expression of CD14 and CD163. The gene expression profiles obtained were then compared to publically available data from monocyte subsets in human and mouse. This thesis also investigated the expression of genes that are known to be differentially expressed between human and mouse. To do this gene expression in porcine bone marrow derived macrophages was analyzed across an LPS time course. Like human macrophages, pig macrophages did not induce nitric oxide nor any arginine metabolizing genes in response to LPS. Instead they responded with robust induction of indoleamine 2,3-dioxygenase (IDO) and other enzymes of the tryptophan metabolism pathway such as kynurenine hydroxylase, kynureninase and tryptophan-tRNA synthetase. The tryptophan metabolism pathway has been implicated in sepsis in man and the absence of this pathway in the mouse may be one of the reasons why an adequate rodent model of sepsis has not been developed. The IDO inhibitor 1-methyl-tryptophan (1-MT) has been used to treat mouse macrophages where it had a protective effect after LPS administration. Similar experiments on pig macrophages did not show the same protective effect and induction of key immune genes was increased after treatment with 1-MT suggesting IDO is involved in feedback control of the immune system. With the completion of the genome sequence and the characterisation of many key regulators and markers, the pig has emerged as a tractable model of human innate immunity and disease that should address the limited predictive value of rodents in preclinical studies. This project aimed to address the gap in our knowledge of the control of innate immunity in the pig and provided further evidence that the pig can function as an ideal model to study innate immunity.
5

Modulation of human monocyte/macrophages in vitro by interferons and other agents

Mokoena, T. R. January 1986 (has links)
No description available.
6

Macrophage membrane glycoproteins defined by wheat germ agglutinin

Rabinowitz, S. S. January 1988 (has links)
No description available.
7

Pulmonary intravascular macrophages in the rabbit

Duke, Tanya 24 February 2010
Pulmonary intravascular macrophages (PIMs) promote lung inflammation and are found in ruminants, horses, pigs, cats, and dolphins, but not in primates, rats and mice. Rabbits are used to study mechanisms of lung inflammation in humans, but disagreement exists whether rabbits have PIMs. This study examined rabbits for PIMs, and their influence on endotoxin-induced lung inflammation.<p> Rabbits were treated with gadolinium chloride (10 mg/kg intravenous: Group GC, n=6) to produce apoptosis in PIMs, or with saline (Group SAL, n=6). Rabbits were euthanized 48 hours later. Light microscopic examination of epoxy-embedded rabbit lung sections revealed mononuclear phagocytes in alveolar septa. Transmission electron microscopy confirmed PIMs with lysosomes and close attachment to capillary endothelium. Light microscopic immuno-cytochemistry using rabbit anti-macrophage antibody (RAM-11) showed staining of septal and alveolar macrophages. There was no difference in number of RAM-11 positive septal cells between SAL and GC rabbits (P=0.2).<p> Rabbits were administered intravenous E.coli 0127:B8 endotoxin (100 Ýg/kg) 48 hours after GC (GC-LPS; n=5) or SAL treatment (SAL-LPS; n=6), and euthanized 24 hours later. Rabbits in both LPS treated groups were hypocalcaemic and exhibited compensated metabolic acidosis compared to SAL rabbits. Four rabbits died in the SAL-LPS group within 24 hours of the endotoxin treatment and were replaced. None died in the GC-LPS group (Chi-square comparison for survival P=0.063). Greater numbers of septal heterophils were found in groups SAL-LPS and GC-LPS compared to SAL and GC. TNFÑ protein in serum, and IL-1Ò and IL-6 mRNA in lung tissues were increased in SAL-LPS compared to SAL and GC rabbits. Lung tissues from SAL-LPS rabbits but not in GC-LPS showed moderate inflammation, but lung wet/dry ratios were not different. Lung tissue TNFÑ, IL-1Ònand IL-6 mRNA, myeloperoxidase activity, and serum TNFÑ were reduced in GC-LPS animals compared to SAL-LPS. Immuno-electron microscopy revealed TNFÑ in PIMs in normal and LPS-treated rabbits. Lung and liver tissue TNFÑ, IL-8 and MCP-1 protein concentrations were not different between groups. GC did not appear to reduce liver inflammation. These data show that rabbits have low numbers of PIMs. GC treatment induced apoptosis in PIMs and reduced endotoxin-induced lung inflammation and mortality.
8

<i>Lactobacillus plantarum</i> CONDITIONED MEDIA REDUCES THE SEVERITY OF COLITIS AND INDUCES A SHIFT IN MACROPHAGE PHENOTYPE

TAYLOR, MICHELLE MARIE 29 September 2011 (has links)
Lactobacillus plantarum is known to reduce the inflammatory response of macrophages in vitro and decrease inflammation in vivo during colitis. A predominance of M2, anti-inflammatory, macrophages correlates with a reduced severity of colitis. The purpose of this study was to determine if L. plantarum-conditioned media is able to produce an anti-inflammatory macrophage response during Salmonella-induced colitis while also reducing inflammation. Female C57BL/6 mice were infected with Salmonella after streptomycin pretreatment, then gavaged with L. plantarum-conditioned media (or a control) four hours prior to infection and twenty-four hours post-infection, they were sacrificed forty-eight hours post-infection. Samples of the intestines, blood, peritoneal exudate macrophages, spleen derived macrophages, and bone marrow-derived macrophages were collected. L. plantarum-conditioned media was found to limit inflammation in a dose related manner. Inflammation was measured by cecum histology, myeloperoxidase activity in the intestine, and monocyte chemoattractant protein-1 levels in the blood. IκB-α levels in the intestinal epithelium were measured by Western blot and degradation was reduced by L. plantarum-conditioned media treatment of Salmonella infected mice. Macrophages from L. plantarum-conditioned media treated Salmonella infected mice were found to have an M2 phenotype that was not found in any other treatment group. The phenotype markers arginase-1 and Ym-1 were found to be elevated in L. plantarum-conditioned media treated Salmonella infected mice by Western blot, while Src homology 2-containing inositol phosphatase-1 was reduced. Flow cytometry for the M2 markers CD206 and CD14 along with the M1 markers CD16 and CCR7 showed a similar M2 phenotype shift of macrophages from L. plantarum-conditioned media treated Salmonella infected mice. The cytokine profile of macrophages from L. plantarum-conditioned media treated Salmonella infected mice was anti-inflammatory with elevated IL-10 and decreased IL-6, IL-12, and TNF-α supporting the M2 phenotype. The protective effects of L. plantarum-conditioned media were found to be at least partially macrophage dependent in a macrophage transfer experiment. In vitro, L. plantarum-conditioned media was also found to produce M2 phenotype macrophages but have no effect on phagocytic or bactericidal function. In conclusion, L. plantarum-conditioned media provides a novel means of producing an anti-inflammatory immune response during Salmonella infection without compromising the host’s ability to combat infection. / Thesis (Master, Microbiology & Immunology) -- Queen's University, 2011-09-29 10:07:20.666
9

The Role of cIAP2 in Early and Late Atherosclerosis Lesion Development

Sleiman, Lyne 22 September 2011 (has links)
Cellular Inhibitor of Apoptosis 2 (cIAP2) belongs to the IAP family, a group of endogenous proteins that inhibit apoptosis. However, the physiological role of cIAP2 remains poorly defined. Knock-out (KO) and wild type (WT) mice were used to examine the effect of cIAP2 protein on the progression of atherosclerosis in apoE -/- mice. Following the high-fat diet period of 4 and 12 wks, tissues were harvested and analysis focused on the aortic root, the aortic arch, the descending aorta, and the blood. Ex vivo results show a significant decrease in aortic arch lesion area in KO vs. WT in both study groups. Results also show a decrease in aortic root lesion size in KO vs. WT in both study groups. These results support that cIAP2 is an important survival factor for lesion-associated macrophages, since loss of cIAP2 expression in this mouse model reduced atherosclerotic lesion development.
10

The Role of cIAP2 in Early and Late Atherosclerosis Lesion Development

Sleiman, Lyne 22 September 2011 (has links)
Cellular Inhibitor of Apoptosis 2 (cIAP2) belongs to the IAP family, a group of endogenous proteins that inhibit apoptosis. However, the physiological role of cIAP2 remains poorly defined. Knock-out (KO) and wild type (WT) mice were used to examine the effect of cIAP2 protein on the progression of atherosclerosis in apoE -/- mice. Following the high-fat diet period of 4 and 12 wks, tissues were harvested and analysis focused on the aortic root, the aortic arch, the descending aorta, and the blood. Ex vivo results show a significant decrease in aortic arch lesion area in KO vs. WT in both study groups. Results also show a decrease in aortic root lesion size in KO vs. WT in both study groups. These results support that cIAP2 is an important survival factor for lesion-associated macrophages, since loss of cIAP2 expression in this mouse model reduced atherosclerotic lesion development.

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